β2* nicotinic acetylcholine receptor subtypes mediate nicotine-induced enhancement of Pavlovian conditioned responding to an alcohol cue
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 alcohol-associated cue. Male Long-Evans rats with freely available food and water were fi...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2022-10-01
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| Series: | Frontiers in Behavioral Neuroscience |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fnbeh.2022.1004368/full |
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| author | Jean-Marie Maddux Jean-Marie Maddux Leslie Gonzales Leslie Gonzales Nathaniel P. Kregar |
| author_facet | Jean-Marie Maddux Jean-Marie Maddux Leslie Gonzales Leslie Gonzales Nathaniel P. Kregar |
| author_sort | Jean-Marie Maddux |
| collection | DOAJ |
| description | 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 alcohol-associated 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 dihydro-beta-erythroidine (DHβE; 3 mg/kg) or the α7-selective nAChR antagonist methyllycaconitine (MLA; 6 mg/kg), followed by their assigned nicotine or saline injection before assessing their conditioned response to the alcohol-associated cue. Consistent with previous reports, nicotine enhanced the Pavlovian conditioned response to the alcohol-paired cue. DHβE attenuated this enhancement, whereas MLA did not. These results suggest that nicotine acts via β2*, but not α7, 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. |
| first_indexed | 2024-04-12T12:57:13Z |
| format | Article |
| id | doaj.art-c840343578114e7794a373d5cb4b5970 |
| institution | Directory Open Access Journal |
| issn | 1662-5153 |
| language | English |
| last_indexed | 2024-04-12T12:57:13Z |
| publishDate | 2022-10-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Behavioral Neuroscience |
| spelling | doaj.art-c840343578114e7794a373d5cb4b59702022-12-22T03:32:18ZengFrontiers Media S.A.Frontiers in Behavioral Neuroscience1662-51532022-10-011610.3389/fnbeh.2022.10043681004368β2* nicotinic acetylcholine receptor subtypes mediate nicotine-induced enhancement of Pavlovian conditioned responding to an alcohol cueJean-Marie Maddux0Jean-Marie Maddux1Leslie Gonzales2Leslie Gonzales3Nathaniel P. Kregar4Department of Psychology, Lake Forest College, Lake Forest, IL, United StatesNeuroscience Program, Lake Forest College, Lake Forest, IL, United StatesDepartment of Psychology, Lake Forest College, Lake Forest, IL, United StatesNeuroscience Program, Lake Forest College, Lake Forest, IL, United StatesNeuroscience Program, Lake Forest College, Lake Forest, IL, United StatesNicotine 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 alcohol-associated 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 dihydro-beta-erythroidine (DHβE; 3 mg/kg) or the α7-selective nAChR antagonist methyllycaconitine (MLA; 6 mg/kg), followed by their assigned nicotine or saline injection before assessing their conditioned response to the alcohol-associated cue. Consistent with previous reports, nicotine enhanced the Pavlovian conditioned response to the alcohol-paired cue. DHβE attenuated this enhancement, whereas MLA did not. These results suggest that nicotine acts via β2*, but not α7, 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.https://www.frontiersin.org/articles/10.3389/fnbeh.2022.1004368/fullnicotineethanolPavlovian conditioned approachgoal-trackingnicotinic acetylcholine receptorassociative learning |
| spellingShingle | Jean-Marie Maddux Jean-Marie Maddux Leslie Gonzales Leslie Gonzales Nathaniel P. Kregar β2* nicotinic acetylcholine receptor subtypes mediate nicotine-induced enhancement of Pavlovian conditioned responding to an alcohol cue Frontiers in Behavioral Neuroscience nicotine ethanol Pavlovian conditioned approach goal-tracking nicotinic acetylcholine receptor associative learning |
| title | β2* nicotinic acetylcholine receptor subtypes mediate nicotine-induced enhancement of Pavlovian conditioned responding to an alcohol cue |
| title_full | β2* nicotinic acetylcholine receptor subtypes mediate nicotine-induced enhancement of Pavlovian conditioned responding to an alcohol cue |
| title_fullStr | β2* nicotinic acetylcholine receptor subtypes mediate nicotine-induced enhancement of Pavlovian conditioned responding to an alcohol cue |
| title_full_unstemmed | β2* nicotinic acetylcholine receptor subtypes mediate nicotine-induced enhancement of Pavlovian conditioned responding to an alcohol cue |
| title_short | β2* nicotinic acetylcholine receptor subtypes mediate nicotine-induced enhancement of Pavlovian conditioned responding to an alcohol cue |
| title_sort | β2 nicotinic acetylcholine receptor subtypes mediate nicotine induced enhancement of pavlovian conditioned responding to an alcohol cue |
| topic | nicotine ethanol Pavlovian conditioned approach goal-tracking nicotinic acetylcholine receptor associative learning |
| url | https://www.frontiersin.org/articles/10.3389/fnbeh.2022.1004368/full |
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