Term
| What are the three configurations of neurons? |
|
Definition
bipolar=single dendrite and single axon (retina)
pseudo-unipolar (DRG)- has two axons and no dendrite
multipolar neurons-short dendrites, long and dendrites with many spines |
|
|
Term
| What kind of microtubule associated proteins are found in the different parts of the neuron |
|
Definition
dendrite-MAP2
axon-MAP Tau |
|
|
Term
| How is polysome protein synthesis different from endoplasmic reticulum protein synthesis? |
|
Definition
polysome- free ribosomes on a single mRNA, synthesis of cytoplasmic proteins
ER- ribosomes on membrane of ER. transmembrane or vesicle proteins |
|
|
Term
| Where are neurotransmitters formed and what kind of vesicles are they found in? |
|
Definition
synthesized in presynaptic terminal by enzymes via modification of a single enzyme.
found in small clear vesicle.
released only in presynaptic terminal and have a rapid response. |
|
|
Term
| Where are neuropeptides found and how are they synthesized? |
|
Definition
synthesized in soma on ribosomes via addition of a peptide bond to multiple amino acids.
found in large dense core vesciles
released at presynaptic terminals and along axons.
slow and long lasting response |
|
|
Term
| What form of secretion do synaptic vesicles use? |
|
Definition
Regulated secretion (as opposed to constitutive).
Synaptic vesicles are only found at axon terminals. |
|
|
Term
| What two molecule motors move along microtubules and in which directions? |
|
Definition
Kinesin-minus
Dynein- positive |
|
|
Term
| what is the function of intermediate filaments? What is their structure? |
|
Definition
strong rope-like proteins that resist stretch.
twisted monomers form dimers, then tetramers (protofilaments). protofilaments form a profibril which form a filament. each filament=32 monomers. |
|
|
Term
| What are the two intermediate filament types unique to nervous system cells? |
|
Definition
Glial fibrillary acidic protein: astrocytes and nonmyelinating schwann cells
Neurofilament (NF)- most neurons and not other cell types |
|
|
Term
| What are the three types of axonal transport? What do they transport? |
|
Definition
rapid anterograde: 200-400mm per day toward terminal- neuropeptides, neurotransmitters in vesicles, mitochondria and transmembrane proteins.
rapid retrograde 100-200mm per day toward cell body-membrane bound organelles, prelysomal vesicles, multivesicular bodies, recycled proteins
slow anterograde 1-2mm per day toward terminal: bulk flow cytoskeletal and cytoplasmic elements (eg actin, microtubules, clathrin) |
|
|
Term
| How does herpes zoster spread to the skin? |
|
Definition
| primary sensory neurons are infected with virus. virus produced in the soma is spread by rapid anterograde axonal transport to the ending in the skin. The skin in the infected area becomes painful, red with blisters and distribution follows the infected dorsal root ganglion. |
|
|
Term
| How is rabies transfered from bite to neuron body? |
|
Definition
| retrograde axonal transport. time required for transport back to soma is the incubation period. |
|
|
Term
| In a psuedounipolar neuron, where is the initial segment found? |
|
Definition
| because the sensory receptor is electronic, the initial segment is right behind the sensory modality. |
|
|
Term
| Why is a synapse described as having rectifier function? |
|
Definition
| action potential arrives, converts electrical activity to chemical then back to electrical. only travels in one direction. |
|
|
Term
| What are polysomes? What do they synthesize? |
|
Definition
| Polysomes are ribosomes that synthesize soluble or non-membrane proteins |
|
|
Term
| What is the morphology of an excitatory synapse and where are they found? |
|
Definition
| round, prominent dense presynaptic projections, wide synaptic cleft and thick postsynaptic density. found on dendrites and dendritic spines |
|
|
Term
| what is the morphology of inhibitory synapses and where are they found? |
|
Definition
| flattened synaptic vesicles, reduced dense presynaptic projections, narrow synaptic cleft and thin postsynaptic density. tend to be found on cell bodies |
|
|
Term
| During the spinal stretch reflex of the patellar tendon, how is the flexor inhibited? |
|
Definition
| The primary afferent fiber simultaneously excites an interneuron in the spinal cord that then inhibits any excitatory action of the flexor motor neuron i.e. the biceps |
|
|
Term
| How does the presynaptic sorting compartment receive vesicles and where does it send vesicles to? |
|
Definition
From: 1. cell body (rapid anterograde axonal transport) 2. synaptic vesicle recycling from terminal endocytosis
Sends: 1. synaptic vesicle pool 2. retrograde axonal transport |
|
|
Term
| How are synaptic vesicles loaded with neurotransmitter? |
|
Definition
| After budding from the PSC, a proton pump pumps hydrogen into the vesicle and uses ATP in the process. The pH in the vesicle drops and neurotransmitter is transported into the vesicle by an H+ exchange transporter specific for each class of neurotransmitter. |
|
|
Term
| How are synaptic vesicles addded to the pool of vesicles? |
|
Definition
| -attach to actin filaments which are attached to presynaptic dense projections. -synapsin I will attach the vesicle to the actin only when it is not phosphorylated. -enzyme CAM kinase II is activated by Ca++ and phosphorylates synapsin I. |
|
|
Term
| When an action potential arrives at a synapse, it triggers voltage gated Ca++ channels. What cascade of effects does this have? |
|
Definition
Ca++ activates CAM kinase II. CAM kinase II phosphorylates synapsin I. Phosphorylated synapsin releases vesicles from actin.
