Variation of CS salience reveals group II mGluR-dependent and -independent forms of conditioning in the rat.

There is good evidence that metabotropic glutamate receptors (mGluRs) are involved in some types of learning, and we have previously suggested that this involvement may reflect the modulation by mGluRs of the signal-to-noise ratio in neural networks. This hypothesis supposes that unspecific activation of mGluRs increases background noise level, so reducing the effectiveness of behaviourally relevant stimuli as signals in the network. We report here that intraperitoneal (i.p.) injection of 4-aminopyrrolidine-2,4-dicarboxylic acid (APDC), a specific agonist of group II mGluRs, disrupts conditioning to context (but not to cue) using conventional procedures. The hypothesis predicts, however, that the effect of the drug should be counteracted by the use of more salient stimuli, which would provide stronger signals to the network. In accordance with this prediction, we find that increases in the salience of either the CS (context) or the UCS (shock) abolish the drug-induced disruption of conditioning. These results suggest that group II mGluRs modulate neural networks involved in association formation.

Impairment of contextual fear conditioning in rats by Group I mGluRs: reversal by the nootropic nefiracetam.

The blockade of Group I metabotropic glutamate receptors (mGluRs) may be a potential strategy for prevention therapy of neurotoxicity. We here confirm previous reports that systemic application of the Group I antagonist, 1-aminoindan-1,5-dicarboxylic acid (AIDA), causes amnesia in a contextual fear conditioning paradigm in rats. This deficit was fully reversed by long-term pretreatment with the nootropic nefiracetam, which in fact obtained supranormal performance. Our data suggest that application of Group I antagonists to prevent neurotoxicity, combined with nootropic treatment to prevent cognitive deficits, may be a therapeutic strategy for the development of novel antineurotoxic treatments.

A critique of the neuroecology of learning and memory.

Recent years have seen the emergence of neuroecology, the study of the neural mechanisms of behaviour guided by functional and evolutionary principles. This research has been of enormous value for our understanding of the evolution of brain- and species-specific behaviour. However, we question the validity of the neuroecological approach when applied to the analysis of learning and memory, given its arbitrary assumption that different 'problems' engage different memory mechanisms. Differences in memory-based performance in 'natural' tasks do not prove differences in memory capacity; similarly, differences in the use of memory in the natural environment do not provide a sound basis for expecting differences in anatomical structures that subserve learning and memory. This critique is illustrated with examples taken from the study of the neurobiology of food storing and song learning in birds.