MARCH 25 Flashcards

1
Q

what can shape emotional processing throughout life?

A

experiences in early life

experience shapes NORMATIVE EMOTIONAL DEVELOPMENT and risk for PSYCHIATRIC DISORDERS

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2
Q

paper: “sensitive periods in affective development: ________ maturation of fear learning”

A

nonlinear

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3
Q

this paper makes use of an analogy to what?

A

to sensory systems

we know how sensory systems develop

ie. visual system - we need normative visual experience in order to develop functional vision

can we apply this to fear learning?

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4
Q

what 2 processes play out simultaneously across development?

A
  1. GENETIC program refined by evolution (to coordinate species-typical developmental emergence of behaviours)
  2. SPECIALIZATION that’s responsive to individual’s unique experiences (to shape brain and behaviour to demands of the specific environment)
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5
Q

sensitive periods in development

A

each functional process (and its underlying neural circuit) is subject to a SENSITIVE PERIOD in which neural development is MAXIMALLY SENSITIVE to experience

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6
Q

how does brain organization occur?

A

in an ORGANIZED, SEQUENTIAL manner

lower-order functions develop before higher-order functions

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7
Q

what happens after a sensitive period closes?

A

neural circuits stabilize

as do their behavioural functions

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8
Q

sensitive period strict definition

A

“a sensitive period is a temporally restricted window during development when a particular part of the brain is especially responsive to environmental stimuli and can undergo significant, enduring changes during this period”

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9
Q

critical period

A

extreme version of a sensitive period

if brain doesn’t receive the typical inputs during a critical period, it can lead to LASTING DYSFUNCTION

some functions are EXTREMELY DEPENDENT on the appropriate experience for normal development

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10
Q

critical periods in brain development

A

windows of EXTREME INTERDEPENDENCE BETWEEN EXPERIENCE & DEVELOPMENT

after them, a DECREASE IN PLASTICITY typically renders the BEHAVIOURAL OUTCOME IRREVERSIBLE

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11
Q

what fixes the function after the critical period has closed?

A

a decrease in neuroplasticity

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12
Q

T/F: the brain remains capable of learning and adapting even after the sensitive period has pased

A

true

ie. second language learning

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13
Q

T/F: after the critical period, it may be very difficult to develop the skill or ability if the necessary experiences weren’t encountered during the critical period

A

tue

ie. vision

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14
Q

neural circuits that mediate affective experience continue to mature into what?

A

young adulthood

(variations in early life experience persistently alter development and function of affective circuits)

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15
Q

early life stress sensitizes responses to what?

A

to future stress

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16
Q

when do many psychiatric disorders have their onset?

A

during adolescence

ie. anxiety, substance use disorder

this is why understanding sensitive periods in affective development could have important THERAPEUTIC IMPLICATIONS

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17
Q

sensitive and critical periods in visual system

A

SENSITIVE PERIODS:

^ early in life, sensitive period where brain is ESPECIALLY RESPONSIVE TO VISUAL INPUT

^ experience strongly influences development of PERCEPTUAL SKILLS

^ exposing infants to RANGE OF VISUAL STIMULI helps develop perceptual abilities

CRITICAL PERIODS:

^ for development of BINOCULAR VISION (ie. depth perception)

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18
Q

critical period plasticity within visual system

A

for normal binocular vision to develop, brain must receive VISUAL INPUT FROM BOTH ETES during the critical period

this is because visual input shapes the development of CORTICAL OCULAR DOMINANCE COLUMNS through competition

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19
Q

visual input shapes development of what?

A

cortical ocular dominance columns

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20
Q

manipulations that deprive brain of visual input from one or both eyes leads to…

A

abnormal development of ocular dominance columns

monocular deprivation = over-representation of the non-occluded eye, under-representation of the occluded eye

this is IRREVERSIBLE by restoring visual input

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21
Q

functional result of monocular deprivation during critical period

A

amblyopia

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22
Q

does monocular deprivation in adulthood result in amblyopia?

A

no (because it’s outside of the critical period)

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23
Q

what delays the onset of the critical period in the visual system?

A
  1. DARK REARING (binocular deprivation)
  2. manipulations that PREVENT the DEVELOPMENTAL INCREASE in GABAergic INHIBITION delay the onset of the critical period plasticity
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24
Q

what manipulations 1) advance and 2) delay the onset of critical period plasticity?

A
  1. advance:

^ increasing GABA signalling (inhibitory) advances onset of critical period plasticity

  1. delay:

^ decreasing GABA signaling (inhibitory) delays onset of critical period plasticity

