Abstract
An unique synaptic feature of ventrobasal (VB) thalamic relay neurons (which is a relay station of somatosensory information) is that, in addition to receiving primary sensory synapses, they receive massive feedback synapses originating from the neocortex. It is previously reported that cholinergic systems modulate neuronal activities in VB relay neurons. However, its mechanisms on synaptic transmission are not well examined. In the present study, we investigated the effects of exogenously applied acetylcholine (ACh) on synaptic transmissions of the mouse VB thalamic relay cell. Using whole-cell patch-clamp technique, bath-application of ACh (0.01-10 mM) elicited the direct postsynaptic inward current in a dose-dependent manner. Relatively high doses of ACh (1 and 10 mM) reduced amplitudes of both corticothalamic EPSCs and IPSCs mediated by thalamic reticular nucleus. On the other hand, ACh didn't affect EPSCs from the medial lemniscus tract which delivers somatosensory information. Both the direct excitation of the postsynaptic membrane and the regulation of synaptic transmissions of ACh were mimicked by a nicotinic ACh receptor agonist, but not by a muscarinic ACh receptor agonist. Thus, these results indicate that the activation of nicotinic ACh receptors resulted in reduction of non-lemniscal inputs and depolarization of relay cells in the VB thalamus. [J Physiol Sci. 2008;58 Suppl:S131]
