Basolateral amygdala and ventral hippocampus in stress-induced amplification of nicotine self-administration during reacquisition in rat

Guoliang Yu, Burt Sharp

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Rationale: Cigarette smoking remains the leading cause of preventable morbidity and mortality in the USA, although only 3-5 % of quitters are successful for 6-12 months. Stress during abstinence increases the likelihood of relapse to smoking. We recently reported that repeated stress during abstinence from operant nicotine self-administration (SA) amplifies the reacquisition of nicotine SA and affects the diurnal intake of nicotine in rats. Herein, we sought to identify brain regions critical for the expression of stress-enhanced nicotine SA during reacquisition. Methods: Rats acquired nicotine SA (FR5) with virtually unlimited drug access (23 h/day). During abstinence (8 day), 30 min of restraint stress was applied on days 1, 3, 5, and 7. Beginning day 8, nicotine SA was reacquired over 5 days, and basolateral amygdala (BLA) was inactivated bilaterally or disconnected from nucleus accumbens core (NAcc). Similarly, ventral hippocampus (vHP) was inactivated or disconnected from BLA. Results: Bilateral inactivation (muscimol∈+∈baclofen) of BLA or disconnection from NAcc abolished the stress-enhanced reacquisition of nicotine SA without affecting basal levels of nicotine SA. Similarly, bilateral inactivation of vHP or disconnection of vHP and BLA also abolished stress-enhanced reacquisition of nicotine SA. Conclusion: BLA, vHP, and functional interactions between BLA-NAcc and vHP-BLA are required for expression of stress-enhanced nicotine SA during reacquisition. However, without stress, these functional interactions are not necessary for reexpression of nicotine SA during reacquisition. Therefore, BLA, vHP, and these regional interactions specifically mediate the effects of repeated stress on the reacquisition of nicotine SA behavior.

Original languageEnglish (US)
Pages (from-to)2741-2749
Number of pages9
JournalPsychopharmacology
Volume232
Issue number15
DOIs
StatePublished - Aug 24 2015

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Self Administration
Nicotine
Hippocampus
Nucleus Accumbens
Basolateral Nuclear Complex
Smoking
Muscimol
Baclofen

All Science Journal Classification (ASJC) codes

  • Pharmacology

Cite this

Basolateral amygdala and ventral hippocampus in stress-induced amplification of nicotine self-administration during reacquisition in rat. / Yu, Guoliang; Sharp, Burt.

In: Psychopharmacology, Vol. 232, No. 15, 24.08.2015, p. 2741-2749.

Research output: Contribution to journalArticle

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abstract = "Rationale: Cigarette smoking remains the leading cause of preventable morbidity and mortality in the USA, although only 3-5 {\%} of quitters are successful for 6-12 months. Stress during abstinence increases the likelihood of relapse to smoking. We recently reported that repeated stress during abstinence from operant nicotine self-administration (SA) amplifies the reacquisition of nicotine SA and affects the diurnal intake of nicotine in rats. Herein, we sought to identify brain regions critical for the expression of stress-enhanced nicotine SA during reacquisition. Methods: Rats acquired nicotine SA (FR5) with virtually unlimited drug access (23 h/day). During abstinence (8 day), 30 min of restraint stress was applied on days 1, 3, 5, and 7. Beginning day 8, nicotine SA was reacquired over 5 days, and basolateral amygdala (BLA) was inactivated bilaterally or disconnected from nucleus accumbens core (NAcc). Similarly, ventral hippocampus (vHP) was inactivated or disconnected from BLA. Results: Bilateral inactivation (muscimol∈+∈baclofen) of BLA or disconnection from NAcc abolished the stress-enhanced reacquisition of nicotine SA without affecting basal levels of nicotine SA. Similarly, bilateral inactivation of vHP or disconnection of vHP and BLA also abolished stress-enhanced reacquisition of nicotine SA. Conclusion: BLA, vHP, and functional interactions between BLA-NAcc and vHP-BLA are required for expression of stress-enhanced nicotine SA during reacquisition. However, without stress, these functional interactions are not necessary for reexpression of nicotine SA during reacquisition. Therefore, BLA, vHP, and these regional interactions specifically mediate the effects of repeated stress on the reacquisition of nicotine SA behavior.",
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N2 - Rationale: Cigarette smoking remains the leading cause of preventable morbidity and mortality in the USA, although only 3-5 % of quitters are successful for 6-12 months. Stress during abstinence increases the likelihood of relapse to smoking. We recently reported that repeated stress during abstinence from operant nicotine self-administration (SA) amplifies the reacquisition of nicotine SA and affects the diurnal intake of nicotine in rats. Herein, we sought to identify brain regions critical for the expression of stress-enhanced nicotine SA during reacquisition. Methods: Rats acquired nicotine SA (FR5) with virtually unlimited drug access (23 h/day). During abstinence (8 day), 30 min of restraint stress was applied on days 1, 3, 5, and 7. Beginning day 8, nicotine SA was reacquired over 5 days, and basolateral amygdala (BLA) was inactivated bilaterally or disconnected from nucleus accumbens core (NAcc). Similarly, ventral hippocampus (vHP) was inactivated or disconnected from BLA. Results: Bilateral inactivation (muscimol∈+∈baclofen) of BLA or disconnection from NAcc abolished the stress-enhanced reacquisition of nicotine SA without affecting basal levels of nicotine SA. Similarly, bilateral inactivation of vHP or disconnection of vHP and BLA also abolished stress-enhanced reacquisition of nicotine SA. Conclusion: BLA, vHP, and functional interactions between BLA-NAcc and vHP-BLA are required for expression of stress-enhanced nicotine SA during reacquisition. However, without stress, these functional interactions are not necessary for reexpression of nicotine SA during reacquisition. Therefore, BLA, vHP, and these regional interactions specifically mediate the effects of repeated stress on the reacquisition of nicotine SA behavior.

AB - Rationale: Cigarette smoking remains the leading cause of preventable morbidity and mortality in the USA, although only 3-5 % of quitters are successful for 6-12 months. Stress during abstinence increases the likelihood of relapse to smoking. We recently reported that repeated stress during abstinence from operant nicotine self-administration (SA) amplifies the reacquisition of nicotine SA and affects the diurnal intake of nicotine in rats. Herein, we sought to identify brain regions critical for the expression of stress-enhanced nicotine SA during reacquisition. Methods: Rats acquired nicotine SA (FR5) with virtually unlimited drug access (23 h/day). During abstinence (8 day), 30 min of restraint stress was applied on days 1, 3, 5, and 7. Beginning day 8, nicotine SA was reacquired over 5 days, and basolateral amygdala (BLA) was inactivated bilaterally or disconnected from nucleus accumbens core (NAcc). Similarly, ventral hippocampus (vHP) was inactivated or disconnected from BLA. Results: Bilateral inactivation (muscimol∈+∈baclofen) of BLA or disconnection from NAcc abolished the stress-enhanced reacquisition of nicotine SA without affecting basal levels of nicotine SA. Similarly, bilateral inactivation of vHP or disconnection of vHP and BLA also abolished stress-enhanced reacquisition of nicotine SA. Conclusion: BLA, vHP, and functional interactions between BLA-NAcc and vHP-BLA are required for expression of stress-enhanced nicotine SA during reacquisition. However, without stress, these functional interactions are not necessary for reexpression of nicotine SA during reacquisition. Therefore, BLA, vHP, and these regional interactions specifically mediate the effects of repeated stress on the reacquisition of nicotine SA behavior.

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