Term
|
Definition
| the timing of important biological and behavioural changes, marked by transition points, such as time of conception, weaning, puberty. It proves a more accurate measure of development then chronological age which is just your age in numbers since time of conception |
|
|
Term
|
Definition
| examines sources of behavioural variability in an inviduals development over a lifespan |
|
|
Term
|
Definition
| the stages/process in which a human embryo or fetus gestates during pregnancy until birth. Most of the brain and organs develop during prenatal development |
|
|
Term
|
Definition
| the period of development beginning immediately after birth. The body grows and matures during postnatal development and exposure to certain environmental toxins can effect this. |
|
|
Term
| How signals control development of physical and mental traits? |
|
Definition
- extracellular messengers bind to receptors (hormones, nts )
- intracellular messengers activate 2nd messenger systems (camp_
- gene is activated
- transcription happens
- protein, enzyme, hormone synthesis,
- leads to physical development (cell and nerve growth), mental development (axon and dendrite growth) and behavioural development (nerve and muscle activity
- hormones, and other chemicals activate genes, thus environmental influences which alter hormone,nt or neuropeptide release during critical periods of development, may lead to abnormal physical, mental or behavioural development. |
|
|
Term
|
Definition
| certain time period during development which the presence of specific external or internal stimulis conditions are necessary for normal development of NS |
|
|
Term
|
Definition
| time during which harmful stimuli can damage the developing nervous system |
|
|
Term
|
Definition
| - time where the developing nervous system or organ can be adversely effected by negative stimuli or lack of required stimuli |
|
|
Term
|
Definition
| is the time where the developing nervous system or organ could be positively affected by external stimuli (correction of abnormalities is most effective) |
|
|
Term
| 1-4) Behavioural teratology |
|
Definition
| the study of abnormally developed/deformed fetuses and teratogens which caused such deformations. Abnormal development and the production of congenital anomalies |
|
|
Term
|
Definition
| drug/chemical/ disease/ bacteria which alter neurochemical signals and disrupt/change the course of normal development |
|
|
Term
| CRITICAL PERIOD FOR - HEART |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| developmental test batteries- q1/6 |
|
Definition
| examine changes in developmental parameters caused by abnormal neuroendocrine or environmental stimuli, therefor can determine the effect of drugs on development of behaviour |
|
|
Term
|
Definition
| mental/motor tests- 1-15 months of age |
|
|
Term
|
Definition
| 37 behaviours- neonatal newborns |
|
|
Term
|
Definition
| 0- 6 years- motor skills and language |
|
|
Term
|
Definition
| done by parents-6 monts-6 years |
|
|
Term
|
Definition
organize nervous system development during critical periods- eg- prenatal testosterone masculinizes females
- permanent effects, perinatally, critical periods, permanent structural changes in brain cells
more imp for masculinization then feminization |
|
|
Term
|
Definition
activate neural pathways that are already present- eg estrogen in female sexual behaviour
- short term effects, occur later in life, cannot be activated until organization occurs, transient modulation- equal for both genders |
|
|
Term
| 1.9. How do hormones organize developmental processes? |
|
Definition
hormones, activate genes, thus environmental influences which alter hormone,nt or neuropeptide release during critical periods of development, may lead to abnormal physical, mental or behavioural development.
