β2* nicotinic acetylcholine receptor subtypes mediate nicotine-induced enhancement of Pavlovian conditioned responding to an alcohol cue.

Autor: Maddux, Jean-Marie, Gonzales, Leslie, Kregar, Nathaniel P.
Předmět:
Zdroj: Frontiers in Behavioral Neuroscience; 10/12/2022, Vol. 16, p1-17, 17p
Abstrakt: Nicotine enhances Pavlovian conditioned responses to reward-associated cues. We investigated through which nicotinic acetylcholine receptor (nAChR) subtypes nicotine acts to produce this behavioral effect to an alcoholassociated cue. Male Long-Evans rats with freely available food and water were first accustomed to drinking 15% ethanol in their home cages using an intermittent access, two-bottle choice procedure. Then the rats were given 15 Pavlovian conditioning sessions in which a 15-s audiovisual conditioned stimulus (CS) predicted the delivery of 0.2 ml of ethanol, the unconditioned stimulus (US). Each session contained 12 CS-US trials. A control group received explicitly unpaired presentations of the CS and US. We measured Pavlovian conditioned approach to the site of US delivery during presentations of the CS, accounting for pre-CS baseline activity. Before each conditioning session, rats were injected subcutaneously with nicotine (0.4 mg/kg) or saline (1 ml/kg). During nAChR antagonist test sessions, rats were first injected systemically with the β2*-selective nAChR antagonist dihydrobeta-erythroidine (DHbE; 3 mg/kg) or the a7-selective nAChR antagonist methyllycaconitine (MLA; 6 mg/kg), followed by their assigned nicotine or saline injection before assessing their conditioned response to the alcoholassociated cue. Consistent with previous reports, nicotine enhanced the Pavlovian conditioned response to the alcohol-paired cue. DHbE attenuated this enhancement, whereas MLA did not. These results suggest that nicotine acts via β2*, but not a7, nAChRs to amplify Pavlovian conditioned responding to an alcohol cue. These findings contribute to a growing literature that identifies nAChRs as potential targets for pharmacological treatment of co-morbid alcohol and tobacco use disorders. [ABSTRACT FROM AUTHOR]
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