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Complex Control of Striatal Neurotransmission by Nicotinic Acetylcholine Receptors via Excitatory Inputs onto Medium Spiny Neurons

Journal article
Authors Valentina Licheri
Oona Lagström
Amir Lotfi
X. H. Patton
Holger Wigström
B. Mathur
Louise Adermark
Published in Journal of Neuroscience
Volume 38
Issue 29
Pages 6597-6607
ISSN 0270-6474
Publication year 2018
Published at Institute of Neuroscience and Physiology, Department of Physiology
Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Pages 6597-6607
Language en
Keywords addiction, basal ganglia, dorsolateral striatum, dopamine, electrophysiology, nAChR, positron-emission-tomography, long-lasting disinhibition, dopamine, release, nucleus-accumbens, cholinergic interneurons, in-vivo, muscarinic receptors, glutamate release, dorsal striatum, rat striatum, Neurosciences & Neurology
Subject categories Neurosciences


The prevalence of nicotine dependence is higher than that for any other substance abuse disorder; still, the underlying mechanisms are not fully established. To this end, we studied acute effects by nicotine on neurotransmission in the dorsolateral striatum, a key brain region with respect to the formation of habits. Electrophysiological recordings in acutely isolated brain slices from rodent showed that nicotine (10 nM to 10 mu M) produced an LTD of evoked field potentials. Current-clamp recordings revealed no significant effect by nicotine on membrane voltage or action potential frequency, indicating that the effect by nicotine is primarily synaptic. Nicotine did not modulate sIPSCs, or the connectivity between fast-spiking interneurons and medium spiny neurons, as assessed by whole-cell recordings combined with optogenetics. However, the frequency of sEPSCs was significantly depressed by nicotine. The effect by nicotine was mimicked by agonists targeting alpha 7-or alpha 4-containing nAChRs and blocked in slices pretreated with a mixture of antagonists targeting these receptor subtypes. Nicotine-induced LTD was furthermore inhibited by dopamine D2 receptor antagonist and occluded by D2 receptor agonist. In addition, modulation of cholinergic neurotransmission suppressed the responding to nicotine, which might reflect upon the postulated role for nAChRs as a presynaptic filter to differentially govern dopamine release depending on neuronal activity. Nicotine-induced suppression of excitatory inputs onto medium spiny neurons may promote nicotine-induced locomotor stimulation and putatively initiate neuroadaptations that could contribute to the transition toward compulsive drug taking.

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