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J Neurophysiol (December 18, 2002). doi:10.1152/jn.00714.2002
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Submitted on August 22, 2002
Accepted on December 16, 2002

NMDA-RECEPTOR DEPENDENT LONG-TERM SYNAPTIC DEPRESSION IN THE ENTORHINAL CORTEX IN VITRO

Said Kourrich1 and C. Andrew Chapman1*

1 Department of Psychology, Concordia University, Montreal, Quebec, Canada

* To whom correspondence should be addressed. E-mail: chapman{at}csbn.concordia.ca.

The entorhinal cortex receives a large projection from the piriform (primary olfactory) cortex and, in turn, provides the hippocampal formation with most of its cortical sensory input. Synaptic plasticity in this pathway may therefore affect the processing of olfactory information and memory encoding. We have recently found that long-term synaptic depression (LTD) can be induced in this pathway in vivo by repetitive paired-pulse stimulation, but not by low-frequency (1 Hz) stimulation with single pulses. Here, we have used field potential recordings to investigate the stimulation parameters and transmitter receptors required for the induction of LTD in the rat entorhinal cortex in vitro. The effectiveness of low-frequency stimulation (900 pulses at 1 or 5 Hz) and repeated delivery of pairs of stimulation pulses (30 ms interpulse interval) was assessed. Only repeated paired-pulse stimulation resulted in lasting LTD, and a low-intensity paired-pulse stimulation protocol that induces LTD in vivo was only effective in the presence of the GABAA receptor antagonist bicuculline (50 µM). LTD could also be induced in normal ACSF, however, by increasing the number of pulse-pairs delivered, and by increasing the stimulation intensity during LTD induction. The induction of LTD was blocked by constant bath application of the NMDA glutamate receptor antagonist APV (50 µM), indicating that LTD is dependent on NMDA receptor activation. However, LTD was not blocked by the group I/II metabotropic glutamate receptor antagonist E4-CPG (500 µM), or by bicuculline (50 µM). The induction of LTD in the entorhinal cortex in vitro is therefore dependent on intense stimulation that recruits activation of NMDA receptors, but does not require concurrent activation of metabotropic glutamate receptors or inhibitory synaptic inputs.




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