Term
| Amino Acid Derived Neurotransmitters |
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Definition
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Term
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Definition
| Ach, Catecholamines (dopa, norepi), Serotonin |
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Term
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Definition
| Choline (diet) by choline acetyltransferase |
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Term
| What neurotransmitter is used in the ventral horn of the spinal cord? |
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Definition
| Ach. Also usd in preganglionic neurons and postganglionic parasympathetic. |
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Term
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Definition
Autoimmune or congenital. Disorder of synapse between cholinergic motor neurons and skeletal muscle.
Clinical - severe weakness of skeletal tissue
Tx: Anticholesterase |
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Term
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Definition
Degeneration of cholinergic neurons in nucleus basalis and loss of projection to neocortex, hippocampus, amygdala.
Cortical Ach deficiency
Tx: Inhibitors of acetylcholinesterase |
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Term
| Nicotinic Ach receptors found? |
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Definition
| Skeletal muscle and preganglionic autonomics. |
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Term
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Definition
| Turns into dopa after crossing blood brain barrier. Parkinson's tx for low dopa. |
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Term
| Amphetamine effect on neurotransmitters? |
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Definition
| Increased monoamine release (enhances release) |
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Term
| Effect of benzos and barbituates |
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Definition
Benzos - increase frequency of opening of GABA Cl- channels.
Barbituates - Increase duration of open GABA Cl- channels. These serve to enhance transmission. |
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Term
| Effect of morphine on neurotransmitter? |
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Definition
| Mimmics opiouds (effect on GPCR), causes analgesia. |
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Term
Effect of fluoxetine on neurotransmission?
Cocaine? |
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Definition
| Both block removal. Fluoxetine blocks serotonin reuptake. Cocaine blocks monoamine reuptake. |
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Term
| Effect of Pyridostigmine (Mestonin) |
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Definition
| Blocks degradation - used in myasthenia graves (blocks acetylcholinesterase). |
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Term
| Six things that enhance transmission of neurotransmitters |
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Definition
1. Enhance synthesis/packaging
2. Enhance release
3. Effect on neurotransmitter-gated ion channels
4. Effects on G protein coupled neurotransmitter receptors.
5. Blocking removal of neurotransmitter
6. By blocking Degradation |
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Term
| How do drugs/toxins depress transmission of neurotransmitters? |
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Definition
1. By interfering with synthesis or packaging of neurotransmitters.
2. By interfering with neurotransmitter release
3. By effects on neurotransmitter-gated ion channels
4. By effects on G protein-coupled neurotransmitter receptors |
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Term
| How does reserpine affect transmission? |
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Definition
| Blocks transport of monoamines into synaptic vesicles. |
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Term
| How does Botulinum affect neurotransmission? |
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Definition
| Blocks release of Ach, causes paralysis. |
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Term
| Effect of strychnine, phencyclidine (PCP), curare (arrow tip poison) on neurotransmission? |
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Definition
Strychnine - blocks glycine gated Cl- channels.
Phenycyclidine blocks NMDA receptors
Curare blocks nicotinic Ach receptors
Note these are ion gated! |
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Term
Effect of Haloperidol on neurotransmission?
Atropine? |
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Definition
Haloperidol - blocks dopamine receptors
Atropine - blocks muscarinic Ach receptors.
Note these are G protein! |
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Term
| What is the rate limiting set of catecholamine synthesis? |
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Definition
| Tyrosine Hydroxylase. Tyrosine->Dopa->Dopamine->Norepinephrine->Epinephrine |
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Term
| Degredation of Dopamine (intra and extracellular) |
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Definition
MAO degrades dopamine to DOPAC (intracellular)
Extracellular - Dopamine is converted to homovanillic acid (HVA) through the sequential action of COMT and MAO. HVA is used as indicator of functional activity of dopaminergic neurons....PRIMARY METABOLITES OF DOPAMINE ARE HVA AND DOPAC |
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Term
Where are DA receptors found?
D1 receptors?
D2? |
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Definition
Presynaptic terminal - autoreceptors
Postsynaptic somato-dendritic process.
D1 - stimulate adenylyl cyclase (and D5)
D2 - Inhibit or have no effect on adenylyl cyclase. (and D3,D4) |
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Term
| Where is norepi used as a transmitter? |
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Definition
| Sympathetic ganglia (smooth+cardiac muscle), locus ceruleus, and reticular formation. |
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Term
| Where is Dopamine used a neurotransmitter? |
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Definition
| Substantia nigra, VTA (spared in parkinson's), Hypothalamus, Retina, Olfactory bulb |
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Term
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Definition
| Raphe nuclei (widespread in CNS) |
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Term
| Parkinson's Disease (degeneration of what?) |
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Definition
Degeneration of substantia nigra pars compacta.