Ca++ also binds to synaptotagmin. This leads to the Core Complex finishing its twisting(with release of synaptotagmin); bringing the vesicle membrane into contact with the plasma membrane. |
|
|
Term
| How does docking at the plasma membrane of the synaptic vesicle occur? |
|
Definition
| Synaptic vesicle approaches the membrane and fits between presynaptic dense projections. Core Complex is formed by binding of synaptobrevin(on vesicle) with SNAP25 and syntaxin(on synapse membrane) |
|
|
Term
| How is the synaptic vesicle primed? |
|
Definition
| priming involves the addition of synaptogamin to the Core Complex. When these proteins are present the vesicle is primed and able to release neurotransmitter |
|
|
Term
| how is a synaptic vesicle recycled? |
|
Definition
| The patch of membrane is recycled into the presynaptic terminal via endocytotic mechanism involving AP2, clathrin and dynamin. This patch of membrane is defined by synaptotagmin. |
|
|
Term
| What are the ways neurotransmitter is inactivated after "use"? |
|
Definition
| 1. Diffusion 2. Taken into the presynaptic terminal by transmitter specific transporters. |
|
|
Term
| How is the uptake of neurotransmitter different in neuromuscular junctions? |
|
Definition
| NMJs does not use uptake to inactivate ACh. In the cleft there is acetylcholinesterase that breaks down ACh to choline and acetate. Choline is the molecule taken back up into the presynaptic terminal. |
|
|
Term
| What is the mechanism of action of botulism toxin? |
|
Definition
| Digests synaptobrevin, SNAP-25 and syntaxin in NMJs. This prevents vesicle exocytosis leading to flaccid paralysis and retraction of the presynaptic terminal. |
|
|
Term
| What is the mechanism of tetanus toxin? |
|
Definition
| tetanus toxin binds the presynaptic terminal at the NMJ. It is taken up by vesicles and transported retrogradely. It is released in the CNS on inhibitory interneurons. This inhibits the release of inhibitory neurotransmitters leading to spastic paralysis. |
|
|
Term
| What is Myasthenia gravis caused by? How can it be treated? |
|
Definition
| It is an autoimmune disease where antibodies are produced to the ACh receptor. This leads to fewer than normal receptors and droopy eyelid. Tx: plasmapheresis of antibodies or cholinesterase inhibitors which enhance ACh lifetime to improve muscle contraction and strength. |
|
|
Term
|
Definition
| psychiatric disorders except personality disorders and mental retardation |
|
|
Term
|
Definition
| personality disorders and mental retardation |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| global assessment of functioning 0-100 |
|
|
Term
|
Definition
| unpleasant feelings of sadness, depression or anger (mood) |
|
|
Term
|
Definition
|
|
Term
| What are some advantages of MRI over CT? |
|
Definition
-better contrast between gray and white matter
-superior visualization of posterior fossa
-better visualization of spinal cord
-more sensitive for demyelination, edema, stroke and tumor
-contrast agent well tolerated compared with iodinated contrast. |
|
|
Term
| What are some disadvantages of MRI over CT? |
|
Definition
-cost
-can't use with metal objects
-obesity/clasutrophobia |
|
|
Term
|
Definition
| injection of contrast dye into subarachnoid space to outline cords and roots. |
|
|
Term
| What are some of the contraindications for lumbar puncture? |
|
Definition
1. intracranial mass lesions
2. coagulopathy
3. compression of spinal cord lesions
4. infection of skin or sequamous tissue at LP site. |
|
|
Term
| What is basic lumbar puncture technique? |
|
Definition
| 1. lateral decubitus, spine flexed. 2. L3-L5 at level of iliac crest. 3. prep and rape 4. lidocaine 5. insert slowly until "pop" |
|
|
Term
| what are the normal lab values for CSF of WBC, RBC, glucose and protein? |
|
Definition
| pressure <180mm WBC <5/ul RBC=either hemorrhage or traumatic tap differentiate by RBC tube clearance, xanthochromia, ratio of WBC to RBC (1:700) protin <45mg/dl glucose 60-80% of serum glucose. if otherwise indicates meningitis or inflammation |
|
|
Term
| what does an increase in oligoclonal bands in the CSF indicate? |
|
Definition
| abnormal immune activation i.e. MS |
|
|
Term
| What are the three methods for blood vessel evaluation? |
|
Definition
| 1. carotid ultrasound 2. cerebral angiography 3. MR angiography |
|
|
Term
| what does elevated total protein in the CSF indicate? |
|
Definition
|
|
Term
| What are the four different types of electrophysiological studies? |
|
Definition
| 1. EEG electroencephalography, records electrical activity through scalp electrodes. 2. EP evoked potential- recording of electrical activity in response to appropriate stimuli in specific afferent pathways. 3. Electromyography EMG, assessment of electrical activity within discrete region of muscle. (needle in muscle). normally quiet during rest, denervated muscle is irritable and shows fibrillation potentials. 4. Nerve conduction studies. |
|
|
Term
| What would you expect to see for a nerve conduction study in a demyleinating neuropathy vs axonal neuropathy? |
|
Definition
| demylinateing neuropathy- conduction velocity is slowed and conduction block may occur. axonal neuropathy-conduction velocity is normal but nerve action potentials are smaller in amplitude. |
|
|
Term
|
Definition
| tumors, HSV, abcess or encephalitis |
|
|
Term
|
Definition
| vasculitis, sarcoidosis, metabolic storage disease |
|
|
Term
|
Definition
| inflammatory myopathies such as polymyositis and dystrophies |
|
|
Term
|
Definition
| Failure of anterior end of neural tube to close. Rarely survives more than a few hours. Associated with raised alpha fetoprotein levels. Cranial vault is missing and base of skull is flat. |
|
|
Term
| What are the 3 major periods of development? |
|
Definition
| neural tube formation: 4th week segmentation and cleavage: 8th week proliferation and migration: 8 weeks to birth |
|
|
Term
| What is myelomeningocele? |
|
Definition
failure of posterior end of neural tube to close. There is herniation of both meninges and spinal cord through vertebral defect. Cystic mass covered by a delicate membrane or skin OR open lesion with mass of vascular connective and neural tissue.
associated with maternal alpha fetoprotein |
|
|
Term
|
Definition
| mesodermal defect with herniation of brain tissue through a midline defect in the cranial cavity. often located in occipital or posterior fossa region. can be frontal. fluctant mass covered by skin. contain jumbled fragments of neural tissue in small lesions. large encephaloceles can contain large portions of cerebral hemisphere leaving intracranial contents skewed |
|
|
Term
| What are the different categories of developmental abnormaility? |
|
Definition
| 1. neural tube defects 2. disturbances of cleavage 3. disorders of neuronal migration 4. misc 5. posterior fossa abnormalities 6. perinatal damage |
|
|
Term
| What is holoprosencephaly? What it is a disorder of? |
|
Definition
| disorder of cleavage- failure in outgrowth/cleavage of prosencephalic vesicle. incomplete seperation of cerebral hemispheres across the midline. single ventricle with fused basal ganglia. associated with trisomy 13 and 18. increased incidence with diabetes, rubella, toxo, fetal alcohol syndrome |
|
|
Term
|
Definition
| agenesis of olfactory bulbs, tracts and related structures. incidental or with holoprosencephaly. |
|
|
Term
|
Definition
| absence of gyri and sulci. results in a small brain with a smooth cerebral surface. |
|
|
Term
| What is pachy(macro)gyria? |
|
Definition
| reduced number of broad gyri. decreased number of neurons reaching the neocortex resulting in simplification of gyral folds. |
|
|
Term
|
Definition
| numerous, small irregularly formed thin gyri giving a cobblestone appearance. there is a loss of external contour of the convulations of the brain. associated with genetics, twinning, VZV, CMV, toxo and syphilis. |
|
|
Term
| What is microcephaly? What is it associated with? |
|
Definition
| abnormally small brain associtaed with fetal alcohol syndrome and viral infections. |
|
|
Term
| agenesis of corpus callosum is associated with what other conditions? |
|
Definition
| absence of white matter bundle connecting both hemispheres. sporadic or inherited. associated conditions are holoprosenchephaly, midline tumors. |
|
|
Term
|
Definition
| cerebral hemispheres largely absent, fluid filled cerebral cavity. associated with fetal hypoxia, maternal intoxication and twining. |
|
|
Term
| What is arnold-chiari malformation? |
|
Definition
| small posterior fossa with downward displacement of cerebellar tissue through foramen magnum. associated with hydrocephalus and lumbar meningomyelocele |
|
|
Term
| What are the two major causes of perinatal damage? |
|
Definition
| physical trauma and hypoxia |
|
|
Term
| what are the 3 patterns of perinatal damage |
|
Definition
| germinal matrix hemorrhage, periventricular leukomalacia and perinatal hypoxic injury |
|
|
Term
| what is germinal matrix hemorrhage? |
|
Definition
| associated with prematurity. hemorrhage may be localized or spread into ventricles or beyond. Due to hypoxia |
|
|
Term
| what is periventricular leukomalacia? |
|
Definition
| common in premature babies, usually hypotensive mechanism of injury, periventricular white matter necrosis and mineralization |
|
|
Term
|
Definition
| perinatal hypoxic injury which involves depths of sulci. may result in thinned out, mushroom shaped gyrus. |
|
|
Term
| what are some common causes of cerebral palsy? Is it a progressive disease? |
|
Definition
| neonatal hypoxia, trauma, kernicterus and neonatal meningitis. NO it is not a progressive disease. Mental retardation in 50% and seizures in 50% |
|
|
Term
List the following cells found in the brain by their sensitivity to hypoxia :
astrocytes, oligodendrocytes, neurons, mesodermal elements |
|
Definition
| 1.neuron 2.oligodendrocyte 3.astrocyte 4.mesodermal elements |
|
|
Term
| what are the general effects of hypoxia and ischemia? |
|
Definition
| 1. cerebral edema 2. microscopic brain damage resulting from decreased blood perfusion or decreased oxygenation |
|
|
Term
| how is ischemic cell damage/necrosis manifested histologically? |
|
Definition
| as red neurons. cytoplasm has increased eosinophilia and there is shrinkage. the nuclease is pyknotic or karyorrhectic. |
|
|
Term
| The neurons in which three areas of the brain are more susceptible to hypoxic/ischemic damage? |
|
Definition
| 1. segments of Ammon's horn ie. CA 1. CA 2 is the most resistant. 2. purkinje cells in the cerebellum 3. neurons of layers III and V of the cerebral cortex: this may appear as a laminar necrosis. |
|
|
Term
| besides ischemic damage, what 2 other types of reaction can neurons have? |
|
Definition
| 1. Central chromatolysis: reactions within the neuron after damage to the axons=swell with peripheral displacement of nucleus and dispersal of Nissl substance. 2. simple atrophy and neuronal degeneration |
|
|
Term
| what histological changes occur during reactive astrocytosis? |
|
Definition
| nuclear enlargement, eosinophillic cytoplasm-astrocytes are connected to each other to make a barrier to lesions. (reactive gliosis) |
|
|
Term
| what are the two categories of cerebral edema |
|
Definition
vasogenic- damage to epithelial cells: fluid leaks through damaged capillaries.