extracellular messengers which initiate the cascade |
|
|
Term
| 1.11. Why is the neuroendocrine system considered the “motor” that powers development? |
|
Definition
|
|
Term
|
Definition
| peptides/proteins which stimulate cells to divide, or increase in size and thus regulate cell growth |
|
|
Term
|
Definition
| gfs which regulate cell differentiation, survival, phenotype expression, plasticity and growth |
|
|
Term
|
Definition
| nerve growth factor- promotes growth and survival of PNS and CNS (sensory) |
|
|
Term
|
Definition
| neurotrophin-3- b. promotes growth of hippocampal, cerebellar and somatosensory neurons |
|
|
Term
|
Definition
| brain derived neurotrophic factor- promotes peripheral sensory neurons and cns neurons which dont respond to ngf |
|
|
Term
|
Definition
| epithelial growth factor- stimulates cell division of skin and other epidermal cells |
|
|
Term
|
Definition
| fibroblast growth factor- proliferation of fibroblasts, endothelial cells and other cell types, bvs, neurons, and adrenal cells |
|
|
Term
|
Definition
| insulin like growth factors- somatomedins- stimulate proliferation and growth of connective tissue- activated by gh |
|
|
Term
| GF synth, storage, release, receptors |
|
Definition
synth- pre-propeptides in neural and non-neural cells- stored in secretory vesicles- deactivated by peptidaze
recp- gpcr, trk, p75 |
|
|
Term
| 2.4. How does NGF stimulate development of a "bipotential" adrenal medulla cell? |
|
Definition
| -release of NGF from target cell, attracts neurons and promotes synapse formation, survival and maturation of these cells in neurons. NGF stimulates development of the cell into a neuron? |
|
|
Term
| formation of endocrine cell |
|
Definition
| glutocorticoids prevent the bipotential cells from developing info neurons, so when these cells are stimulated by fgf, they develop into endocrine cells |
|
|
Term
| how do gfs block cell death? |
|
Definition
| block cell death by blocking actions of p53 and activating cell survival genes- bcl2 - if none- biochemical activity is reduced, cell dies- gf stimulation must occur before endonuclease activation |
|
|
Term
| 2.5. In a developing synapse, which cell releases the neurotrophic factor, NGF? |
|
Definition
| target cell releases NGF where it is taken up by presynaptic cell, and attracts axonal projections stimulated by fgf |
|
|
Term
| 2.6. What type of receptors to NGF and other neurotrophins bind to? |
|
Definition
|
|
Term
| 2.8. What are four different ways that growth factors prevent apoptosis? |
|
Definition
1) they activate dna replicatoin, 2) activate mrna and protein synthesis
3) amino acid and glucose uptake
4) block actions of p53 and activate cell survival genes
5) prevent endonuclease activation |
|
|
Term
| Q3.1. Does the rat have its brain growth spurt before or after birth? What does this suggest about the role of external stimuli in brain development? |
|
Definition
| brain growth spurt in rats and humans occurs after birth, therefore postnatal factors have considerable influence on neural development- environment plays a big role |
|
|
Term
| Q3.2. What are the six phases of neural development? |
|
Definition
- neurogenesis
- nerve cell growth
- migration & differentiation
- establishment of neural connections (synaptogenesis)
- modifaction of connections
- myelenation
- |
|
|
Term
|
Definition
birth of berve cells from stem cells, glial cells or progenetors- rats -e10
- cells can develop differently depending on gfs
- absense of ngf here causes fewer drg neurons and increased apoptoses |
|
|
Term
|
Definition
nerve cells migrate from progentor cells (subventricular zone) to surfact of brain (marginal zone)= bdnf and nt4 promote radial migration of granular cells in cerebral cortex and cerebellem
egf- promotes mig to telencephalon |
|
|
Term
|
Definition
| cells migrate within layers of the cortex- cortex is on a tangent |
|
|
Term
|
Definition
e16-b10
- migrate to cortical plate
- electrical activity develops in response to ca ions
- ngf is essential for dev of NA neurons |
|
|
Term
| Q3.7. An SNS precursor cell can develop into a noradrenergic neuron if stimulated by the neurotrophin ( A ), but stimulation of the precursor cell by neurturin (NTN) plus the neurotrophins ( B, C, and D ) is required for the development of a cholinergic neuron. |
|
Definition
|
|
Term
|
Definition
| terminal enlargments at the ends of neurites which promote growth by attaching their filipodia to the surfaces of other cells of tissue- they follow guidance pathways and are guided by external neurotrophic factors such as ngf, bdng of target cells |
|
|
Term
| Q3.9. What does it mean to say that a neurotrophin acts as an "axon guidance molecule" during brain development? |
|
Definition
neurotrophins can act as axonal guidance molecules to direct axon growth toward particular target cells.
