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Volume 16, Number 20, Issue of October 15, 1996 pp. 6342-6352
Copyright ©1996 Society for NeuroscienceGABAB Receptors, Monoamine Receptors, and Postsynaptic Inositol Trisphosphate-Induced Ca2+ Release Are Involved in the Induction of Long-Term Potentiation at Visual Cortical Inhibitory Synapses
Received March 28, 1996; revised July 22, 1996; accepted July 24, 1996.
Yukio Komatsu Department of Physiology, Kyoto Prefectural University of Medicine, Kyoto 602, Japan
-Aminobutyric acid (GABA)A receptor-mediated inhibitory synaptic transmission in visual cortex undergoes long-term potentiation (LTP), which is input-specific and associative. The present study, conducted under a blockade of ionotropic glutamate receptors, demonstrates an induction mechanism of LTP considerably different from those of associative LTP at excitatory synapses. Inhibitory responses of layer V cells 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 GABAB receptors but not for GABAA or metabotropic glutamate receptors. Inhibition of postsynaptic G-proteins, phospholipase C, inositol trisphosphate (IP3) receptors, or Ca2+ increase prevented the generation of LTP, as did the blockade of GABAB receptors.
In rat cerebral cortex, GABAB receptor activation is not known to affect the IP3 level by itself. However, it facilitates IP3 formation induced by the activation of
1 adrenoceptors, which are believed to be located postsynaptically. Accordingly, I examined the involvement of these and other amine receptors, including histamine H1, muscarinic acetylcholine, and serotonin 5-HT2 receptors, all of which are coupled to IP3 formation. Only the blockade of
Key words: long-term potentiation; inhibitory synaptic transmission; visual cortex; GABAA receptor; GABAB receptor;
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