Whole-cell patch-clamp recording in embryonic chick brain slices was used to examine the effect of nicotinic receptor activation on synaptic activity in neurons of the ventral lateral geniculate nucleus (LGNv). In LGNv neurons with input resistances < 250 M omega, bath perfusion of the nicotinic agonist, carbachol (10-30 microM), in the presence of 0.5-1.0 microM tetrodotoxin (TTX) and 1.0 microM atropine, produced a dramatic increase in the frequency of spontaneous postsynaptic currents (n = 8/8), while eliciting little or no direct postsynaptic response. The nicotinic antagonist, dihydro-beta-erythroidine (DH beta E; 30-100 microM) had no effect on basal synaptic currents, but blocked the carbachol-induced enhancement of spontaneous currents, demonstrating that activation of nicotinic receptors is responsible for this effect. 2. The gamma-aminobutyric acid A (GABAA) receptor antagonist, bicuculline (10-20 microM), blocked the basal spontaneous synaptic currents (n = 4) as well as the carbachol-induced enhancement of these events (n = 3), indicating that these currents are likely to be GABAergic inhibitory postsynaptic currents (IPSCs). 3. Because the nicotinic agonist-induced increase in IPSC frequency occurred during blockade of synaptic transmission with TTX, the enhancement of synaptic activity is not dependent upon action potential propagation. This is in marked contrast to our results in chick lateral spiriform neurons in which nicotinic agonist-induced increases in spontaneous GABAergic IPSCs were completely abolished in the presence of TTX. The data indicate that the nicotinic receptors mediating the increase in IPSC frequency in the LGNv are likely to be located directly on presynaptic nerve terminals.