cytotoxic: metabolic derangement causes intracellular sodium and water accumuluation. edemia is usually a combo of both. |
|
|
Term
| What is a high intracranial pressure? |
|
Definition
|
|
Term
| what are the 4 causes of mass effect? |
|
Definition
| 1.edema 2. hemorrhage 3. tumor 4. increased volume of CSF |
|
|
Term
| what are the 3 types of brain herniation? |
|
Definition
| 1. transtentorial (Uncal) 2. subfalcine (cingulate gyrus) 3. cerebellar tonsillar (foraminal) |
|
|
Term
| where does a transtentorial herniation occur? what secondary affects can result? |
|
Definition
| medial temporal lobe herniates. results in hemiparesis, 3rd nerve compression, posterior cerebral artery compression. |
|
|
Term
| How does duret hemorrhage occur? |
|
Definition
| when an uncal herniation occurs, this can push the brainstem downards. since the basilar artery is in a fixed position, this can lead to all the pontine capillaries to be broken. |
|
|
Term
| where does cerebellar tonsillar herniation occur? |
|
Definition
| supratentorial or posterior fossa mass causes tonsils to push through the foramen magnum leading to coma and death. |
|
|
Term
| what complications can result from subfalcine herniation? |
|
Definition
| infarctions and corpus callosum damage. |
|
|
Term
| what are the two types of hydrocephalus? |
|
Definition
| non-communicating (no communication between ventricles and lumbar subarachnoid space). communicating-CSF flows between ventricles and lumbar subarachnoid space. |
|
|
Term
| How is ectoderm induced to produce neurons? |
|
Definition
| involuting mesodermal cells release molecules that block BMP signals between ectodermal cells. These molecules include CHORDIN AND NOGGIN |
|
|
Term
which end does the neural tube close first?
On what day does neural tube folding start and what day does it finish? |
|
Definition
| neural tube closes in the cervical region initially. The neural folds begin to fuse at the cerical level at around day 21. The rostral end closes day 24 and caudal end day 26 |
|
|
Term
| After neural tube closure there are floor plates formed. What are they and where are they found? What are their derivatives? |
|
Definition
floor plate-most ventral roof plate-most dorsal aspect
alar plate-more dorsal becomes dorsal horn, sensory nuclei in medulla and cerebellum
basal plate-becomes ventral horn and motor nuclei in medulla |
|
|
Term
| what is the sulcus limitans? |
|
Definition
| fissure between the alar and basal plates in of the neural tube |
|
|
Term
| Where do neuroepithelial cells go through M phase? |
|
Definition
| at the ventricular surface |
|
|
Term
| Describe how neuroepithelial cells migrate during proliferation |
|
Definition
| - The proliferating neural stem cells are in S-phase when the cell bodies are located in central region of the wall of the neural tube. -The stem cells then undergo mitosis at the ventricular surface. - When daughter cells exit the cell cycle and begin to differentiate as neurons, they migrate radially from the ventricular zone to the mantle zone. -The progenitor cells span the thickness of the neural tube, and their nuclei translocate to the mantle zone during the S-phase of the cell cycle. - The nuclei return to the ventricular surface during G2 and the M-phase of the cell cycle always occurs at the ventricular surface. |
|
|
Term
| How does sonic hedgehog influence the dorsal ventral patterning of the neural tube and where is it expressed? |
|
Definition
| expressed first in the notochord and later in the floor plate. induces ventral differentiation of neural tube. |
|
|
Term
| What induces dorsal differentiation of the neural tube and where is it produced? |
|
Definition
| BMPs expressed in the ectoderm overlying the neural tube and eventually in dorsal neural tube cells. |
|
|
Term
| what type of cells do gliablasts give rise to? |
|
Definition
| astrocytes, oligodendrocytes |
|
|
Term
| what do neuroepithelial cells give rise to? |
|
Definition
|
|
Term
| what type of cells does neural crest give rise to? |
|
Definition
| all neurons whose cell bodies are found outside the brain and spinal CNS. 1. cranial and spinal nerve ganglia 2. autonomic nervous system ganglia 3. enteric plexus in gut 4.adrenal medulla Also give rise to cells other than neurons: 1. schwann cells 2. melanocytes |
|
|
Term
| What are the three swellings of the neural tube that give rise to the general structure of the brain? |
|
Definition
| prosencephalon, mesencephalon and rhombencephalon |
|
|
Term
| what does prosencephalon give rise to? |
|
Definition
| diencephalon-thalamus telencephalon-cerebral hemisphere |
|
|
Term
| what does rhombencephalon give rise to? |
|
Definition
| myelencephalon-medulla metencephalon-pons and cerebellum |
|
|
Term
| how is cerebral cortex formed? |
|
Definition
| radial glial cells span the neuroepithelium. neurons migrate from the mantle layer into the marginal layer following the apical processes of the radial glia. |
|
|
Term
| How is the fourth ventricle formed? |
|
Definition
| the walls of the neural tube are spread apart by the pontine flexure so that they and the sulcus limitans become the floor of the ventricle and roof becomes a thin membrane. |
|
|
Term
| where do the precursors of the cerebellar granule cells come from? |
|
Definition
| a region of the rhombencephalon known as the rhombic lip |
|
|
Term
| during granule cell production, what is the order of migration of the neurons? |
|
Definition
| The opposite of cortex formation, granule cell layers from by neurons migrating from the external layer to the internal layers underneath the purkinje cells. |
|
|
Term
| When considering developmental abnormalities, what is the most important factor to take into consideration? |
|
Definition
| The timing of the insult, not the specific cause. Many agents can produce the same injury if damage occurs at a specific stage of developement |
|
|
Term
|
Definition
| general term for a neurologic disorder of the spinal cord. |
|
|
Term
| what are some of the etiologies for complete transverse lesions? |
|
Definition
| 1. spinal cord trauma 2. transverse myelitis 3. cord compression |
|
|
Term
| What is Brown-Sequard syndrome? |
|
Definition
| hemisection of the cord due to trauma, tumor or ischemia |
|
|
Term
| How does Brown-Sequard manifest? |
|
Definition
| sensory: loss of propioception/vibration ipsilateral. loss of pain/temperature contralateral. motor-ipsilateral paresis or plegia below the level of damage to the CST |
|
|
Term
| what is syringomyelia? What is the other etiology for central cord syndrome? |
|
Definition
central cord syndrome where there is loss of pain and temperature at the level of the lesion. depending on whether the lesion has extended outward to the corticospinal tracts, there can also be motor defecits.
