There is still a lot of debate as to what each individual region contributes to the attainment and expression of those memories, but the basic (and I think very reasonable model) is that the memories are 'stored' in the amygdala, and become expressed when certain contextual information is processed at the hippocampus and prefrontal cortex. You've got a number of things right - fear memories attained through Pavlovian conditioning are predominantly mediated through activity in the amygdala, prefrontal cortex and hippocampus in rodents. Hey, you've got a lot of questions there and I don't think that I will be able to answer them all succinctly here, but I will try to help and hopefully point you in the right direction :) As well, the studies show that allosteric medication acting the CRHR1 can inhibit fear response. It would seem that fear is not interpreted in part of the brain. has pathways that regulate the limbic system. The aforementioned thalamus, hippocampus etc. A person can still feel fear with impairments (or in the strange case of one woman, the complete removal).īut they mention other areas of the basil ganglia which is linked to the amygdala. It is more intrinsic in emotional interpretation. I don’t know why the amygdala wasn’t mentioned exclusively, but it isn’t needs for a fear response necessarily. The authors seem to be summarizing a few things, but mostly you have it right. The pathways are a cascade effect, and the authors were speaking about the various pathways that will have CRHR1 regulating neurons from the PFC (forebrain) down to the Limbic centers for fear response. I think you mean “formulate” as formate is a compound anion from Formic Acid.īut yes, they formulate in those respective areas. ''The stimulus reaches the thalamus (FROM WHERE? Cortex/sensory systems?), and information is passed to the lateral nucleus, then the basolateral system, and immediately to the central nucleus where a response is then formed'' ''The lateral nuclei receives the majority of sensory information, which arrives directly from the temporal lobe structures, including the hippocampus and primary auditory cortex'' ''The septal nuclei receive reciprocal connections from the olfactory bulb, hippocampus, amygdala, hypothalamus, midbrain, habenula, cingulate gyrus, and thalamus.'' Im confused why they didnt mention the amygdala above? also what do they mean by cortex (do they mean PFC since they said forebrain?) and what is septum?(septal nuclei? or septum pellucidum?) As the limbic system, these regions are linked and, as the current study shows, trigger fear-inducing behaviour in glutamatergic neurons.'' ''in regions of the forebrain (cortex, hippocampus, thalamus, septum), CRHR1 is detectable in glutamatergic and GABAergic neurons. This article says something different tho: This leads me to the question, what decides how much activity is in these areas? Hormones / neurontransmitters? Are these areas activated by CRHR1 activation? (CRH binding to CRHR1 receptors?). Is it true these parts of the brain formate fear learning memory? So I imagine if increased activity in these regions (hippocampus, basal and central amygdala) means more fear learning.
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