Hippocampus-dependent learning facilitated by a monoclonal antibody or D-cycloserine

Lucien T. Thompson*, Joseph R. Moskal, John F. Disterhoft

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

167 Scopus citations


Persistent neuronal plasticity, including that observed at some hippocampal synapses, requires N-methyl-D-aspartate (NMDA)-mediated transmission. NMDA receptor activation may be necessary for hippocampus-dependent learning as antagonists block acquisition in many such tasks. The behavioural effects of NMDA agonists are less well defined. We have shown that a monoclonal antibody (B6B21) displaced [3H]-glycine that was bound specifically to the NMDA receptor, and enhanced the opening of its integral cation channel in a glycine-like fashion, effects that were competitively antagonized by 7-chlorokynurenic acid1. B6B21 also enhanced long-term potentiation in hippocampal slices1. We report here that intraventricular infusions of B6B21 significantly enhances acquisition rates in hippocampus-dependent trace eye blink conditioning in rabbits, halving the number of trials required to reach a criterion of 80% conditioned responses. Peripheral injections of D-cycloserine, a partial agonist of the glycine site on the NMDA receptor which crosses the blood-brain barrier, also doubles rabbits' learning rates. Pseudoconditioning control experiments indicated a lack of nonspecific behavioural sensitization effects. Our data suggest that enhanced activation of the glycine coagonist site on the NMDA receptor/channel complex facilitates one form of associative learning and may be used in other learning tasks.

Original languageEnglish (US)
Pages (from-to)638-641
Number of pages4
Issue number6396
StatePublished - Jan 1 1992

ASJC Scopus subject areas

  • General


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