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SUMMARY:Neurocircuitry of Stress Adaptation
DTSTART:20180416T163000
DTEND:20180416T173000
DTSTAMP:20260501T165528Z
UID:35049555f8bb83cbfb79f09aa2a1289760edd7cfd240f9db0d81b4c4
CATEGORIES:Conferences - Seminars
DESCRIPTION:Prof. James P. Herman\,  Department of Psychiatry and Behavio
 ral Neuroscience\,  University of Cincinnati \, USA\nMulti-component cir
 cuits are critical for control of physiology and behavior\, both in the co
 ntext of adaptation and pathology. Neuroanatomical and functional studies 
 have defined tripartite regulation of stress reactivity\, involving prefro
 ntal and hippocampal inputs that limit stress responses and amygdala input
 s that appear excitatory. Importantly\, all three of these structures expr
 ess an abundance of glucocorticoid receptors (GRs)\, which integrate stres
 s hormone signals into appropriate changes in network reactivity. To query
  the role of the prefrontal cortical GR in stress homeostasis\, we have us
 ed viral vector-based technologies to drive GR knockdown in the infralimbi
 c cortex (IL).  In rats\, shRNA-mediated knockdown of GR in the IL (but n
 ot prelimbic) cortex causes enhanced HPA axis responsiveness to both acute
  and chronic stress\, and enhanced immobility in the forced swim test\, su
 ggesting a role for the IL GR in limiting behavioral and physiological str
 ess reactivity. In addition\, chronic stress causes a marked enhancement o
 f inhibitory synaptic drive in the IL\, consistent with a loss of function
 . Enhanced inhibition is associated with marked reductions in number of GR
  immunoreactive GABAergic interneurons\, suggesting a selective impact of 
 stress on this cell population.  Current studies are using rat model of c
 onditional GR deletion (generated using CRSIPR/Cas9 methods) to test cell 
 type and circuit mechanisms mediating prefrontal stress control.
LOCATION:SV 1717 https://plan.epfl.ch/?room==SV%201717
STATUS:CONFIRMED
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