Trauma |
|
|
Term
| what can a vitamin B12 deficiency cause? |
|
Definition
| subacute combined degeneration: degeneration of the posterior columns with prominent propioceptive loss and some degree of injury to descending corticospinal tracts. there is bilateral loss of vibration/propioception as well as bilateral paresis/plegia below level. |
|
|
Term
| which tracts does subactue combined degeneration involve? |
|
Definition
| posterior columns and descending corticospinal tract |
|
|
Term
| What is Tabes dorsalis and which tracts does it affect? |
|
Definition
| a form of tertiary neurosyphillis. causes injury to the posterior columns as well as the dorsal roots that carry sensory information to the spinal cord. Leads to sensory ataxia. There is bilateral loss of vibration/propioception especially in the legs. |
|
|
Term
| anterior spinal cord syndrome? |
|
Definition
| infarct, emboli to anterior spinal artery. causes loss of pain and temperature below level. vibration and propioception is preserved. tehre is bilateral paresis and plegia below the level however |
|
|
Term
| what is one cause of anterior spinal cord syndrome? |
|
Definition
| extended cross clamping of the aorta during vascular sugery. |
|
|
Term
| what is the difference in ion content between CSF and blood plasma? |
|
Definition
| higher levels of Cl-, Na+ and Mg and lower levels of K+, Ca++, glucose and protein |
|
|
Term
| Describe the order of flow for CSF |
|
Definition
| CSF is produced by the choroid plexus in the ventricles--> exits fourth ventricle via the foramina of luschka and Magendie to enter the subarachnoid space.--> absorbed into venous system at the arachnoid villi. |
|
|
Term
| What are the two categories of hydrocephalus? |
|
Definition
| obstructive and commmunicating |
|
|
Term
| what is an arnold chiari malformation? |
|
Definition
| malformation with downward displacement of cerebellar tonsils through the foramen magnum. may cause headache, swallowing difficulties and balance problems. |
|
|
Term
| what is dandy walker malformation? |
|
Definition
| malformation of the cerebellar vermis, cystic dilatation of the fourth ventricle and enlargement of the posterior fossa. |
|
|
Term
| what are common sites of obstruction that result in hydropcephalus? |
|
Definition
| intraventricular foramen, cerebral aqueduct, foramina of the fourth ventricle |
|
|
Term
| In adults and older children what are the signs and symptoms of hydrocephalus? |
|
Definition
| headache, nausea, vomiting, blurred double vision, eyes fixed downward, problems with balance coordination or gait. slowed developement and cognitive problems. urinary incontinence also common |
|
|
Term
| what symptoms can be seen in infants with hydrocephalus? |
|
Definition
| sunsetting eyes, vomiting, macrocephaly due to suture parting, seizures |
|
|
Term
| what are the two different treatment options for obstructive hydrocephalus? |
|
Definition
| excision or shunt placement |
|
|
Term
| communicating hydrocephalus is caused by malabsorbption or increased production of CSF...what are some etiologies? |
|
Definition
| congenital absence of arachnoid villi, high CSF protein (tumor or inflammatory response), hemorrhage into CSF, exceedingly high venous pressure |
|
|
Term
| what is the clinical triad for normal pressure hydrocephalus? |
|
Definition
|
|
Term
| what is the treatment for normal pressure hydrocephalus? |
|
Definition
| ventriculoperitoneal shunt placement |
|
|
Term
| normal pressure hydrocephalus |
|
Definition
| one of the potentially reversible causes of dementia |
|
|
Term
| idiopathic intracranial hypertension is associated with what things? |
|
Definition
| obesity in younger women, vit A toxicity, several drugs |
|
|
Term
| what is idiopathic intracranial hypertension? |
|
Definition
| increased CSF pressure with ventricular enlargement |
|
|
Term
| what is the treatment for idiopathic intracranial hypertension? |
|
Definition
| CSF drainage by lumbar puncture, acetazolamide to decrease CSF produciton, weight loss...or shunt. |
|
|
Term
|
Definition
| An individual's loss of contact with external reality |
|
|
Term
| What are the "positive" symptoms of schizophrenia? |
|
Definition
| delusions, hallucinations, disorganized speech, disorganized or catatonic behaviour |
|
|
Term
|
Definition
| a firmly held false belief outside of a patient's social context |
|
|
Term
| what can catatonic motor behavior range from? |
|
Definition
| complete unawareness of environment, rigid postures to purposeless agitation and excessive or repetitive motor activity. |
|
|
Term
| What are the negative symptoms for schizophrenia? |
|
Definition
| loss of affective responsiveness, verbal expression, personal motivation, social drive and attention to the environment |
|
|
Term
| What is the DSM-IV-TR criteria for schizophrenia? |
|
Definition
| at least 2 of the following for most of a 1 month period: 1)delusions 2)hallucinations 3) serious disorganized speech 4) grossly disorganzied or catatonic behavious 5) one or more negative symptoms: affective flattening, alogia or avolition OR if one of the A symptomes is really bad |
|
|
Term
| what are the BCDEF parts of the DSM-IV? |
|
Definition
| B. decline in functioning C. 6months of illness D. exclude other disorders. E. exclude general medical conditions F. exclude development disorders. |
|
|
Term
| what are the five types of schizophrenia |
|
Definition
| catatonic, disorganized, paranoid, undiffereniated type, residual type |
|
|
Term
|
Definition
| delirium is a syndrome of abnormal consciousness and is caused by an underlying medical problem. It always involves the impairment of conciousness. |
|
|
Term
| what is the dopamine hypothesis? |
|
Definition
| excessive dopamine activity in the limbic regions led to the psychotic states associated with schizophrenia. May be the end state of other possible mechanisms? |
|
|
Term
| what factors increase the hospitalization risk for schizophrenic people? |
|
Definition
| failure to take maintenance medication, exposure to life stresses, alcohol and illicit drug use. |
|
|
Term
| what neurobiologic abnormalities can be found in schizophrenics? |
|
Definition
| -loss of brain volume -smaller brains -decreased gray matter volume and density -enlarged cerebral ventricules -decreased hippocampal volume -decreased thalamic volume. |
|
|
Term
| What is the Weinberger or neurdevelopmental hypothesis of schizophrenia? |
|
Definition
| That abnormalities of early brain development increase the likelihood of eventual clinical symptoms. |
|
|
Term
| what foramen does the glossopharyngeal nerve exit? |
|
Definition
|
|
Term
| where do the motor fibers for the glossopharyngeal nerve originate? |
|
Definition
| inferior salivary nucleus: otic nucleus ambiguus: innervate stylopharyngeus |
|
|
Term
| where are the glossopharyngeal sensory fibers located? |
|
Definition
| 1. pinna and auditory canals: cell bodes in superior ganglion and terminate in spinal trigeminal nucleus 2. GVA from parotid gland, pharynx and carotid body 3. primary afferent GVA fibers carrying taste from posterior third of the tongue enter the solitary tract to the solitary nucleus. |
|
|
Term
| what does ipsilateral CN IX palsy cause? |
|
Definition
| ipsilateral loss of pharyngeal sensation i.e. decreased gag reflex. ipsilateral loss of pharyngeal taste and parotid gland secretion. rare: glossopharyngeal neuralgia |
|
|
Term
| Where do the general visceral efferent fibers of the vagus originate? somatic visceral efferent? |
|
Definition
GVE originates in dorsal motor nucleus of vagus: parasympathetic preganglionic fibers to trachea, bronchi heart etc
SVE nucleus ambiguus: pharyngeal constrictor muscles, laryngeal, palatine etc |
|
|
Term
| What are the general sensory afferent aspects of the vagus nerve? where are the cell bodies? |
|
Definition
| GSA fibers from small area of ear and external auditory meatus. cell bodies in superior ganglion that enter the spinal trigeminal tract |
|
|
Term
| what are the general visceral afferent aspects of vagus? where do they travel? |
|
Definition
| GVA from heart pharynx, larynx, lungs and gut via the solitary tract to the solitary nucleus |
|
|
Term
| special visceral afferent fibers for X. where from and where to? |
|
Definition
| taste for epiglottis and base of tongue, cells in inferior ganglion enter brainstem in vagus n. and join solitary tract to solitary nucleus. |
|
|
Term
| what occurs during an isolated CN X lesion? |
|
Definition
1. dysphagia due to unilateral paralysis of pharyngeal and laryngeal musculature. milk through nose!
