HSM330 article 4 summary

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Ryerson University
Health Services Management
HSM 330
Daolun Chen

LeDoux 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 on 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 conditioning -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. -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 ygdala -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 -most extensively studied form of LTP occurs in CA1 and involves interaction btw n presynaptic glutamate and 2 classes of postsynaptic receptors 1) glutamate binds to AMPA receptors and depolarizes postsynaptic cell - depolar ization removes Mg block on NMDA receptors 2) Ca flows into cell through NMDA channel and voltage-gated Ca channels and tri ggers intracellular events that result in gene induction and synthesis of new proteins - these then help st abilize the changes over long periods of time -many in vitro studies of LTP in amygdala, mostly involving pathways carrying in fo from thalamus or cortex to LA and B -as in CA1, LTP in thalamo-amygdala pathway requires an elevation of postsynapti c Ca, and that the Ca enters through either NMDA receptors or voltage-gated Ca channels (VGCCs)
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