1. In vivo effects of intracortical administration of NMDA and metabotropic glutamate receptors antagonists on neocortical long-term potentiation and conditioned taste aversion.
- Author
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Escobar ML, Alcocer I, and Bermúdez-Rattoni F
- Subjects
- 2-Amino-5-phosphonovalerate pharmacology, Animals, Benzoates administration & dosage, Benzoates pharmacology, Excitatory Amino Acid Agonists administration & dosage, Excitatory Postsynaptic Potentials drug effects, Glycine administration & dosage, Glycine pharmacology, Male, Microinjections, N-Methylaspartate administration & dosage, Piperazines administration & dosage, Piperazines pharmacology, Rats, Rats, Wistar, Avoidance Learning drug effects, Excitatory Amino Acid Agonists pharmacology, Excitatory Amino Acid Antagonists pharmacology, Glycine analogs & derivatives, Long-Term Potentiation drug effects, N-Methylaspartate pharmacology, Neocortex physiology, Receptors, Metabotropic Glutamate antagonists & inhibitors, Taste drug effects
- Abstract
It has been proposed that long-term potentiation (LTP), a form of activity-dependent modification of synaptic efficacy, may be a synaptic mechanism for certain types of learning. Recent studies on the insular cortex (IC), a region of the temporal cortex implicated in the acquisition and storage of conditioned taste aversion (CTA), have demonstrated that tetanic stimulation of the basolateral nucleus of the amygdala (Bla) induce an N-methyl-D-aspartate (NMDA) dependent LTP in the IC of adult rats in vivo. Here we present experimental data showing that intracortical administration of the NMDA receptor competitive antagonists CPP (-3(-2 carboxipiperazin-4-yl)-propyl-1-phosphonic acid, 0.03 microg per hemisphere) and AP-5 (D(-)-2-amino-5-phosphonopentanoic, 2.5 microg per hemisphere) disrupt the acquisition of conditioned taste aversion, as well as IC-LTP induction in vivo. In contrast, administration of the metabotropic glutamate receptor antagonist MCPG ((RS)-alpha-methyl-4-carboxyphenylglycine, 2.5 microg per hemisphere) does not disrupt the acquisition of CTA nor IC-LTP induction. These findings are of particular interest since they provide support for the view that the neural mechanisms underlying NMDA-dependent neocortical LTP constitute a possible mechanism for the learning-related functions performed by the IC.
- Published
- 2002
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