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PSY1004 SEMESTER 2 > PSY1004 SEMESTER 2 - WEEK 3 > Flashcards

PSY1004 SEMESTER 2 - WEEK 3 Flashcards

1
Q

define prenatal development

A

development of humans before they are born

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2
Q

define postnatal development

A

development of humans after they are born, usually in infancy

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3
Q

define neonate

A

an infant less than one month old

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4
Q

define differentiation

A

specialisation of cells allowing accumulation of more specific particular function

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5
Q

what is 22 GW referred as

A

age of viability, baby can survive

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6
Q

outline germinal period

A

0-10 gestation day
from single-cell zygote into morula into blastocyst
from conception to attached to uterine wall

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7
Q

what GW is the embryonic period

A

2-8 GW

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8
Q

what has happened by 8GW

A

embryo is fully attached to uterine wall, basic organs formed, sexual differentiations occur, begin respond direct stimulation (turns head in response to light mouth touches - reflexive)

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9
Q

what is gastrulation (2-8GW)

A

early embryo transform into very simple ball of cells into more complex embryo with multiple layers of different cell types
forms 3 distinct germ layers = mesoderm, endoderm, ectoderm

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10
Q

whats endoderm (gastrulation)

A

inner lining of some systems and organs such as liver, pancreas

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11
Q

whats mesoderm (gastrulation)

A

middle layer = bones, muscles, heart and circulatory system, internal sex organs

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12
Q

whats ectoderm (gastrulation)

A

outer layer = skin, brain, nervous system, becomes neural plate (differentiates into forebrain, midbrain, hindbrain), folds to become neural tube where all neurons comprising brain originate from single indentical cell layer in neural tube wall

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13
Q

what does forebrain comprise of?

A

cerebral hemispheres, thalamus, hypothalamus

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14
Q

what does midbrain comprise of?

A

superior and inferior colliculi, substantia nigra

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15
Q

what does hindbrain comprise of?

A

medulla oblongata, pons

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16
Q

what is present in 5-6 GW

A

basic structure of hindbrain, midbrain, forebrain

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17
Q

what time period is ‘foetal period’

A

9GW-birth

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18
Q

what happens at 14GW

A

division of brain hemispheres now visible

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19
Q

what happens at 26 GW

A

nerve cells generated, cortex begin to wrinkle, myelination

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20
Q

give indirect methods of studying prenatal development

A
  1. present loud sounds on abdominal surface and ask mother to report movements
  2. inference from non-human animal models
  3. autopsies of human embryos and foetuses
  4. inference from studies measuring perception and memory of neonates
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21
Q

state issues of indirect measures of prenatal development

A

animal models lacking applicability (differing gestations and development course)
both animal/human post-mortem highly regulated, very controversial which comes with its own issue
conceptual and practical problems

22
Q

define direct measures for studying prenatal development

A

measure autonomic nervous system activity with/without an external stimuli`

23
Q

give 2 direct measures of studying prenatal development

A

foetal ultrasound (good for studying behaviours, deformities, developmental problems)
foetal brain activity using fMRI (doesnt make sense until studying brains action, so only later GW)

24
Q

brain development stage 1- explain primary neurulation

A

ectoderm become neural plate (patch of tissue on embryos dorsal surface that become nervous system)
development induced by chem signals, growth factors

