NMDA RECEPTOR AND THE TYROSINE PHOSPHORYLATION OF ITS 2B SUBUNIT IN TASTE LEARNING IN THE RAT INSULAR CORTEX

Citation
K. Rosenblum et al., NMDA RECEPTOR AND THE TYROSINE PHOSPHORYLATION OF ITS 2B SUBUNIT IN TASTE LEARNING IN THE RAT INSULAR CORTEX, The Journal of neuroscience, 17(13), 1997, pp. 5129-5135
Citations number
56
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
02706474
Volume
17
Issue
13
Year of publication
1997
Pages
5129 - 5135
Database
ISI
SICI code
0270-6474(1997)17:13<5129:NRATTP>2.0.ZU;2-X
Abstract
We demonstrate that the NMDA receptor is involved in taste learning in the insular cortex of the behaving rat and describe two facets of thi s involvement. Blockage of the NMDA receptor in the insular cortex by the reversible antagonist APV during training in a conditioned taste a version (CTA) paradigm impaired CTA memory, whereas blockage of the NM DA receptor in an adjacent cortex or before a retrieval test had no ef fect. When rats sampled an unfamiliar taste and hence learned about it , either incidentally or in the context of CTA training, the tyrosine phosphorylation of the NMDA receptor subunit 2B (NR2B) in the insular cortex was specifically increased, The level of tyrosine phosphorylati on on NR2B was a function of the novelty of the taste stimulus and the quantity of the taste substance consumed, properties that also determ ined the efficacy of the taste stimulus as a conditioned stimulus in C TA; however, blockage of the NMDA receptor by APV during training did not prevent tyrosine phosphorylation of NR2B. We suggest that tyrosine phosphorylation of NR2B subserves encoding of saliency in the insular cortex during the first hours after an unfamiliar taste is sampled an d that this encoding is independent of another, necessary role of NMDA receptors in triggering experience-dependent modifications in the ins ular cortex during taste learning. Because a substantial fraction of t he NR2B protein in the insular cortex seems to be expressed in interne urons, saliency and the tyrosine phosphorylation of NR2B correlated wi th it may modulate inhibition in cortex.