2. dysarthria-weakness of laryngeal muscles and vocalis muscle
3. taste loss is not noticed by patient, nor is loss of sensation from small area of ear. |
|
|
Term
| injury to CN XI results in what? |
|
Definition
| ipsilateral weakness of shoulder elevation and impaired shoulder stability. |
|
|
Term
| what does a hypoglossal nerve lesion result in? |
|
Definition
| ipsilateral weakness and wasting of the tongue. causes dysphagia and dysarthria |
|
|
Term
| what cranial nerves pass through the jugular foramen? |
|
Definition
|
|
Term
| what are the symptoms of medial medullary syndrome? |
|
Definition
anterior spinal artery infarct:
1. right hypoglossal-right side of tongue paralysis
2. right pyramid- left sided hemiparesis
3. right medial lemniscus- left sided loss of propioception and vibration
ALTERNATING HEMIPLEGIA |
|
|
Term
| If there is occlusion of the smaller penetrating branches of PICA what type of lesion does this result in? |
|
Definition
| occlusion of PICA penetrating branches affects a smaller area of the medulla than a full PICA occlusion. It can affect the nucleus ambiguus-voluntary muscles of pharynx and larynx. also the ipsilateral lateral spinothalamic tract=pain and temperature on left side of body. |
|
|
Term
| what causes a lateral medullary lesion (wallenberg's) and what symptoms result? |
|
Definition
| occlusion of PICA causes stroke of dorsolateral medulla 1. inferior cerebellar peduncle-ipsilateral ataxia 2. nucleus ambiguus-ipsilateral paralysis of soft palate, pharynx and larynx 3. spinal nucleus and tract of CN V-loss of ipsilateral pain/temp on face 4. lateral spinothalmic tract-contralateral loss of pain/temp of trunk and limbs. 5. Ispilateral Horner's sydrome: sympathetic fibers: papillary constriction, ptosis and loss of sweating on half of face. 7. vestibular nuclei-mystagmus and vertigo. 8. vesitbular nucleus- vertigo |
|
|
Term
| which nerves are at the pontomedullary junction? |
|
Definition
|
|
Term
| what are some of the disease processes that affect CN VIII? |
|
Definition
| tumors, toxins(aminoglycoside antibiotics), trauma, infections and degenerative disorders |
|
|
Term
| what is the general sensory afferent component of the facial nerve and where are its cell bodies? |
|
Definition
| pinna and external auditory canal. cell bodies are in the geniculate ganglion |
|
|
Term
| what are the special visceral afferent components of the facial nerve and where is the nucleus? |
|
Definition
| taste from anterior 2/3 of tongue via lingual nerve and chorda tympani. travel from intermediate nerve to solitary tract and then nucleus solitarius |
|
|
Term
| what is the visceral motor component of the facial nerve? |
|
Definition
| preganglionic parasympathetic axons from the superior salivary nucleus got the the salivary and lacrimal glands, nasal mucosa |
|
|
Term
| What symptoms are there for a peripheral VII palsy? |
|
Definition
| 1. lower motor neuron palsy 2. hyperacusis due to paralysis of the stapedius muscle 3. loss of taste to anterior 2/3 of tongue 4. decreased secretion of tears and saliva. |
|
|
Term
|
Definition
| probably due to herpes simplex viral infection. lower motor neuron facial nerve inflammatory process. treated with prednisone and acyclovir |
|
|
Term
| what is Ramsay-Hunt syndrome |
|
Definition
| reactivated varicella infection with rash on ext auditory canal and auricle. |
|
|
Term
| what disease can affect CN VII bilaterally? |
|
Definition
|
|
Term
| what is the difference between a peripheral and central facial palsy? |
|
Definition
| peripheral-full face palsy central-spares forehead because upper part of the facial motor nucleus that serves the forehead muscles is innervated bilaterally by corticobulbar neurons. the lower facial motor neuron receives supranuclear input from only contralateral motor cortex |
|
|
Term
| which nerve nucleus does CN VII loop around? |
|
Definition
|
|
Term
| what has the longest intracranial course and what can it be injured by? |
|
Definition
| abducens and it can be injured by increased intracranial pressure. |
|
|
Term
| What is an etiology for abducens palsy? |
|
Definition
|
|
Term
| where are the cell bodies of all the sensory fibers for CN V located? except for which division? |
|
Definition
| the trigeminal ganglion expect for the mesecephalic nuclues=propioceptive fibers |
|
|
Term
| describe the path of CN V pain and temperature nerve fibers |
|
Definition
| enter the brainstem, turn caudally to form the spinal tract of the trigeminal nerve and terminate in the spinal nucleus of V. second order neurons cross to the opposite side of the pons and ascend as the ventral trigeminothalamic tract to the VPM. |
|
|
Term
| describe the path of tactile CN V fibers |
|
Definition
| trigeminal fibers project to principal sensory nucleus and rostral part of the nucleus of the spinal tract. these nuclei then send fibers across the midline to join the contralateral VTT. |
|
|
Term
| If there is a lesion in the lateral part of the medulla or lower pons, cause loss of pain and temperature sensation on which side of the face? |
|
Definition
| It would cause deficits on the ipsilateral side of the face but the contralateral side of the body. |
|
|
Term
| if there is a lesion in the upper pons or midbrain, which side of the face would have pain and temperature sensation loss? |
|
Definition
| the contralateral side of the face and contralateral side of the body |
|
|
Term
|
Definition
| trigeminal neuralgia with terrible lancinating pains brought on by minimal stimuli or occurring spontaneously |
|
|
Term
| which nerves will a cerebellopontine angle lesion possibly affect? |
|
Definition
| V, VI, VII, VIII and cerebellum. treat with surgery or gamma knife radiation |
|
|
Term
| what is the paramedian pontine reticular formation? |
|
Definition
| a pontine nucleus in charge of ipsilateral conjugate gaze. It is adjacent to the abducens nucleus. |
|
|
Term
| how is internuclear opthalmoplegia caused? |
|
Definition
| lesions of the median longitudinal fasiculus unyoke conjugate gaze. (paramedian pontine reticular formation sends signals to both VI and III(via MLF)) |
|
|
Term
| what is acoustic neuroma? |
|
Definition
| most common lesion of CPA region. arises from schwann cells in the sheath of nerve VIII near the attachment of the nerve to the brainstem. these benign tumors grow slowly compressing CN VIII with progressive hearing loss. nystagmus (vestibular nerve injury) eventual ataxia may occur due to compression of the cerebellar peduncles. |
|
|
Term
| How can lock in syndrome occur? |
|
Definition
| hemorrhage into base of pons causes bilateral paralysis of limbs, face, tongue etc. only movement preserved is vertical eye movements or sight blinking. |
|
|
Term
| lesions of the trochlear nerve cause what deficits? |
|
Definition
| inability for eye to rate downward and outward |