- act as chemoattractants for growing azons- drg- attracted by ngf, not bdng- attract or repel growth of neurites |
|
|
Term
| Q3.10. What are the three phases of synaprogenesis? |
|
Definition
synaptic contact- growth cone is converted into nerve terminal, post synaptic cell develops dendritic spines- increases nt synthesis
synaptic maturation- pre-synaptic axon terminal forms synaptic vesicles cluster and receptors migrate- neurotrophins stimulate ca ion channels.
maintenance- neurotrops released from post syn cell are absorbed by pre-syn to stimulate production of nts- ngf- prevents cell death |
|
|
Term
| Q3.11. What happens if the axon of a developing neuron is cut? |
|
Definition
| - dont know yet- cutting the axon blocks ngf transport |
|
|
Term
| Q3.12. At what age do nerve cell proliferation, migration and differentiation occur in the rat? |
|
Definition
| prolif, growth, differentiation occur bw e11-p8, migration and growth continue to occur until p30 |
|
|
Term
|
Definition
| ater postnatal day 3- cells whos axons fail to reach suitable target cells may die.- non-supported neurons- 50% die |
|
|
Term
| Q3.13. What two changes occur in neural circuits during the period of synaptic reorganization? |
|
Definition
- neural connections with lact of activity are lost- lead to loss of snapses
- environmental input maintains some connections- activity releases tropic factors which faciliate nt release |
|
|
Term
| Q3.14. What are four different actions of neurotrophins during synaptogenesis? GPCP |
|
Definition
1) attract growth cone and facilitate synaptic contact
2) alter membrane permeability to promote nt synth
3) promote maturation by stimulating ca ion channel activity
4) neurotrophs released from post syn neuron are takein into presyn cell and stimlate production and release of nts |
|
|
Term
| Q3.15. In humans, the largest number of neurons and synapses in the brain occurs between the ages of ? and ? , after which the numbers decline. |
|
Definition
|
|
Term
| Q3.16. Handling infant rats for a short time on postnatal day 1 has been shown to facilitate the release of which neurotrophin? |
|
Definition
|
|
Term
| Q3.17. What is "activity-dependent synaptic change" and how is BDNF involved? |
|
Definition
| Exposure to increased activity levels and enrichment, stimulates ngf and bdnf in brain areas to increase neurogenesis- bdnf is released presynaptically upon increased activity and triggers and stimulate post synaptic neurons like a nt to increase /strengthen connection |
|
|
Term
| Q3.18. Which two neurotrophins facilitate myelination? |
|
Definition
|
|
Term
| bone morphogenic proteins |
|
Definition
| proteins promote differentiation of symp neurons- inhibit glial differentialion |
|
|
Term
| how does bdnf modulate activty dependant synaptic activity? |
|
Definition
| - at active synapses, bdnf is released, binds to truncated trk b receptors and increases cell activity and ca influz, internalizes the bdnf and stimulates nucleus of cell |
|
|
Term
| Q3.19. At what age does catecholamine synthesis begin in rats? humans? |
|
Definition
rats- e10, humans- week 5
da and ser first, then na- present by 16
- axon growth and formation of nerve terminals occur bw e15-e18, synaptogen-e16
humans- na 5-6 weeks gestational age, da: 6-8 weeks |
|
|
Term
| cholinergiv neurons- when do they develop |
|
Definition
| rats- e12-17 (functional by e17, humans 20 weeks |
|
|
Term
| GABA AND GLUTAMATE prenatal dev |
|
Definition
nmda develop first (excitatory)e12-15 rats, 16018 weeks humans ampa develops later (inhibitory) e15 rats, 18-26 humans.
