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.
Miura
Masami
M
Department of Neurobiology and Behavior, University of California, Irvine, California, USA. mmiura@tmig.or.jp
Ishii
Katsuyoshi
K
Aosaki
Toshihiko
T
Sumikawa
Katumi
K
D000818:Animals; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects; D018755:GABA Agonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D008810:Mice, Inbred C57BL; D017072:Neostriatum / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects*; D009538:Nicotine / Q000494:pharmacology*; D018722:Nicotinic Agonists / Q000494:pharmacology*; D018408:Patch-Clamp Techniques; D013268:Stimulation, Chemical; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D018755:GABA Agonists; D018756:GABA Antagonists; D018722:Nicotinic Agonists; D005680:gamma-Aminobutyric Acid; D009538:Nicotine