|
|
Term
| what is the viceral efferent aspect of CN III? |
|
Definition
| edinger westphal nucleus sends out preganglionic parasympathetic fibers to the ciliary ganglion. postganglionic fibers from the ciliary ganglion innervate the ciliary muscle for accomadation and iris sphincter for papillary constriction |
|
|
Term
| what are the symptoms of CN III lesion? |
|
Definition
| 1. outward deviation of the eye because of unopposed lateral rectus 2. ptosis 3. pupillary mydriasis |
|
|
Term
| what are some causes of third nerve lesions? |
|
Definition
| ischemia, diabetes, compression, optic neuritis or other inflammatory conditions. |
|
|
Term
| what nerves will cavernous sinus syndromes affect? |
|
Definition
|
|
Term
| describe Weber's syndrome. what deficits can it cause? |
|
Definition
| lesion at medial basal part of the pons. produces contralateral hemiplegia with involvement of face, arm and leg combined with ipsilateral CN III palsy |
|
|
Term
| Describe the affect of a midbrain tegmental lesion |
|
Definition
| 1)ipsilateral CN III palsy 2)medial lemniscus-contralateral loss of discriminative touch 3) anterolateral system-loss of contralateral pain and temperature sensation from both body and face 4) contralateral cerebellar ataxia-ataxia and involuntary movements of leg and arm |
|
|
Term
| what deficits will result from injuries to the mesencephalic tectum? |
|
Definition
| superior colliculus will cause paralysis of conjugate upward gaze AKA parinauds syndrome. pupils may be unreactive to light. |
|
|
Term
| what is parinauds syndrome? (tectal compression syndrome) |
|
Definition
| paralysis of vertical gaze because of injury to superior colliculi |
|
|
Term
| what will a bilateral lesion to the RF of the midbrain or pains cause? |
|
Definition
|
|
Term
| what are the two types of synapse? |
|
Definition
| directed-one to one non-directed-one to many |
|
|
Term
| what is a heteroreceptor? |
|
Definition
| a receptor that regulates the release or synthesis of mediators other than its own ligand |
|
|
Term
|
Definition
| sits on the presynaptic membrane and responsive to the neurotransmitter that the synapse releases. part of a feedback loop. |
|
|
Term
| what are the four types of "circuit" in the nervous system? |
|
Definition
1. long-hierachical pathways
2. projection
3. local circuit neurons
4. single-source divergent systems |
|
|
Term
what is the function of long hierachical pathways?
what are the neurotransmitters utilized at the motor and sensory junctions? |
|
Definition
functions to transfer information over long distances from the periphery to the CNS and return.
neuromuscular junciton=ACh
sensory neurons=substance P or other peptide. |
|
|
Term
| what is the function of a projection neuron? what neurotransmitters does it use? |
|
Definition
| interconnect pathways in the brain and transfer info over long distances in the CNS: uses excitatory amino acid transmitters for some pathways i.e. glutamate |
|
|
Term
| what can happen following hypoxia/ischemia in the brain to neurons? |
|
Definition
| superabundance of excitatory transmitters released onto receptors increasing intracellular Ca++. this activates calcium dependent lipases and proteases killing the neuron. |
|
|
Term
| what is the function of local circuit neurons? what neurotransmitters does it utilize? |
|
Definition
| regulate flow of info in immediate domain i.e. feedback systems. utilizes inhibitory amino acid transmitters i.e. GABA and glycine |
|
|
Term
| what is the function of single-source divergent systems? |
|
Definition
contain one of the monoamine neurotransmitters. cell bodies are found in a limited number of sites with projections to most of the brain. e.g. locus coruleus...norepinephrine.
also dopamine, serotonin or a peptide. |
|
|
Term
| what can happen to NO after a stroke? |
|
Definition
| NO may combine with superoxide to form peroxynitrate |
|
|
Term
| How does the intensity of receptor activation vary with number of receptors? |
|
Definition
| inversely. intense activation of receptors results in a fall in the number of receptors. |
|
|
Term
| CNS drugs are additive with physiological state of a patient and the effects of stimulants and depressents. why is this dangerous? |
|
Definition
| depressent drugs are additive and fatal eg alcohol and barbituates |
|
|
Term
| what strucutre on astrocytes maintains the BBB? |
|
Definition
|
|
Term
| what is the result of denervation of an autonomic nervous system neuron? |
|
Definition
| continued function, denervation or supersensitivity. |
|
|
Term
| what is the postganglionic neurotransmitter for the parasympathetic nervous system? |
|
Definition
|
|
Term
| what is the neurotransmitter for the sympathetic nervous system? |
|
Definition
| norepinephrine or epinephrine. ADRENERGIC because adrenaline |
|
|
Term
| what is the ganglionic transmitter for parasympathetic and sympathetic? |
|
Definition
|
|
Term
| what are the two exceptions to neurotransmitter postganglionic release? |
|
Definition
1. adrenal medulla releases epinephrine and norepinephrine into the circulation
2. sympathetic nerves to renal smooth muscle release dopamine |
|
|
Term
| most structures are dually innervated however some are single innervation and this is always excitatory. which are the sympathetic ones and which are the parasympathetic ones? |
|
Definition
sympathetic: adrenal medulla, sweat glands, piloerector muscles of skin, radial muscle of iris
parasympathetic: circular muscle of iris, ciliary muscle of eye |
|
|
Term
| which enzyme synthesizes ACh? |
|
Definition
| ChAT=choline acetyltransferase |
|
|
Term
| what enzyme breaks down ACh? |
|
Definition
|
|
Term
| Nicotinic receptors are coupled with what types of channels? Muscarinic? |
|
Definition
nicotinic=ionic
muscarinic= G protein |
|
|
Term
|
Definition
| autonomic ganglia=depolarization |
|
|
Term
|
Definition
| heart=decreased rate and force of contraction |
|
|
Term
|
Definition
| smooth muscle and secretory glands=contraction and increased secretion |
|
|
Term
|
Definition
|
|
Term
|
Definition
| neuromuscular=muscle contraction |
|
|
Term
|
Definition
| autonomic ganglia, CNS=firing of postganglionic neuron |
|
|
Term
| what enzyme converts tyrosine into DOPA? |
|
Definition
|
|
Term
| what enzyme conversts DOPA into DA |
|
Definition
|
|
Term
| what enzyme converts DA(dopamine) into norepinephrine? |
|
Definition
| DBH=dopamine beta hydroxylase |
|
|
Term
| what converts NE into EPI? |
|
Definition
| PNMT=phenylethanolamine-N methyltransferase present in the adrenal medulla |
|
|
Term
| what two enzymes metabolize catecholamines? |
|
Definition
MAO=monoamine oxidase (on mitochondria)
catechol-O-methyltransferase (COMT) |
|
|
Term
| contrast the metabolism of cholinergic and adrenergic neurotransmiters |
|
Definition
action of ACh is terminated by metabolsim and/or diffusion away.