excitatory and facilitate development of nmda receptors for glutamate |
|
|
Term
| Q3.20. What two excitatory functions does GABA have during neural development? |
|
Definition
1) facilitates development of nmda receptors for glutamate, which facilitates developmend of ampa receptos after and switch it to inhibitory
- facilitates proliferation and radial migration in development |
|
|
Term
| Q3.21. Neurotransmitter activity can stimulate neural growth by activating ? channels in neurons? |
|
Definition
second messenger systems and post synaptic target cells
- |
|
|
Term
| when does hypothalamus differentiate |
|
Definition
6-12 weeks fetal age, hormos become detectable in neursecretory cells of hypothatl- gnrh first one
4 weeks- rathkes pouch, 6 neurophypophyseal bud, 16-both functional |
|
|
Term
| what is anterior pituitary developed from? posterior pituitary? |
|
Definition
ant- rathkes pouch
posteriour- neurohypohyseal bud- diencephalon |
|
|
Term
|
Definition
originates from olfactory bulb, failure of migration to hypothal results in lack of LHRH secretion, kallmans syndrome and anosmia
by e16 lhrh is detected in hypothal |
|
|
Term
|
Definition
no lhrh in poa so nerves fail to migrate to hypothaol- gonads fail to develop and anosmia, cant smell
males
- respnd do lhrh treatment |
|
|
Term
| Q4.4. At what age are pituitary LH and hypothalamic LH-RH first detected in the rat? |
|
Definition
| e16 hypothalamus, none is seen before e14 |
|
|
Term
| role of hormones as neurotrophic factors |
|
Definition
| -cell prolif, nerual size, migrarion, neuronal differntiation, synaptogen and org, mylenation |
|
|
Term
|
Definition
| promote cell division, nt synthesize |
|
|
Term
|
Definition
inhibit cell division and reduce brain weigh inhibit prolif- levels must be low in brain
stimulate se and catecholamine synth by increasing tryptophan hydrozuylaz in criticap periods |
|
|
Term
| what two hormones increase myelentation? |
|
Definition
|
|
Term
| Q4.6. What are the organizational effects of hormones? |
|
Definition
1) influence prolif and dif
2) modulate neurite growth and establishment of connections
3) direct modification by influencing cell death and synapse elimination
- during perinatal period, baseline level of hormone secretion is determined- presence or absenese alters feedback or release |
|
|
Term
| what are activational effects of hormones? |
|
Definition
trigger puberty or inhibit it
gonads- sexual differentiation and agression
thyroids- physical parameters, inteligence
corts- motor responses |
|
|
Term
| Q4.7. How do hormones influence neural development? |
|
Definition
| there presence or absence will indicate dif levels of development? |
|
|
Term
| what is septo-optic dysplasia? |
|
Definition
birth defect with malformed optic disc and nerve, pituitary defficiences and absnense of thing separating ventricles
- causes visual impairment and decreases growth hormones
- blindness, involuntary eye movement, lack of pituitary stalk |
|
|
Term
| what age is thyroxine produced? and htp functional? |
|
Definition
| 7th week, 90 days fully functional, iodize is necessary |
|
|
Term
| Q5.1 What stimulates the surge in T3 and T4 secretion at birth? |
|
Definition
| exposure to cold stiluated surge ot tsh for 30 min to regualte body temp |
|
|
Term
|
Definition
lack of thyroid hormones due to
1) disruption of hpa system and low trh and tsh
2) lack of receptors for tsh and trh
3) lack of enzymes necessary for tsh of thry synth
4) lack of iodine |
|
|
Term
| Q5.2 What effect does neonatal hypothyroidism have on body temperature? |
|
Definition
reduced body temp, reduced growth, reduced brain weight, mylenation, blood vessels, lower intelligence
adults- anorexia, thick hair, pale skin |
|
|
Term
|
Definition
hypofunction of thyroid
low bmr, increased sensitivty to cold
can be improved through thyroid injection |
|
|
Term
| congenital hypothyroidism |
|
Definition
| due to lack of iodine- cretinism, gh secretion is reduced in absense of thyrozine therefore thyroxine is necessary for brain frowth bc it stimulates ngf |
|
|
Term
| Q5.3 Give 2 effects of neonatal hypothyroidism on brain development. |
|
Definition
| decreased brain weight, decreased mylenation, decrease dendrite devel |
|
|
Term
| Q5.4 Using maze learning as a measure, what is the "critical period" for the replacement of thyroid hormones in rats in order to ensure "normal" cognitive development? rats? humans? |
|
Definition
| 0-7 days for rats, 1 month for humans? |
|
|
Term
|
Definition
over active thyroid, to much thyroid hormones= graves disease
elevated body emp, increased hr, nervous, hyper |
|
|
Term
|
Definition
| weight loss, nervousness, heat intolerance, giareah, insomnia, protrusion of eyebals |
|
|
Term
| what is a goiter? what causes it? |
|
Definition