L-dopa is tx |
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Term
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Definition
Overactivity of mesolimbic and or mesocortical dopamine neurotransmission.
Haloperidol or chrloropmazine are tx - dopamine receptor antagonists. |
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Term
| Steps in dopa synthesis, release, deg |
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Definition
1. Synthesis of DOPA from tyrosine (stimulated by L-Dopa, blocked by alpha-methyltyrosine)
2. Storage: resperpine and tetrabenazine interfere with uptake and storage of dpa. (reserpine longer)
3. Reelease Amphetamine and tyramide enhance release
4. Receptor interaction
5. Reuptake (cocaine, amphetamine, benztropine inhibit).
6. Degradation by MAO - inside cell (pargyline inhibits). |
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Term
NE is stored where in the presynaptic terminal?
What does it interact with? |
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Definition
VMAT (vesicular monoamine transporter) in the axoplasm. Once released, NE can interact with alpha or beta adrenergic receptors. alpha2 modulate synthesis and release of NE (on nerve terminals).
Once released, can interact with alpha or beta adrenergic receptors. |
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Term
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Definition
| What NE is metabolized to by MAO and COMT for brain NE metabolite. |
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Term
| How is NE action terminated? |
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Definition
Reuptake into presynaptic terminal by NET (plasma membrane norepi transmitter).
NE broken down by MAO to 3,4-dihydroxyphenylglycolaldehyde. Aldehyde Dehydrogenase turns this to DOMA or aldehyde reductase pathway turns it to MHPG. DOMA broken down by COMT to VMA
alternatively NE metabolized by COMT first in a pathway that ultimately leads to VMA.
EITHER WAY YOU EITHER GET VMA (if COMT or VMA OR MHPG/Sulfate conjugate) if MAO. |
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Term
| Dopamine is degraded how? |
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Definition
| By MAO or COMT first, then the other ultimately yeilding HVA and then a sulfate conjugate. QUESTIONABLE ON COMT - MAINLY MAO. THEREFORE COMT INHIBITORS HAVE AN EFFECT ON NE reuptake, BUT NOT Dopa |
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Term
Acetylcholine degraded by?
Dopa/Norepi/Epi? |
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Definition
Acetylcholine - acetylcholinesterase
Dopa/Norepi/Epi - MAO/COMT/reuptake |
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Term
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Definition
Noradrenergic deficiency in monoamine hypothesis of depression.
Drugs which deplete monoamines can induce depression.
tx monoamine reuptake inhibitors (imipramine) and tricyclics |
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Term
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Definition
| Norepinephrine disfunction |
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Term
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Definition
| Tryptophan is precursor. Synthetic enzyme is tryptophan hydroxylase. Tryptophan is precursor. Synthetic enzyme is tryptophan hydroxylase. (5HT acetylase in converted by pineal gland to melatonin). |
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Term
| How is serotonin terminated? |
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Definition
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Term
What type of receptors are 5-HT receptors?
Where do they normally occur? |
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Definition
7 transmembrane spanning - g protein coupled receptors.
Also subtypes (5HT1-7, 5HT3 is ligand gated, not g protein).
5HT2 uses PLC pathway.
5HT1 -Normally occur in brain and cerebral blood vessels. Mediate neural inhibition and vasoconstriction.
5HT2 - CNS+periphery
5HT3 - PNS - nociceptor afferent neurons and autonomic and enteric neurons (excitatory - ion gated).
5HT4 - Brain and peripheral organs like heart, bladder, GI tract.
5HT5 - ?
5HT6 - ?
5HT7 - ? dont know. |
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Term
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Definition
| Synthesized from tryptophan, vesicular storage, release, reuptake, degraded by MAO (released back outside of cell as 5-HIAA) |
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Term
| Properties of neuropeptide transmitters |
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Definition
| Synthesized as larger precursor proteins at the soma (must be transported). Slow postsynaptic effects. Actions terminated by extracellular proteases or by diffusion. Co-released with classical neurotransmitters. Can trigger complex coordinated behavior, and actions do not require point to point synaptic connections. |
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Term
| Stress and Depression and Neuropeptides |
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Definition
| Depression - excessive secretion of ACTH leads to excessive cortisol release. Increased levels of CRF have been correlated to depression. |
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