catecholaminergic neurons activation of receptors is terminated by recapture by the nerve terminal or capture by surrounding tissue |
|
|
Term
| alpha 2A, 2B and 2C receptors are found where? what do they do? |
|
Definition
| these adrenergic receptors are presynaptic and postsynaptic autoreceptors. results in decreased release of NE and contraction of vascular smooth muscle. |
|
|
Term
|
Definition
|
|
Term
|
Definition
| smooth muscle of lung=bronchodilationa and vasodilation |
|
|
Term
|
Definition
|
|
Term
| What is the dopamine hypothesis of schizophrenia? |
|
Definition
That schizophrenia results form a biochemical abnormality of hyperactive dopaminergic neuronal systems; particularly the mesocortical dopaminergic system. Based on three lines of evidence:
1. most antipsychotic drugs block dopamine receptors
2. L-DOPA administration causes schizophreniform psychosis
3. abuse of amphetamines that release dopamine produce paranoid states that resemble schizophrenia. |
|
|
Term
Dopamine receptors belong to which superfamily of receptors?
Dopamine receptors are classified as either D1 family or D2 family. Which cloned receptors fall into each family? What effect does the stimulation of each receptor family have? |
|
Definition
Dopamine receptors=G-protein coupled receptors
D1=increased cyclic AMP production. cloned receptors D1 and D5 fall into this group.
D2=stimulation leads to inhibition of cyclic AMP production and modulation of K+ and Ca++ currents. D2, D3 and D4 cloned receptors fall into this group |
|
|
Term
What is the major advantage of newer "atypical" antipsychotic drugs over older "typical" ones?
On the molecular level why does this occur? |
|
Definition
Atypical antipsychotic drugs have fewer exrapyramidal symptoms.
Older antipsychotic drugs are "neuroleptic" and resulted in 100% blockade of D2 receptor activity. This was more likely to results in EPS. Atypical antipsychotic drugs have low affinity for D2 receptors blocking receptors by about 80% or less. This means they are less likely to elicit EPS. |
|
|
Term
| How can antipsychotic drugs result in galactorrhea? |
|
Definition
| Dopamine receptor blockade of the anterior pituitary inhibits the release of prolactin. Antipsychotic drugs block D2 receptors and disinhibit receptors so that there is increased prolactin production resulting in excess lactation |
|
|
Term
| What are the three families of "typical" antipsychotic drugs? |
|
Definition
| phenothiazines, thioxanthines, butyrophenones |
|
|
Term
| What constitute extrapyramidal symptoms? |
|
Definition
movement disorders that can include:
1. acute dystonic reactions
2.akathasia (restlessness)
3.Parkinson's syndrome
4. tardive dyskinesia |
|
|
Term
| How do antipsychotic drugs result in tardive dyskinesia? |
|
Definition
Use of antipsychotic drugs result in denervation supersensitivity of D2 receptors. This results in a cholinergic deficiency.
It is characterized by repetiive involuntary purposeless movements |
|
|
Term
| How do antipsychotics cause Parkinson's syndrome? |
|
Definition
| Antipsychotic drugs block the D2 receptors for substantia nigra leading to dysregulation of the extrapyramidal system |
|
|
Term
| What is malignant neuroleptic syndrome? |
|
Definition
When an initial large dose of neuroleptic drug results in high fever, mutism, extrapyramidal and autonomic disturbances.
Treat by cooling, rehydrating and bromocriptine(dopamine receptor agonist) |
|
|
Term
| What antipsychotic drugs can result in agranulocytosis? |
|
Definition
|
|
Term
What is the response rate for a placebo?
What factors can affect the effectiveness of placebos? |
|
Definition
25%
Color, size, route of administration, physician's attitude and const |
|
|
Term
| What does phase IV clinical drug development consist of? |
|
Definition
| postmarketing surveillence |
|
|
Term
| Besides positive and negative controls during drug trials, what other type of control is valid? |
|
Definition
| Historical control e.g. if there is 100% mortality for the condition prior to any interventions being tried. |
|
|
Term
| Give the two examples of pregnancy category X drugs mentioned in lecture |
|
Definition
| radioactive iodine and birth control pills |
|
|
Term
| What is a schedule IV drug? |
|
Definition
| A drug with limited physical or psychological dependence. |
|
|
Term
| Heroin would be classified as a schedule ? drug? |
|
Definition
|
|
Term
| In a pregnancy Cat C drug, is there a risk to the fetus? |
|
Definition
| There is an uncertain risk. No human studies have been done. Animal studies do show fetal risk however. |
|
|
Term
| Where are the minus ends of the microtubules found? |
|
Definition
|
|
Term
| What is the function of astrocytes? |
|
Definition
To regulate the extracellular environment around neurons. They regulate ionic levels and the pH of surrounding neurons. In addition they remove neurotransmitter from EC fluid.
Some of the material taken from astroctyes is transported to glial endfeet on capillaries where it is taken into the bloodstream |
|
|
Term
| What is the function of microglia? |
|
Definition
| Scavenger cells derived from macrophages |
|
|
Term
What is the function of oligodendrocytes?
What cell performs this function in the peripheral nervous system? |
|
Definition
They are the myelinating cell of the CNS. They are capable of myelinating multiple segments of an axon of several axons.
Schwann cells myelinate axons in the PNS. They can only myelinate a single segment of a single axon. |
|
|
Term
| Describe the properties of Ia and Ib neurons. Which organs are they associated with? |
|
Definition
| Aα, sensory neuron. 13-22 microns diameter, 80-120 m/sec i.e. largest and fastest. muscle spindles, golgi tendon organs |
|
|
Term
| What are the properties of type II neurons and which organs are they associated with? |
|
Definition
| Aß, 6-12 microns, 35-75 m/sec. also pretty fast many sensory modalities, muscle spindles and golgi tendon organs |
|
|
Term
| What are the properties of type III neurons? |
|
Definition
| Aδ and B, 1-5 microns diamters, 5-30 m/sec. free nerve endings, fast pain and temperature |
|
|
Term
| What are the properties of type IV neurons? |
|
Definition
| C, 0.2-1.5 microns diameter, 0.5-2.0 m/sec slow pain, temperature, some mechanoreceptors and NO MYELIN |
|
|
Term
| α neurons innervate what type of organ? what properties do they have? |
|
Definition
| α motor neuron, 12-20 micron diamter, 72-120 m/sec skeletal muscles |
|
|
Term
| γ(gamma) neurons ennervate what kind of organs and have what properties? |
|
Definition
| γ neurons are motor neurons, 2-8 micron diamter, 12-40 m/sec skeletal muscles within muscle spindle sense organs |
|
|
Term
| What kind of neuron is not myelinated? |
|
Definition
| type IV sensory neurons. they carry slow pain and temperative fibers |
|
|
Term
| Where are neurotransmitters synthesized? |
|
Definition
| They are synthesized in enzymes in the synaptic terminal |
|
|
Term
| What are the four types of neurotransmitter? |
|
Definition
1. Acetylcholine
2. Biogenic amines
3. excitatory amino acids
4. inhibitory amino acids |
|
|
Term
| How are the catecholamine neurotransmitters inactivated? Contrast this with how acetylcholine is inactivated. |
|
Definition
A specific plasma membrane pump for catecholamines moves them into the presynaptic terminal. The enzyme monoamine oxidase(on mitochondria) or COMT then degrades them.