25
brain development stage 1- explain secondary neurulation
neural tube closure, cranial (anterior) neuropore closes then caudal (posterior) neuropore closed), both completley closed by 4GW
26
when can neural tube defects (NTDs) arise and what can cause them?
during secondary neurulation (4GW) genetics/env factor contribute but no precise mechanism experimental models used to inform preventative measures or prenatal treatments
27
what can prevent NTDs
maternal folic acid supplements. effective in reducing risk, but varying study effect size
28
name some NTDs
1. cranioarchischsisis (open brain+spinal cord) 2. anencephaly (open brain, lacks skull vault) 3. encephalocele (meninges and brain herniation) 4. iniencephaly (occipital skull and spine defects and extreme head retroflexion) 5. spina bifida (clsoed asymptomatic, vertebrae not completely closed) 6. meningocele (meninges protusion, filled with CSF by skull/spine defects) 7. myelomeningocele (open spinal cords)
29
brain development stage 2- outline neurogenesis/neural proliferation
neurogenesis continues post-birth and includes proliferation of new cell via mitosis multipotent cells into neuroblasts glioblast become neurons, glial cell during migration links to Autism spectrum disorder
30
outline what genetic factors and GW can risk Autism Spectrum conditions (ASC)
links to 100s genes interacting with disrupted prenatal processes, around 10-20 GW in neural proliferation
31
outline pathology of autism, including processes of causes
excess neurons in prefrontal cortex disrupted prenatal/postnatal neuronal migration, neuronal maturation and synaptogenesis from autopsies
32
brain development stage 3- explain process for migration/ neuronal migration
radial glial cell acts as guide wires for neuronal migration. migrating cell is immature, lack dendrites cells post-migration aligns with other cells, forms structure (aggregates) can cause neuronal migration disorders (NMD)
33
when does neuronal migration disorder (NMD) occur, what can it be characterised by and common symptoms
during migration. childhood neurological deficits, commonly are intractable epilepsy (hard to treat pharmlogicallu)
34
what are causes of NMD (neuronal migration disorder), outline pathology
varying cause, genetic, multiple genetic disruption/mutation disrupted gene responsible for radial migratory processes of neuroblasts to cerebral cortex lead to malformation of cortex pre and postnatally
35
outline the example of lissencephaly (neuronal-migration-disorder)
epilepsy, severe intellectual disability, gyri don't form properly so smoother brain appearances
36
brain development stage 4- outline maturation and dendritic/axon growth
post-migration, formed structures, dendrites begin to grow to mature size axons have growth cones on end (critical for this stage actions), dendrites form synapse with other neurons/tissues
37
brain development stage 5- explain synaptogenesis
formation of new synapses at 23 GW, multistage process dependant on glial cell presence (particularly astrocytes) many synapses form randomly, chemical signal exchange between pre and postsynaptic neuron needed
38
what can prenatal methamphetamine exposure during stage 5- synaptogenesis cause
learning and memory deficits, accounts for postnatal cognitive deficits persisting into childhood/adulthood animal models of mice support impact of methamphetamine on brain from postnatal to adult life, disruption in axon growth of neuron in hippocampus
39
brain development stage 6- explain apoptosis/neuronal death
40-75% neurons intentionally die post-migration due to failure to compete for chemicals provided by targets impact of neurotrophins
40
what are neurotrophins
promote growth and survival, guide axons, stimulate synaptogenesis
41
brain development stage 7- explain myelogenesis/formation of myelin, in PNS
in PNS 2 months gestation, preventing message leaks along nerves (quicker, more efficient) myelinate motor before sensory roots
42
brain development stage 7- explain myelogenesis/formation of myelin, in CNS
third trimester, first occur in sensory tracts in cerebral cortex and complex association pathway occur post-birth (seen by increasing motor ability in first year of life) in corticospinal tracts (main connection inbetween cerebral cortex, motor nerves from spinal cortex) myelination only occur caudally to medulla by 40 GW
43
explain development of cerebral cortex around 9GW
develops from forebrain, rapidly increase size, expands to form differing regions. later becomes highly specialised
44
explain cerebral cortex development at 4 month gestation
cells in cerebral hemisphere proliferate, migrate
45
explain cerebral cortex development at 6 month gestation
surface of cortex no longer smooth due to rapid proliferation causing gyri, sulci differentiated frontal, parietal, occipital lobes
46
why is immaturity at birth seen as an adaptive feature?
allows brain to adapt to differing environments
47
outline synaptic pruning during development, and its importance
improves brain efficiency, transmission of signals between neurons is prenatally relatively slow, most rapid post 2nd-year of life issues results in Fragile x syndrome
48
outline fragile x syndrome
genetic disorder with developmental delay, learning disabilities, behavioural problems. defective FMR1 gene suppressing production of proteins stimulating pruning, result in excess synapses not sufficently pruned, with noise in neural system causing attentional deficit
49
outline prenatal learning at 6 months gestation
can learn despite immature nervous system, showing basic forms of memory (habituating response to repeated auditory stimulus)
50
outline foetal behavioural organisation at 34 GW
no longer moves continually, distinct period of rest/activity. 20-30% of time spent in motionless sleep (steady HB, BR) 70-80% active sleep (irregular HR, BR, responsive to sensory stimuli in uterine env, eye movement, responsive to touch/sound, early neural network stimulated by internal/external stimuli)
51
outline foetal behavioural organisation at 38 GW
no longer spend so much time in active sleep, "maturer" brain, more inhinitory pathway = reduced movements amount
52

PSY1004 SEMESTER 2 (9 decks)

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