Abstract
It has been shown previously that baclofen, the GABB beta receptor agonist, reduces the excitability of ventrobasal thalamic relay neurons measured by increases in latency and decreased discharge probability, while thyrotropin releasing hormone (TRH) analogues have the opposite effects. The present experiments have shown that the excitability reducing effects of baclofen on ventrobasal transmission are antagonised by the administration of TRH analogue CG3703. These results are discussed in the context of possible GABAergic and TRHergic modulation of VBT transmission from the thalamic reticular nucleus.