In contrast acetylcholine is the only neurotransmitter that is inactivated by an extracellular enzyme: acetylcholinesterase. Choline is the molecule that is eventually reuptaken. |
|
|
Term
| What are the four "criteria" for neurotransmitters/neuropeptides. |
|
Definition
1. synthesis
2. release
3. identity
4. removal |
|
|
Term
| Describe the cascade that follows the ligand receptor binding of a metabotropic receptor. |
|
Definition
1. receptor activates G coupled proteins.
2. G proteins activate adenylyl cyclase producing cAMP
3. cAMP activates PKA
4. PKA phosphorylates ion channel and results in the activation of other pathways. |
|
|
Term
| There are four classes biogenic amine. Name them and give examples of each. Also give the amino acid each is derived from. |
|
Definition
1. Catecholamines: dopamine, norepinephrine, epinephrine. From tyrosine
2. indolamines: serotonin (5-HT) from tryptophan
3. Imidazole amines: histamine from histidine
4. Purines: ATP from adenosine |
|
|
Term
What are the two excitatory amino acid neurotransmitters? How are they inactivated? What are the inhibitory amino acids?
Which of these neurotransmitters are associated with cation ion channels and which are associated with anion ion channels? |
|
Definition
excitatory: glutamate, aspartate. cation ion channels e.g. Ca++, Na+
inhibitory: glycine, GABA, anion permeable channels e.g. Cl-
These neurotransmitters are inactivated by reuptake by specific transporters either into the presynaptic terminal or glial cells. |
|
|
Term
| What type of receptors do neuropeptides use? What is the duration of the response? |
|
Definition
| Metabotropic receptors with a slow onset and long responses. |
|
|
Term
How are neuropeptides inactivated?
What are the representative neuropeptides given in lecture? |
|
Definition
extracellular peptidase
opioids and tachykinins |
|
|
Term
| what are the group characteristics of neuro-gases? where are they synthesized? |
|
Definition
-low molecular weight
-diffuse through membranes because no vesicles
-short biosynthetic pathway
synthesized in the POSTsynaptic terminal and then diffuse back to the presynaptic terminal. |
|
|
Term
| What are the three different types of ion channel? |
|
Definition
1. leak (g-protein modulated)
2. voltage gated (responsible for rapid depolarizing phase of action potential)
3. ligand gated |
|
|
Term
| What is the resting membrane potential maintained by? |
|
Definition
| Mostly due to K+ leak channels. Na+K+ATPase pump also contributes to resting potential by pumping out 3 Na+ ions for every 2K+ brought in. |
|
|
Term
The nernst equation represents the balance between which two forces. What are they?
Keeping this in mind explain why extracellular hyperkalemia results in membrane potential becoming more depolarized. |
|
Definition
1. concentration/chemical gradient: ions want to move from high to low concentration.
2. electrical gradient across a membrane:ions want to move toward opposite charge until equilibrium.
During hyperkalemia, the extracellular concentration of K+ increases whilst the intracellular concentration remains the same. Therefore the concentration gradient is reduced, making the membrane potential less negative. The electrical gradient is increased (as there is now more positive charge extracellularly) but this effect is less than the chemical gradient effect. The net effect is depolarization. |
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Term
| What is the ligand for the NMDA receptor? What is necessary for it to be fully activated? What ions travel through this channel? |
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Definition
glutamate(excitatory neurotransmitter). There is a Mg2+ plug so that the ion channel only fully opens during depolarization.
Na+, K+ and Ca++ travel through this channel. |
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Term
| One of the postsynaptic glutamate receptors is activated regardless of membrane potential. What ions is it permeable to? |
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Definition
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Term
| Define the length constant. Upon what factors does it depend? |
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Definition
Distance over which the voltage decreases to 37% of that at input site. Length constant is determined by both core resistance and membrane resistance. e.g.
larger diamter axon=lower core resistance=higher length constant
more open channels=lower membrane resistance=lower length constant |
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Term
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Definition
length of time it takes for membrane potential to rise to 63% of its steady state level.
Determined by membrane resistance and capacitance. Because phospholipid membranes are the same, capacitance is the same for all cells and time constant depends on membrane resistance. Higher membrane resistance=higher time constant |
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Term
what is spatial summation?
what is temporal summation? |
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Definition
spatial summation=achieving action potential via the input of multiple cells. Summation of EPSPs can result in action potential while IPSPs will make it less likely.
temporal summation=effect where input from a single neuron can achieve action potential. Occurs when time constant is long enough and frequency of rises in potential are high enough that one begins before the previous one ends. |
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Term
| What two voltage gated channels is action potential dependent on? |
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Definition
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Term
| Voltage gated Na+ ion channels involved with action potential have 3 states and 2 gates. For each of the states describe which of the gates are open or closed. |
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Definition
1. resting: inactivation gate open, activation gate closed
2. open: inactivation gate open and activation gate open
3. inactivated: inactivation gate closed, activation gate open |
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Term
| During repolarization after action potential generation, what ion channels are open? |
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Definition
| sodium channel is closed(inactivation gate closed, activation gate is still open) and pottasium channel is open. |
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Term
| what are the two types of refractory period? |
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Definition
absolute- cell incapable of responding to subsequent depolarization
relative-cell capable of responding to subsequent depolarization only if stimulus is high |
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Term
| How does myelin insulation affect the length constant? |
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Definition
| myelin increases the membrane resistance which results in a longer length constant. |
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Term
| Why is an action potential not generated in the dendrites or soma even though the EPSPs will be higher in these region than in the initial segment? |
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Definition
| The concentration of voltage gated channels will be highest at the initial segment resulting in a lower threshold for AP generation |
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Term
| What is saltatory conduction? |
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Definition
| propagation of action potential along myelinated axons from one node of ranvier to the next. |
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Term
| What nerves are involved in the blink reflex? |
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Definition
V1= detects stimulus to cornea/conjunctiva
VII=motor response |
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Term
| Most structures in the nervous system are dually innervated. For some tissues one system predominates. List the exceptions for the parasympathetic and sympathetic systems. |
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Definition
Parasympathetic: pacemaker of heart, smooth muscle of gut, urinary tract, most exocrine glands
Sympathetic: vascular smooth muscle |
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Term
| For the sympathetic nervous system and parasympathetic nervous system list the nomenclature for agents that 1)have action the system, 2)mimic the transmitter and 3)block the transmitter |
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Definition
sympathetic: 1)adrenergic drugs 2)sympathomimetic 3) sympatholytic
parasympathetic: 1) Cholinergic drugs 2) parasympathomimetic 3) parasympatholytic |
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