The NMDA receptor antagonist CPP impairs conditioned taste aversion and insular cortex long-term potentiation in vivo

Brain Res. 1998 Nov 23;812(1-2):246-51. doi: 10.1016/s0006-8993(98)00931-7.


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 antagonist CPP (-3(-2 carboxipiperazin-4-yl)-propyl-1-phosphonic acid) disrupts the acquisition of conditioned taste aversion, as well as, the IC-LTP induction in vivo. 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Avoidance Learning / drug effects*
  • Excitatory Amino Acid Antagonists / pharmacology*
  • Excitatory Postsynaptic Potentials / drug effects
  • Long-Term Potentiation / drug effects*
  • Male
  • Piperazines / pharmacology*
  • Rats
  • Rats, Wistar
  • Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors*
  • Taste / physiology*
  • Temporal Lobe / drug effects*


  • Excitatory Amino Acid Antagonists
  • Piperazines
  • Receptors, N-Methyl-D-Aspartate
  • 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid