PMID- 8983983 OWN - NLM STAT- MEDLINE DCOM- 19970103 LR - 20210107 IS - 0014-4819 (Print) IS - 0014-4819 (Linking) VI - 106 IP - 3 DP - 1995 TI - NMDA and non-NMDA receptors mediate taste afferent inputs to cortical taste neurons in rats. PG - 391-402 AB - Two main subclasses of ionotropic receptors for excitatory amino acids (EAAs), N-methyl-D-aspartate (NMDA) receptors and non-NMDA receptors, are involved in neurotransmission in the cortex of mammals. To examine whether EAAs are transmitters at the cortical taste area (CTA) in rats and to elucidate which types of the two ionotropic receptors operate at these synapses, we studied the effects of microiontophoretic administration of EAA antagonists on the responses of 64 taste cortical neurons to four basic taste stimuli in urethane-anesthetized rats. Both D-2-amino-5-phosphonovalerate (APV), a selective antagonist for NMDA receptors, and 6-cyano-7-nitro-quinoxaline-2,3-dione (CNQX), a selective antagonist for non-NMDA receptors, suppressed most of the taste responses. The percentage of neurons suppressed by APV (70.3%) was almost the same as that suppressed by CNQX (64.1%). These suppressive effects were independent of the effects of background discharges during the prestimulus, water-rinsing period. The percentage of neurons suppressed by the antagonists did not differ between any pairs of taste stimuli. The number of neurons possessing both receptors was larger in the granular insular area (area GI), one of the two CTAs, than in the dysgranular insular area (area DI). In addition, taste responses were suppressed by CNQX or by both APV and CNQX in area GI in a significantly larger number of layer V neurons than in area DI. The present results indicate that normal excitatory transmission of taste afferents in the CTA in rats was mediated by both NMDA and non-NMDA receptors. The finding that a large fraction of neurons in the CTA in rats mediated taste information through NMDA receptors in normal transmission might be related to the higher potency of the plasticity observed in the CTA. FAU - Otawa, S AU - Otawa S AD - Department of Physiology, Kumamoto University School of Medicine, Japan. FAU - Takagi, K AU - Takagi K FAU - Ogawa, H AU - Ogawa H LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - Germany TA - Exp Brain Res JT - Experimental brain research JID - 0043312 RN - 0 (Excitatory Amino Acid Antagonists) RN - 0 (Receptors, Glutamate) RN - 0 (Receptors, N-Methyl-D-Aspartate) RN - 6384-92-5 (N-Methylaspartate) RN - 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione) RN - 76726-92-6 (2-Amino-5-phosphonovalerate) RN - SIV03811UC (Kainic Acid) SB - IM MH - 2-Amino-5-phosphonovalerate/pharmacology MH - 6-Cyano-7-nitroquinoxaline-2,3-dione/pharmacology MH - Animals MH - Cerebral Cortex/cytology/*physiology MH - Electrophysiology MH - Excitatory Amino Acid Antagonists/pharmacology MH - Kainic Acid/pharmacology MH - N-Methylaspartate/pharmacology MH - Neurons/*physiology MH - Neurons, Afferent/drug effects/*physiology MH - Rats MH - Rats, Sprague-Dawley MH - Receptors, Glutamate/*physiology MH - Receptors, N-Methyl-D-Aspartate/*physiology MH - Stimulation, Chemical MH - Taste/*physiology EDAT- 1995/01/01 00:00 MHDA- 1995/01/01 00:01 CRDT- 1995/01/01 00:00 PHST- 1995/01/01 00:00 [pubmed] PHST- 1995/01/01 00:01 [medline] PHST- 1995/01/01 00:00 [entrez] AID - 10.1007/BF00231062 [doi] PST - ppublish SO - Exp Brain Res. 1995;106(3):391-402. doi: 10.1007/BF00231062.