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25
what NT is needed for onset of critical period development?
GABA
26
closure of critical period = associated with other adaptations that put a "brake" on plasticity. what are these?
perineuronal nets (PNNs)
27
perineuronal nets
PNNs part of the extracellular matrix they form AROUND PARVALBUMIN GABA neurons form a STRUCTURAL BRAKE on further plasticity
28
myelination of axons also regulate what?
the closure of the critical period
29
myelination of cortical areas continues into...
young adulthood
30
manipulations that remove the structural barriers to plasticity or strong modulation of the excitatory-inhibitory balance can do what?
partially restore plasticity after the critical period
31
degradation of PNNs in adulthood can do what?
reopen critical period plasticity
32
lateral amygdala's (LA) role in pavlovian fear learning and extinction
receives info about CS and US plasticity in LA after repeated pairings results in FORMATION OF FEAR MEMORY CS presentations evoke LA riding to activate amygdala, to then trigger fear responses via projections to hypothalamus and brainstem
33
first, CS presentations evoke LA firing - then what?
CS presentations evoke LA firing this activates the CENTRAL NUCLEUS of the amygdala this triggers FEAR RESPONSES via PROJECTIONS to HYPOTHALAMUS and BRAINSTEM
34
LA responses to CS are ______ - so the prelimbic cortex...
LA responses to the CS are TRANSIENT so the PRELIMBIC CORTEX (PL) is necessary for SUSTAINED FEAR EXPRESSION
35
prelimbic cortex is necessary for what?
sustained fear expression (because LA responses to CS are transient) LA sends projections to PL which then send projections to the CE via basal nucleus of amygdala (BA)
36
what does contextual learning of fear involve?
the hippocampus hippocampus generates CONTEXTUAL REPRESENTATION, which becomes associated with the US in the amygdala
37
hippocampus' role in contextual fear learning
it generates the CONTEXTUAL REPRESENTATION which becomes associated with the US in the amygdala
38
PL cortex is critical for...
sustained fear response
39
IL is critical for...
learning, consolidation and retrieval of EXTINCTION following extinction learning, activity of IL neurons modulates fear expression via the intercalated masses (ITC) ITC = inhibitory cells that inhibit LA signalling to the CeA
40
ITC
intercalated masses these are inhibitory cells that inhibit LA signalling to the CeA (following extinction learning, activity of IL neurons modulates fear expression via the ITC)
41
IL and PL regulate fear in what way?
in an opposing manner IL supports fear extinction learning PL supports sustained fear recall
42
what may be the human equivalent of the rodent PL?
the dACC it's activity is associated with fear expression
43
what may be the human equivalent of the rodent IL?
the vmPFC it's associated with extinction learning
44
PL in humans
dACC
45
IL in humans
vmPFC
46
when does fear learning emerge in rodents?
around P10 (postnatal day 10)
47
in rodents, before P10...
fear learning is suppressed odour-shock pairings produce paradoxical approach responses
48
before P10, the fact that odour-shock pairings produces paradoxical approach responses is hypothesized to play role in...
fostering early attachment
49
in rodents, what happens after P10?
fear learning! odour-shock pairings produce AVOIDANCE responses
50
what does P10 coincide with in rodents?
onset of SYNAPTIC PLASTICITY in the AMYGDALA
51
what plays key role in timing the emergence of fear learning in rodents?
the presence of the mother maternal deprivation leads to PRECOCIOUS ONSET of fear learning
52
infantile amnesia
infant fear memories are LESS PERSISTENT and QUALITATIVELY DIFFERENT than adult fear memories
53
what does early life stress do to infantile amnesia?
it REDUCES it leads to extended recall of the fear memory
54
which emerges first: contextual or cued fear learning?
cued this difference is thought to reflect maturation of projections from hippocampus to amygdala (because hippocampus is what generates the context around the fear memory)
55
when does contextual fear learning emerge in rodents?
P24
56
when is contextual fear learning later repressed in rodents?
P29-P45 during ADOLESCENCE
57
why is fear learning thought to be repressed during adolescence?
thought to be important for ENCOURAGING EXPLORATION away from the nest a necessary step towards independence
58
fear learning is developmentally regulated - how?
cued fear learning emerges at P10 - with onset of synaptic plasticity in amygdala contextual fear learning emerges at P24 - with onset of projections to hypothalamus contextual fear learning disappears between P29 and P48 - during adolescence to encourage independence
59
is extinction also developmentally regulated?
yes! in pre-weaning rats, EXTINCTION is PERMANENT doesn't show normal phenomena of renewal, reinstatement and spontaneous recovery
60
juvenile extinction may represent what?
unlearning (because in pre-weaning rats, extinction is permanent)
61
what happens to extinction during adolescence?
it's suppressed adolescent rats show reduced extinction - which is reflected in lack of involvement of IL and PL
62
T/F: both cued fear extinction and contextual fear learning develop nonlinearly
true adolescents showed REDUCED ABILITIES in both, relative to both preadolescents and adults
63
developmental changes in fear learning circuits are likely...
adaptive! 1. adolescence is a TIME OF EXPLORATION and animals must leave safety of home environment ^ suppressing contextual fear may be adaptive 2. yet specific dangers remain, so cued fear learning is adaptive, and resistance to extinction may further increase caution
64
humans: early life stress in institutional rearing is associated with what?
earlier onset of adult-like connectivity between vmPFC and amygdala
65
effects of maternal presence and ELA in rodents and human point to...
existence of SENSITIVE PERIODS for AFFECTIVE DEVELOPMENT
66
molecular mechanisms of sensitive period plasticity
1. switch from approach to avoidance of shock-paired stimuli at P10 = prevented by GABA receptor blockade 2. infantile amnesia is also modulated by GABA signalling 3. juvenile extinction isn't dependent on GABA signalling, unlike adult extinction
67
development of PNNs in amygdala play role in transition from...
infantile extinction (erasure) to adult extinction
68
clinical implications
if extinction is impaired during adolescence, then CBT may not be very effective (because it relies on repeated exposure to diminish fear memories via extinction processes)
69
what clinical implications does renewing developmental-like plasticity carry?
may lead to opportunities to TREAT PERSISTENT FEAR MEMORIES understanding the molecular mechanisms of the 'brakes' on plasticity can lead to new pharmacological treatments for affective disorders that could perhaps overwrite effects of early life experience
70
recap
1. development of THREAT LEARNING and EXTINCTION is NON-LINEAR in rodents and humans 2. early life experience can alter the developmental trajectories of fear learning 3. these phenomenon resemble the phenomenon of sensitive periods in visual system development 4. this suggests hypotheses about potential mechanisms underlying emotional development and the impact of experience 5. could lead to new opportunities to intervene to shape emotional processing into adulthood