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NROC61 - LeDoux article notes

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Le Boutillier

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Hypothalamic theory of emotion (Cannon-Bard)
1) the hypothalamus evaluates the emotional relevance of env events
2) the expression of emotional responses is mediated by dischage of impulses fro
m hypothalamus to brainstem
3) projections from hypothalamus to cortex mediate conscious experience of emoti
Papez: added anatomical circuits in forebrain to theory, but retained central ro
le of ascending & descending
connections from hypothalamus
MacLean: called forebrain emotional circuits the visceral brain, and later the l
imbic system
Weiskrantz: proposed that amygdala lesions dissociate the affective/reinforcing
properties of stimuli from
their sensory representations
-in Pavlovian fear conditioning, an emotionally neutral conditioned stimulus (CS
), usu a tone, is paired w/
an aversive unconditioned stimulus (US), usu a foot shock - after several pairin
gs, CS can elicit responses
that usu occur in presence of danger, such as defensive behaviour (freezing/esca
pe responses), autonomic NS
responses (changes in blood pressure & HR), neuroendocrine responses (release of
hormones from pituitary
and adrenal glands) etc
-the responses are not learned/voluntary, they are innate, species-typical respo
nses to threats
-fear conditioning allows new/learned threats to automatically activate evolutio
nary tuned ways of responding
to danger
-sensory inputs to amygdala terminate mainly in lateral nucleus (LA), damage to
LA interferes w/ fear
-auditory inputs to LA come from auditory thalamus and auditory cortex, and fear
condit. to a simple auditory
CS can be mediated by either pathway
-projection to LA from auditory cortex is involved w/ a more complex auditory st
imulus pattern
-single unit recordings show that the cortical pathway conditions slower over tr
ials than the thalamic pathway
-so plasticity in amygdala occurs initially through the thalamic pathway
-human amygdala shows activity changes during conditioning and these correlate w
/ activity in thalamus, but
not cortex
-animals exhibit fear responses when returned to the chamber in which tone & sho
ck were paired, or chamber in
which shocks occur alone (the chamber becomes a CS)
-this is contextual fear conditioning and reqs amygdala & hippocampus
-areas of ventral hippocampus (CA1 & subiculum) project to basal (B) and accesor
y basal (AB) nuclei of
amygdala, which are also known as the basolateral and basomedial nuclei - damage
to these areas interferes
w/ contextual conditioning, so hippocampal projections to B and AB seem to be in
volved in contextual condit.
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-central nucleus of amygdala (CE) is the interface w/ motor systems
-damage to CE interferes w/ expression of conditioned fear responses
-damage to areas that CE projects to selectively interrupts expression of indivi
dual responses
-eg: damage to lateral hypothalamus affects blood pressure but not freezing resp
onses, and damage to PAG
intereferes w/ freezing but not blood pressure responses)
-damage to bed nucleus of stria terminalis has no effect on blood pressure/freez
ing responses but disrupts
conditioned release of pituitary-adrenal stress hormones
-b/c CE recieves inputs from LA, B, AB it is in a position to mediate expression
of conditioned fear responses
elicited by acoustic & contextual CSs
-direct projection from LA to CE seems sufficient for conditioning to an auditor
y CS, since lesions of B and
AB have no effect on fear conditioning to a tone
-LA and CE may communicate via the intercalated cell mass located btwn LA and CE
Cellular and Molecular Mechs underlying fear conditioning
-cells in LA are responsive to nociceptive stimulation, and some of the same cel
ls respond to auditory inputs
-so, substrate for conditioning (convergence of CS & US info) exists in LA
-during fear conditioning, firing properties of cells in LA are modified
-conditioned plasticity also occurs in auditory cortex
-response latencies in LA w/i trials (<20ms) and rate of acquisition (1-3 trials
) is best explained in terms
of direct auditory thalamo-amygdala transmission, rather than cortico-amygdala t
ransmission, since conditioned
responses in auditory cortex occur later both w/i trials and across trials
-plasticity in auditory thalamus could contribute to LA plasticity
-plasticity has also been observed in B and CE during aversive conditioning, but
acoustic responses latencies
both before and after conditioning are longer than in LA
-thus, LA seems to be initial point of sensory processing and initial site of pl
asticity in amygdala
-plasticity in amygdala has been studied using LTP
-LTP engages the cellular mechs similar to those that underlie natural learning
-success has been achieved in the attempt to related LTP memory in studies of am
-this is b/c specific synapses (those that transmit CS to LA) have been implicat
ed in a specific form of
memory involving amygdala, namely fear condit
-studies using extracellular recordings in vivo of field potentials in LA have s
hown that:
1) LTP occurs in fear processing pathways
2) the processing of natural stimuli similar to those used as a CS in conditioni
ng studies is faciliated
following LTP induction
3) fear conditioning and LTP induction produce similar changes in the processing
of a CS
-hard to explore mechs with in vivo studies, but they provide strong evidence of
relation btwn natural
learning & LTp
-LTP has also been found in vivo in hippocampal-amygdala pathway, which is invol
ved in context conditioning
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