| goiter- enlarged thyroid gland to du excess stimulation of thyroid gland and inhibition of negative feedback- excess tsh and trh but not enough thyroxine to inhibit |
|
|
Term
| Q5.5 How do NGF and thyroid hormones interact to stimulate neural activity in adrenal chromaffin cells? |
|
Definition
| thyroxine promotes ngf, so if you decrease thyroxine, you decrease chromaffin cells and impair growth? |
|
|
Term
| Q5.6 Is the effect of hypothyroidism on IQ in humans completely reinstated by postnatal thyroid hormone treatment? |
|
Definition
| not fully, but if treatment si given early if may improve significantly |
|
|
Term
| Q6.1 Where would you find the testes determining factor TDF gene? |
|
Definition
| SRY genes on y chromosome- top half, provide info for msculination and testes determining gene |
|
|
Term
|
Definition
| smaller then x, 3 gene regions |
|
|
Term
tdf genes must be present for masculinaization
if 46xy genotypic male is missing the top of y chromosome carrying sry gene? |
|
Definition
| develops as female with streak gonads |
|
|
Term
|
Definition
- codes for protein that switches on the development of sertoli cells from supporting cells in undif. gonad
- sertoli cells stimulate production of sperm which stimualte production of leydig cells
w/o it supporting cells develop into follicular cells, |
|
|
Term
| environment and sex- lizards aligators, turtles fish? |
|
Definition
| liz and aligators, males are warm, females are low, turtles oposite |
|
|
Term
|
Definition
| condensed, single x chromaon found in nuclei of somatic cells in females- # of bars is 1 less then # of chroms |
|
|
Term
|
Definition
45X0
female missing one x chromosome, infertile, underdeveloped secondary characteristics, shorter stature, meaning the end x contains genes necessary for normal development |
|
|
Term
|
Definition
47 xxx
1/900girls, 2 or 3 barr boddies, taller thinger btu otherwise normal |
|
|
Term
|
Definition
XXY
- infertile testes, bar boddy, enlarged breasts, elevated fsh levels
1/600, most common after downs syndrome |
|
|
Term
|
Definition
| taller, aggressive, bigger, growth is excelerated, but decreased fertility |
|
|
Term
|
Definition
both overain and testicular tissue, both male and female external genitalia
most, 46xx with sry gene on x chrom
- one of each |
|
|
Term
| Q6.3 Why does the Mullerian duct not develop in a male? |
|
Definition
tdf on y chromosome activates the development of the testes from the medulla of undiferentiated fonad, which develops before ovaries, here the wolfian ducts develop into vas deferns and epidymis
mullerian duct does not develop because it is inhibiited by MIF and activation of sry genes |
|
|
Term
| Q6.4 Why does the Wolffian duct not develop in a female? |
|
Definition
cortex of the gonad develops into ovary in absence of sry gene, mullerian ducts develop into fallopian tubes
w/o androgen stimulation, wolf duct degenerates |
|
|
Term
| Q6.5 What is the effect of castrating a one day old male rat? |
|
Definition
| inhibits testosterone secretion which stops masculinaztion |
|
|
Term
|
Definition
| testosterone, negaitve, est- positive |
|
|
Term
| Q6.6 What is a fetoprotein and what does it do? |
|
Definition
| lower est levels in females, less receptors, all est is bound to fetoprotein- binds to estrogen and prevents it from masculinizing females |
|
|
Term
| Q6.7 How does testosterone masculinize the SDN POA of rats and humans? |
|
Definition
- increases growth and size of neurons
-steroids increase growth
- larger sdn poa in male rat |
|
|
Term
|
Definition
| testosterone is converted to estradiol by enzyme aromataze. thus, in neural cells it is estradiol that serves to masculinize the cells during the critical period/organizational phase |
|
|
Term
|
Definition
| deficiency enxymes in adrenal corezz androgens are synthezied instead of cortisol |
|
|
Term
| testicular feminizing syndrome |
|
Definition
| lack of androgen receptors |
|
|
Term
|
Definition
| inability of cells to respond to androgens- male but looks like female because insensitive to androgens |
|
|
Term
|
Definition
| chronically increased levels of cortisol, causing decrease in growth, obesity |
|
|
Term
| prenatal corticosteriod increases |
|
Definition
| through injections, mothers stress, postnatal infant stress |
|
|
Term
|
Definition
increase the negative feedback of hpa system, bursts of injection cause inhibition in long etrm
- leads to abnormal growth spurts due to gc surge and delayed development during periods of gc inhibition |
|
|
Term
| effects of injections of corticosteroids |
|
Definition
- small, delayed body growth and ear opening, teeth
- smaller brain, lower brain weigh, less cells, myelenation
- delayed stress response
- delayed puberty |
|
|
Term
|
Definition
| cortisol is small, travels through placenta- stress follows into baby |
|
|
