PSYC 371: development and emergence of behaviour

rodent development timecourse

• born with a relatively immature CNS

• first week of postnatal life = third trimester of human gestation

• mobile at 10 days = 6 months in humans

• somatosensory and olfactory systems first to develop = functional at birth = locate mother’s nipple

• hearing and vision begin at around 13 days when eyes and ears open

• amygdala-independent fear and attachment → amygdala-dependent fear → HPC-learning → PFC (higher cognitive function)

HPC-learning

object → place → space → what where when why (episodic memory)

amygdala-independent fear and attachment

• prior to p10 = rats learn to fear odors that are associated w painful stimuli and sickness-inducing foods

• learning occurs in piriform (olfactory) cortex not amygdala cuz not operational atp

• aversive stimuli promote attachment instead

amygdala-dependent fear

• around p10 = amygdala-dependent LTP and fear appears

• human 7 month old baby begin to crawl = fear heights and wide-open eyes = amygdala maturation

• stress and glucocorticoid dependent

• a calm mother or her odour can block fear learning by preventing glucocorticoid release and amygdala activation

context-specific fear

• shocked continue to freeze

• no shock = freezing decreases as they grow older

• takes time to differentiate between context

• takes even longer to appear = delayed HPC development

HPC-learning: water maze

• HPC memory appears around 3 weeks of age where simpler forms of memory may appear before more complex, relational forms

• younger rats show higher path lengths and latencies (time taken to find platform)

• by p24 rats spend more time in the target quadrant

infantile amnesia

• young rats can form HPC memories, but they don’t persist

inhibitory avoidance experiment

• training: rats shocked in dark place

• testing: rats prefer bright spot even tho they would normally rather be in dark

inhibitory avoidance memory

• formed at 17 days, but forgotten a day later

  • can be recovered by a reminder footshock in an unrelated context = memory still exists but just more difficult to access

• 24 day old rats retain IA memory

optogenetics and context fear memory

17 day old mice forget context fear memories but can be artificially activated with optogenetics = infantile amnesia is failure in retrieval process

infant learning

• promotes maturation of HPC circuits

  • BDNF induces synaptic plasticity = expression of mature NMDA receptors = promotes maturation of inhibitory synapses = accelerates subsequent learning

• has persistent effects

nutritional deficiency

• faster brain aging in males when in early stages of gestation

• no changes in cognition: working memory, semantic memory, verbal fluency, etc.

• lower IQ in chinese famine in both sexes

sensory/environmental deficiency

• randomized: half of children in foster care and other half in institutional care

• institutional care: poorer cognitive development and behavioural sensory-motor outcome

  • brain requires patterned stimulation to develop properly

  • institutional care = chaotic, lacks patterns

• critical period: removal from institutional care earlier in life (2-3 years) = better cognitive recovery

effect of neonatal handling on age-related impairments associated with HPC

• neonatal handled group had more glucocorticoid receptors

  • both control and neonatal handled had decreasing amt of glucocorticoid receptors as they grow older

• neonatal handled group have more HPC neurons

• HPC cell loss and pronounced spatial memory (water maze) deficit almost absent in neonatal handled rats as they age

• control group showed elevated basal levels of corticosterone

maternal care buffers stress = improved HPC function

• mothers of handled pups showed increase levels of licking and grooming of pups and arched-back nursing (LG-ABN)

• offspring of low LG-ABN have higher rise of corticosterone (when restraint stressor applied for 20 mins) and stay elevated for longer

ELA → high glucocorticoid sequence

• early-life adversity → methylates glucocorticoid receptor gene → reduces GR expression → reduces negative feedback control of HPA axis = higher glucocorticoids after stressors

• both rodents and humans

early life experience drives adaptive development

• more spines in high-licking and grooming (LG) offspring

• stimulation and vehicle:

  • high-LG: more LTP

  • low-LG: LTD instead

• stimulation and corticosterone:

  • high-LG: no LTP

  • low-LG: more LTP bc being reared in adversed environment = plasticity

• more contextual fear conditioning in low-LG offspring → better learners in stressful environment = ELA optimize brain development for performing under stress later in life

when does development end?

• many circuits and behaviours are stable once animals are sexually mature young adults

• brain changing from birth to death:

  • age-related degenerative processes:

    • decreased HPC neurogenesis

    • less synaptic plasticity

    • decreased neuronal excitability

    • increased brain inflammation

  • continued development:

    • extended synaptic pruning

    • continued neurogenesis

extended synaptic development → late onset PFC behaviours

• synaptic density highest within 1st decade of life

• pruning happens from 10-30

• and 30 the pruning plateaus

• PFC remain plastic for a longgg time = higher cognitive functions continue to develop throughout adulthood

delayed and extended neurogenesis → HPC behaviour in adulthood

• irradiation of the rat HPC in the first postnatal week = 85% fewer DG neurons in adulthood

• DG neurogenesis peaks in the first week of life = measured by counting % of cells labelled with 3H-thymidine at diff ages

emergence of symptoms in diff disorders

• ASD: childhood

• schizo: adolescence

• AD: adulthood

dendritic spine number in diff disorders

• ASD more spines than normal

• Normal > AD > schizo

AD

• type of dementia that is characterized by episodic memory deficits

• as time goes on, irreversible progression towards more general cognitive decline and emotional disturbances

• few years after AD diagnosis = alr around 30% fewer synapses

  • extent of synapse loss is currently the best biomarker for memory deficits

tau pathology

• begins at 30 years