BK21 Seminar

 

▶ Subject : Amygdala, cholecystokinin and compound postsynaptic potentials

▶ Speaker :Leeyup Chung
      (Duke University School of Medicine, Department of Pediatrics )

▶ Date :  13:30~15:00/ Oct. 27(Thu)/2011

▶ Place :  #104 , Life Sience Bldg

 

*Abstract
 I will present my work with Dr. Scott D. Moore in the Department of Psychiatry, Duke University. It is about amygdala, a brain region implicated in fear and anxiety. First, we tested the effect of CCK on spontaneous synaptic events in the basolateral amygdala (BLA) using whole cell patch recordings in rat brain slice preparation. We found that CCK increased the frequency of spontaneous inhibitory postsynaptic potentials (sIPSPs) and currents (sIPSCs). Second, to determine the source of the increased inhibition we examined the direct effect of CCK on local interneurons in this region. CCK most strongly depolarized fast-spiking interneurons. Burst-firing and regular-firing interneurons were also depolarized, although to a lesser degree. However, another distinct group of interneurons was unaffected by CCK. These effects were mediated by the CCKB receptor subtype. The excitatory effect of CCK appeared to be mediated by both a n0nselective cation and a K+ current. Third, we have since observed that CCK induces synchronized rhythmic activity composed of compound postsynaptic potentials (cPSPs). The cPSPs were attenuated by glutamate receptor antagonists or low concentrations of GABAA receptor antagonists, but not by the GABAB receptor antagonist. Low concentrations of tetrodotoxin (10 nM) also attenuated the cPSPs. The Na–K–2Cl cotransporter blocker, bumetanide (1 or 10 µM) also blocked the cPSPs. The anxiogenic neuropeptide corticotropin-releasing factor facilitated cPSPs while anxiolytic neuropeptides attenuated cPSPs. We hypothesize that cPSPs are generated by positive feedback between a subset of interneurons and a subset of glutamatergic projection neurons.

☎ Inquiry : Prof.  Sang Ki Park(279-2349)