Reduction of cortico-thalamic epsps in vivo by antagonists acting at metabotropic glutamate receptors (mGluRs) and NMDA receptors. S.A. Eaton & T.E. Salt. Dept. Visual Science, Inst. Ophthalmology, Bath St., LONDON ECIV 9EL, U.K.

We have previously shown, in the rat ventrobasal thalamus (VB) in vivo, that EPSPs evoked by natural somatosensory (air jet) stimuli can be blocked by the NMDA receptor antagonist CPP and the AMPA receptor antagonist CNQX (Salt & Eaton, 1991, Eur J Neurosci, 3: 296-300). As thalamic relay nuclei receive a substantial cortical input, we have now investigated the synaptic pharmacology of EPSPs evoked by stimulation of the S1 cortex.

Intracellular recordings were made from VB relay neurones in urethane-anaesthetised rats with combination recording/iontophoresis micro-pipettes. Electrical stimulation (0.1ms pulse) of ipsilateral S1 cortex evoked EPSPs, followed by IPSPs which curtailed the EPSPs. Iontophoretic application of the competitive GABAA-receptor antagonist SR95531 reduced the IPSPs and revealed enhanced cortico-thalamic EPSPs. Such EPSPs were reduced by iontophoretic applications of CPP at doses which selectively blocked NMDA -evoked depolarisations. The Group-I metabotropic glutamate receptor antagonist (S)-4-carboxyphenylglycine [(S)-4CPG] also reduced the cortico-thalamic EPSPs, but did not reduce EPSPs evoked by air jet stimulation of the somatosensory afferents to VB at doses which reduced depolarisations evoked by the metabotropic agonist (1S,3R)-ACPD.

These data suggest that cortico-thalamic EPSPs in vivo are mediated by a combination of NMDA receptors and Group-I metabotropic receptors, whereas sensory-evoked EPSPs are mediated via AMPA receptors and NMDA receptors.

Supported by the Wellcome Trust.