Taste responses in the parabrachial nucleus (PBN) are significantly affected by stimulation or lesion of the central nucleus of the amygdala (CeA). To examine if the glutamate receptors in the CeA are involved in this modulation, the effects of microinjection of 6-cyano-7-nitro-quinoxaline-2, 3-dione (CNQX), an AMPA receptor antagonist, into the CeA on the activities of PBN taste neurons were observed by using extracellular recording technique. Responses of PBN taste neurons to taste stimuli were observed before and after CNQX administered to the CeA. In general, drug administration produced a time-dependent suppress of the responses in 30% PBN taste neurons, with the firing rates to HCl and QHCl were significantly lowered (P<0.05). According to the best-stimulus category, 40% NaCl-best (6/15), 30% HCl-best (3/10) and 20% QHCl-best (1/5) neurons decreased their responses to at least one basic taste stimulus after CNQX injection. In HCl- and QHCl-best neurons, the main responses were significantly inhibited after drug injections (P<0.01). The correlation coefficient of responses between the NaCl and the other three tastants decreased after drug administration to the CeA. These results suggest that AMPA receptors within the CeA may be involved in the descending modulation in the PBN taste neurons.
6-Cyano-7-nitroquinoxaline-2,3-dione ; pharmacology ; Amygdala ; drug effects ; physiology ; Animals ; Electric Stimulation ; methods ; Evoked Potentials ; physiology ; Male ; Microinjections ; Pons ; physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA ; antagonists & inhibitors ; Taste ; physiology ; Taste Threshold

LiCl at doses sufficient to induce conditioned taste aversion (CTA) causes c-Fos expression in the brain regions implicated in CTA formation. It has been reported that nitric oxide (NO) may play a role in CTA learning and LiCl increases both the synthesis and activity of NO synthase (NOS) in the brain. In this study, we examined the effect of central N omega-nitro-L- arginine methyl ester (L-NAME) on the brain c-Fos expression and CTA learning induced by lithium in rats. In the results, intracerebroventricular L-NAME given prior to lithium did not change either the lithium-induced CTA or c-Fos in the relevant brain regions. This suggests that the brain NO system may not be involved in the neuronal activation during lithium-induced CTA formation.
Animals ; Avoidance Learning/*drug effects/physiology ; Brain/*physiology ; Conditioning (Psychology) /*drug effects/physiology ; Immunohistochemistry ; Injections, Intraventricular ; Lithium/*pharmacology ; Male ; NG-Nitroarginine Methyl Ester/*pharmacology ; Nitric Oxide/physiology ; Proto-Oncogene Proteins c-fos/*analysis ; Rats ; Rats, Sprague-Dawley ; Support, Non-U.S. Gov't ; Taste/*drug effects/physiology