Chronic nicotine treatment increases GABAergic input to striatal neurons.

Recent studies suggest the involvement of the dorsal striatum in the advanced stages of drug addiction as well as motor functions. We investigated the effect of chronic nicotine treatment on GABAergic synaptic transmission in the striatum of mice. Intrastriatal stimulation evoked GABAA receptor-mediated polysynaptic inhibitory postsynaptic currents more frequently in medium-sized spiny projection neurons of mice treated chronically with nicotine (1 mg/kg, twice-daily subcutaneous injections for 10-15 days) than in those of PBS-treated mice. The multiphasic inhibitory postsynaptic currents consisted of monosynaptic early and polysynaptic, nicotinic acetylcholine receptor-mediated late components. Dihydro-beta-erythroidine, an antagonist of the non-alpha7nicotinic acetylcholine receptor, suppressed only the late inhibitory postsynaptic current. These results suggest that chronic nicotine treatment increases GABAergic input to projection neurons in the dorsal striatum.