GABA(B) RECEPTORS, MONOAMINE RECEPTORS, AND POSTSYNAPTIC INOSITOL TRISPHOSPHATE-INDUCED CA2-TERM POTENTIATION AT VISUAL CORTICAL INHIBITORYSYNAPSES( RELEASE ARE INVOLVED IN THE INDUCTION OF LONG)

gamma-Aminobutyric acid (GABA)(A) receptor-mediated inhibitory synapti c transmission in visual cortex undergoes long-term potentiation (LTP) , which is input-specific and associative. The present study, conducte d under a blockade of ionotropic glutamate receptors, demonstrates an induction mechanism of LTP considerably different from those of associ ative LTP at excitatory synapses, Inhibitory responses of layer V cell s evoked by layer IV stimulation were studied in developing rat visual cortex slices by using intracellular and whole-cell recording methods , LTP induction was prevented by the application of an antagonist for GABA(B) receptors but not for GABA(A) or metabotropic glutamate recept ors, Inhibition of postsynaptic G-proteins, phospholipase C, inositol trisphosphate (IP3) receptors, or Ca2+ Increase prevented the generati on of ITP, as did the blockade of GABA(B) receptors. In rat cerebral c ortex, GABA(B) receptor activation is not known to affect the IP3 leve l by itself. However, it facilitates IP3 formation induced by the acti vation of alpha(1) adrenoceptors, which are believed to be located pos tsynaptically, Accordingly, I examined the involvement of these and ot her amine receptors, including histamine H-1, muscarinic acetylcholine , and serotonin 5-HT2 receptors, all of which are coupled to IP3 forma tion, Only the blockade of alpha(1) adrenoceptors or serotonin 5-HT2 r eceptors prevented LTP induction in most, but not all, of the cells. T hese results suggest that LTP induction requires the activation of pos tsynaptic GABA(B) receptors and that its effect is mediated al least p artly by facilitation of the monoamine-induced IP3 formation, which th en causes Ca2+ release from the internal stores in postsynaptic cells.