MODULATION OF SENSORY NEURON EXCITATORY AND INHIBITORY RESPONSES IN THE VENTROBASAL THALAMUS BY ACTIVATION OF METABOTROPIC EXCITATORY AMINO-ACID RECEPTORS

Several different types of metabotropic excitatory amino acid receptors (mGluRs) are present in the thalamus. We have previously shown that the agonists L-AP4 and CCG-I can have apparently presynaptic effects on GABAergic inhibitory transmission in the thalamus. In this study we attempted to characterize the different receptor types which may mediate these effects and the known post-synaptic excitatory actions of 1S,3R-ACPD in the ventrobasal thalamus, by using a number of agonists with different spectra of activity at the various mGluRs. Inhibitory responses in ventrobasal thalamic neurones of urethane-anaesthetized rats were evoked by air-jet stimuli to the vibrissae and extracellular recording methods were used to reveal inhibitory responses as an inhibition of excitatory responses in a condition-test paradigm. The Group II and Group III mGluR agonists L-AP4, CCG-I, DCG-IV, 1S,3R-ACPD and S-4C3HPG, applied in the vicinity of the recording site by iontophoresis, were found to reduce inhibitions revealed by the condition-test paradigm (by 67, 75, 50, 43 and 77% from control inhibitions, respectively). The endogenous mGluR agonist L-serine-O-phosphate (L-SOP) was found to have similar, although weaker, actions (31% reduction of inhibition), while the Group I agonist 3,5-DHPG had little effect in this test (9% reduction of inhibition). In contrast, both 3,5-DHPG and 1S,3R-ACPD had direct excitatory actions on VB neurones, and these could be antagonized by 4CPG. The effects of CCG-I in the condition-test paradigm could be antagonized by the antagonists MCCG, MCPG, but not MAP4. In contrast, we have previously shown that MAP4 was able to block the effects of L-AP4. These data suggest that there may be at least two types of receptor mediating the disinhibitory effects, which may belong to the Group II and Group III type of mGluR, whereas the postsynaptic excitatory responses to mGluR agonists are probably mediated via Group I receptors (possibly mGluR1).