β2 subunit-containing nicotinic receptors mediate the enhancing effect of nicotine on trace cued fear conditioning in C57BL/6 mice

Jennifer A. Davis, Thomas J. Gould

Research output: Contribution to journalArticle

61 Citations (Scopus)

Abstract

Rationale: Previous research indicates that acute nicotine administration enhances the acquisition of contextual fear conditioning and trace cued fear conditioning. Pharmacological inhibition of α4β2 nicotinic acetylcholine receptors (nAChRs), but not α7 nAChRs, blocked the enhancing effect of nicotine on contextual fear conditioning. Similarly, genetic deletion of the β2 nAChR subunit but not the α7 nAChR subunit blocked the enhancing effect of nicotine on contextual fear conditioning. Objectives: In the present study, nAChR subunit knockout mice were used to compare the involvement of β2 subunit-containing nAChRs and α7 subunit-containing nAChRs in the effects of nicotine on hippocampus-dependent trace cued fear conditioning and contextual fear conditioning. Methods: β2 nAChR subunit knockout mice, α7 nAChR subunit knockout mice, and their wild-type littermates received either nicotine or saline 5 minutes before training and testing. Mice were trained using five conditioned stimulus (CS; 30 s, 85 dB white noise)-trace (30 s)-unconditioned stimulus (US; 2 s footshock) pairings. Freezing to the context and freezing to the CS were assessed 24 h later. Results: Both contextual and trace cued fear conditioning were enhanced by nicotine administration in wild-type littermates and in α7 nAChR subunit knockout mice. In contrast, neither contextual fear conditioning nor trace cued fear conditioning was enhanced by nicotine administration in β2 nAChR subunit knockout mice. Conclusions: These results suggest that β2 subunit-containing nAChRs but not α7 nAChR subunit-containing nAChRs are critically involved in the enhancing effect of nicotine on contextual and trace cued fear conditioning.

Original languageEnglish (US)
Pages (from-to)343-352
Number of pages10
JournalPsychopharmacology
Volume190
Issue number3
DOIs
StatePublished - Feb 1 2007

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Nicotinic Receptors
Nicotine
Inbred C57BL Mouse
Fear
Knockout Mice
Freezing
Conditioning (Psychology)
Hippocampus
Pharmacology

All Science Journal Classification (ASJC) codes

  • Pharmacology

Cite this

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abstract = "Rationale: Previous research indicates that acute nicotine administration enhances the acquisition of contextual fear conditioning and trace cued fear conditioning. Pharmacological inhibition of α4β2 nicotinic acetylcholine receptors (nAChRs), but not α7 nAChRs, blocked the enhancing effect of nicotine on contextual fear conditioning. Similarly, genetic deletion of the β2 nAChR subunit but not the α7 nAChR subunit blocked the enhancing effect of nicotine on contextual fear conditioning. Objectives: In the present study, nAChR subunit knockout mice were used to compare the involvement of β2 subunit-containing nAChRs and α7 subunit-containing nAChRs in the effects of nicotine on hippocampus-dependent trace cued fear conditioning and contextual fear conditioning. Methods: β2 nAChR subunit knockout mice, α7 nAChR subunit knockout mice, and their wild-type littermates received either nicotine or saline 5 minutes before training and testing. Mice were trained using five conditioned stimulus (CS; 30 s, 85 dB white noise)-trace (30 s)-unconditioned stimulus (US; 2 s footshock) pairings. Freezing to the context and freezing to the CS were assessed 24 h later. Results: Both contextual and trace cued fear conditioning were enhanced by nicotine administration in wild-type littermates and in α7 nAChR subunit knockout mice. In contrast, neither contextual fear conditioning nor trace cued fear conditioning was enhanced by nicotine administration in β2 nAChR subunit knockout mice. Conclusions: These results suggest that β2 subunit-containing nAChRs but not α7 nAChR subunit-containing nAChRs are critically involved in the enhancing effect of nicotine on contextual and trace cued fear conditioning.",
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β2 subunit-containing nicotinic receptors mediate the enhancing effect of nicotine on trace cued fear conditioning in C57BL/6 mice. / Davis, Jennifer A.; Gould, Thomas J.

In: Psychopharmacology, Vol. 190, No. 3, 01.02.2007, p. 343-352.

Research output: Contribution to journalArticle

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N2 - Rationale: Previous research indicates that acute nicotine administration enhances the acquisition of contextual fear conditioning and trace cued fear conditioning. Pharmacological inhibition of α4β2 nicotinic acetylcholine receptors (nAChRs), but not α7 nAChRs, blocked the enhancing effect of nicotine on contextual fear conditioning. Similarly, genetic deletion of the β2 nAChR subunit but not the α7 nAChR subunit blocked the enhancing effect of nicotine on contextual fear conditioning. Objectives: In the present study, nAChR subunit knockout mice were used to compare the involvement of β2 subunit-containing nAChRs and α7 subunit-containing nAChRs in the effects of nicotine on hippocampus-dependent trace cued fear conditioning and contextual fear conditioning. Methods: β2 nAChR subunit knockout mice, α7 nAChR subunit knockout mice, and their wild-type littermates received either nicotine or saline 5 minutes before training and testing. Mice were trained using five conditioned stimulus (CS; 30 s, 85 dB white noise)-trace (30 s)-unconditioned stimulus (US; 2 s footshock) pairings. Freezing to the context and freezing to the CS were assessed 24 h later. Results: Both contextual and trace cued fear conditioning were enhanced by nicotine administration in wild-type littermates and in α7 nAChR subunit knockout mice. In contrast, neither contextual fear conditioning nor trace cued fear conditioning was enhanced by nicotine administration in β2 nAChR subunit knockout mice. Conclusions: These results suggest that β2 subunit-containing nAChRs but not α7 nAChR subunit-containing nAChRs are critically involved in the enhancing effect of nicotine on contextual and trace cued fear conditioning.

AB - Rationale: Previous research indicates that acute nicotine administration enhances the acquisition of contextual fear conditioning and trace cued fear conditioning. Pharmacological inhibition of α4β2 nicotinic acetylcholine receptors (nAChRs), but not α7 nAChRs, blocked the enhancing effect of nicotine on contextual fear conditioning. Similarly, genetic deletion of the β2 nAChR subunit but not the α7 nAChR subunit blocked the enhancing effect of nicotine on contextual fear conditioning. Objectives: In the present study, nAChR subunit knockout mice were used to compare the involvement of β2 subunit-containing nAChRs and α7 subunit-containing nAChRs in the effects of nicotine on hippocampus-dependent trace cued fear conditioning and contextual fear conditioning. Methods: β2 nAChR subunit knockout mice, α7 nAChR subunit knockout mice, and their wild-type littermates received either nicotine or saline 5 minutes before training and testing. Mice were trained using five conditioned stimulus (CS; 30 s, 85 dB white noise)-trace (30 s)-unconditioned stimulus (US; 2 s footshock) pairings. Freezing to the context and freezing to the CS were assessed 24 h later. Results: Both contextual and trace cued fear conditioning were enhanced by nicotine administration in wild-type littermates and in α7 nAChR subunit knockout mice. In contrast, neither contextual fear conditioning nor trace cued fear conditioning was enhanced by nicotine administration in β2 nAChR subunit knockout mice. Conclusions: These results suggest that β2 subunit-containing nAChRs but not α7 nAChR subunit-containing nAChRs are critically involved in the enhancing effect of nicotine on contextual and trace cued fear conditioning.

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