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HPA Axis & Hippocampus (Neuroanatomy of fear (Amygdala
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HPA Axis & Hippocampus
Neuroanatomy of fear
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sensory information directed to amygdala
(smell and some somatosensory direct)
Amygdala excites LC and hypothalamus
Acute stress
HPA axis
Hypothalamus releasees CRH (corticotrophin releasing hormone)
Pituatary releases ACTH (adrenocorticotropic hormone)
Adrenal cortex releases cortisol and adrenaline
LC releases noradrenaline
sympathetic nervous system
activated through HPA axis
increased heart rate
blood pressure increase
blood moved to muscles
deep fast breathing (I thought shallow?)
persperation
inhibition of digestion
CNS
activated through noradrenaline
(and also serotonergic systems)
behavioural arrest (freezing)
narrowing of attention
behvioural arousal
augmented startle response
cortical activation
emotional response (fear)
Beyond the amygdala
Hippocampus
lesions have anxiolytic effects
provides contexual information important for fear conditioning
decrease in contextual fear response when BZD injected directly into hippocampus
e.g. freezing in a box where animal previously recieved shock
GABAa alpha2
Chronic stress
chronic activation of gluccocorticoid receptors in hippocampus
increased Ca2+ into neurons
too much Ca2+ cells die
hippocampus can't feedback to limit cortisol production
some anxiety disorders
diminished activity of hippocampus
loss of feedback to amygdala
reduced hippocampal volume in PTSD
lesions of hippocampus have anxiolytic effect, but hippocampal volume reduction associated with increased fear
glucocorticoid/serotonin pup licking epigenetics
couldn't express glucocorticoid receptors in adulthood more anxious phenotype
locus coeruleus
noradrenurgic projections to:
cerebellum, hippocampus, neocortex, thalamus
during survival events
increased firing
increased arousal
Benzos decrease noradrenaline from LC
Raphe nuclei
serotonergic prjections to:
nucleus accumbens, striatum, frontal cortex, hippocampus
punishment stimuli
activates serotonergic
behavioural inhibition (freezing0
benzos decrease serotonergic in raphe nuclei
Depression
heritibility & genetics
moderate - 2 - 3 times more likely if relatives have it
several genes linked
charecteristics of MDD related to different genes
Stress-diathesis hypothesis
(neurogenic hypothesis)
hyperactive HPA axis
high blood levels of cortisol
high brain levels of CRH
Reduced hippocampal volume
correlates with days of untreated depression
administer artificial cortisol
in controls, body stops producing cortisol until CRH administered
in depressives, body still produces cortisol, produces more after CRH
BDNF is reduced by stress
BDNF has been shown to protect cells agaist neuronal death
BDNF reduced in depression
Amygdala threat
HPA axis activation
cortisol released
cortisol to hippocampus (cortisol/glucocorticoid receptors)
negative feedback to HP
chronic stress
increased Ca2+ influx
excitotoxicity
cells die
hippocampus loses negative feedback to HPA
Treatment
antidepressants produce neurogenesis in hippocampus
2-4 weeks for new neurons (coincides with delay in SSRI)