Glutamate and GABA release are enhanced by different subtypes of presynaptic nicotinic receptors in the lateral geniculate nucleus

Abstract

The functional role of nicotinic acetylcholine receptors (nAChRs) in the ventral lateral geniculate nucleus (LGNv) was examined in chick brain slices. Whole-cell patch-clamp recordings of neurons in the LGNv revealed the presence of bicuculline-resistant spontaneous postsynaptic currents (PSCs), which were subsequently blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), an AMPA receptor antagonist. Carbachol and other nicotinic agonists produced marked increases in the frequency of the glutamatergic spontaneous PSCs in the presence of tetrodotoxin, whereas they had little or no effect on current amplitude. The nicotinic receptor antagonist dihydro-β-erythroidine (DHβE) blocked the carbachol-induced enhancement of spontaneous glutamatergic PSCs. α-bungarotoxin (α-BgTx) selectively blocked the nAChR- mediated enhancement of spontaneous glutamatergic PSCs but did not prevent nAChR-mediated enhancement of spontaneous GABAergic PSCs in the LGNv. Methyllycaconitine and strychnine, other blockers of nAChRs containing the α7 subunit, failed to inhibit carbachol's increase of spontaneous glutamatergic and GABAergic PSCs. These results demonstrate that the LGNv neurons receive both glutamatergic and GABAergic inputs and that the release of these transmitters can be modulated by different presynaptic nAChRs. Thus, the regulation of synaptic efficacy in the brain by presynaptic nAChRs can be complex, involving multiple neurotransmitters acting on the same neuron.