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Nicotinic excitation of rat ventral tegmental neurones in vitro studied by intracellular recording
Author(s) -
Calabresi P.,
Lacey M.G.,
North R.A.
Publication year - 1989
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1989.tb16873.x
Subject(s) - hexamethonium , acetylcholine , carbachol , chemistry , nicotine , nicotinic agonist , ventral tegmental area , depolarization , muscarine , muscarinic acetylcholine receptor , tetrodotoxin , neuroscience , biophysics , endocrinology , medicine , dopamine , stimulation , dopaminergic , biology , receptor , biochemistry
1 Intracellular recordings were made from presumed dopamine‐containing neurones in the ventral tegmental area (VTA) in rat brain slices. 2 Nicotine (10–100 μ m ) and acetylcholine (ACh) depolarized the neurones. The depolarization caused by ACh was typically biphasic; both components were increased by neostigmine (0.1–10 μ m ), but only the slower component was blocked by scopolamine (1–10 μ m ). 3 The nicotinic action of ACh, studied in the presence of neostigmine and scopolamine, persisted in the presence of tetrodotoxin (1 μ m ) and cobalt (2–5 mM). 4 ACh or carbachol (30 μ m ) caused inward currents in neurones voltage‐clamped near the resting potential. These currents reversed polarity at around −4mV, were blocked by hexamethonium (1–100 μ m ) in a voltage‐dependent manner, and showed desensitization with prolonged or repeated agonist applications. 5 Depolarizations caused by ACh and carbachol were reduced in slices pretreated with κ‐bungarotoxin, but were not changed by α‐bungarotoxin. 6 These responses to ACh and nicotine resemble those previously described on autonomic ganglion cells. The direct action on VTA neurones may contribute to the positive reinforcement associated with nicotine consumption.

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