Nicotine enhancement of contextual fear conditioning

Gould, Thomas J.; Wehner, Jeanne M.

doi:10.1016/s0166-4328(98)00157-0

Cited by 147 publications

(222 citation statements)

References 40 publications

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“…The β2 KO mice treated chronically with saline had levels of conditioning similar to WT mice, and C57BL/6 mice treated chronically with saline and administered DHβE also showed levels of conditioning similar to controls. These results are in good agreement with past studies that reported that the nAChR antagonists mecamylamine (Gould & Wehner, 1999) and DHβE (Davis & Gould, 2006) did not disrupt conditioning. In addition, other studies have found that young β2 KO mice have normal levels of conditioning (Caldarone, Duman, & Picciotto, 2000;Davis & Gould, 2007).…”

Section: Discussionsupporting

confidence: 93%

“…Extending previous research (Davis et al, 2005;Davis & Gould, 2006;Davis & Gould, 2007;Gould & Wehner, 1999;Gould & Higgins, 2003;Wehner et al, 2004), this study demonstrates that the effects of nicotine are specific to contextual fear conditioning. Throughout all experiments, cued fear conditioning was not affected by withdrawal from chronic nicotine or by DHβE-precipitated withdrawal.…”

Section: Discussionsupporting

confidence: 80%

“…Freezing, used as the behavioral measure of learning, was assessed with a time-sampling procedure described in detail elsewhere (Gould & Wehner, 1999). Briefly, mice were observed for one second every 10 seconds and were scored as freezing or active.…”

Section: Behavioral Procedures: Contextual and Cued Fear Conditioningmentioning

confidence: 99%

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β2 subunit containing acetylcholine receptors mediate nicotine withdrawal deficits in the acquisition of contextual fear conditioning

Portugal

Kenney

Gould

2008

Neurobiology of Learning and Memory

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Acute nicotine enhances contextual fear conditioning, whereas withdrawal from chronic nicotine produces impairments. However, the nicotinic acetylcholine receptors (nAChR) that are involved in nicotine withdrawal deficits in contextual fear conditioning are unknown. The present study used genetic and pharmacological techniques to investigate the nAChR subtype(s) involved in the effects of nicotine withdrawal on contextual fear conditioning. β2 or α7 nAChR subunit knockout (KO) and corresponding wild-type (WT) mice were withdrawn from 12 days of chronic nicotine treatment (6.3 mg/kg/day), and trained with 2 conditioned stimulus (CS; 85 dB white noise) -unconditioned stimulus (US; 0.57mA footshock) pairings on day 13. On day 14, mice were tested for contextual and cued freezing. β2 KO mice did not show nicotine withdrawal-related deficits in contextual fear conditioning, in contrast to WT mice and α7 KO mice. A follow-up study investigated if nicotine withdrawal disrupts acquisition or recall of contextual fear conditioning. The high affinity nAChR antagonist dihydro-beta-erythroidine (DHβE; 3 mg/kg) was administered prior to training or testing to precipitate withdrawal in chronic nicotine-treated C57BL/6 mice. Deficits in contextual fear conditioning were observed in chronic nicotine-treated mice when DHβE was administered prior to training, but not when administered at testing. These results indicate that β2-containing nAChRs, such as the α4β2 receptor, mediate nicotine withdrawal deficits in contextual fear conditioning. In addition, nicotine withdrawal selectively affects acquisition but not recall or expression of the learned response.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 80%

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β2 subunit containing acetylcholine receptors mediate nicotine withdrawal deficits in the acquisition of contextual fear conditioning

Portugal

Kenney

Gould

2008

Neurobiology of Learning and Memory

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“…One ideal animal model for examining the effects of nicotine withdrawal on learning and memory is Pavlovian fear conditioning, in which subjects form an association between a context and a footshock (contextual fear conditioning), and an association between an auditory stimulus and a footshock (cued fear conditioning). Previous studies have shown that acute nicotine enhanced contextual fear conditioning but had no effect on cued fear conditioning in mice (Davis et al, 2005;Davis et al, 2006;Gould and Higgins, 2003;Gould and Wehner, 1999;Wehner et al, 2004). In contrast, withdrawal from chronic nicotine produced impairments in contextual fear conditioning but not cued fear conditioning (Davis and Gould, 2007;Davis et al, 2005).…”

Section: Introductionmentioning

confidence: 97%

Bupropion dose-dependently reverses nicotine withdrawal deficits in contextual fear conditioning

Portugal

Gould

2007

Pharmacology Biochemistry and Behavior

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Bupropion, a norepinephrine and dopamine reuptake inhibitor and nicotinic acetylcholine receptor antagonist, facilitates smoking cessation and reduces some symptoms of nicotine withdrawal. However, the effects of bupropion on nicotine withdrawal-associated deficits in learning remain unclear. The present study investigated whether bupropion has effects on contextual and cued fear conditioning following withdrawal from chronic nicotine or when administered alone. Bupropion was administered alone for a range of doses (2.5, 5, 10, 20 or 40 mg/kg), and dose-dependent impairments in contextual and cued fear conditioning were observed (20 or 40 mg/kg). Follow-up studies investigated if bupropion disrupted acquisition or expression of fear conditioning. Bupropion (40 mg/kg) administration on training day only produced deficits in contextual fear conditioning. Alternatively, bupropion (20 or 40 mg/kg) administration during testing dose-dependently produced deficits in contextual and cued fear conditioning. To test the effect of bupropion on nicotine withdrawal, mice were withdrawn from 12 days of chronic nicotine (6.3 mg/kg/day) or saline treatment. Withdrawal from chronic nicotine disrupted contextual fear conditioning; however, 5 mg/ kg bupropion reversed this deficit. Overall, these results indicate that a low dose of bupropion can reverse nicotine withdrawal deficits in contextual fear conditioning, but that high doses of bupropion produce deficits in fear conditioning.

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“…These binding sites are clearly functional since studies done in laboratory animals and model systems have demonstrated that nicotine treatment produces a broad array of behavioral and physiological effects that are blocked by pretreatment with nicotinic antagonists such as mecamylamine. For example, nicotine injection enhances several components of learning and memory in rats and mice [11,12,13], decreases anxiety [14] and pain perception [15,16], and increases or decreases locomotor activity, depending on dose, species and strain [17,18]. Nicotine treatment also protects animals and neuronal cells in culture from cell death produced by several neurotoxic chemicals [19,20,21,22].…”

mentioning

confidence: 99%

The subtypes of nicotinic acetylcholine receptors on dopaminergic terminals of mouse striatum

Grady

Salminen

Laverty

et al. 2007

Biochemical Pharmacology

232

223

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This review summarizes studies that attempted to determine the subtypes of nicotinic acetylcholine receptors (nAChR) expressed in the dopaminergic nerve terminals in the mouse. A variety of experimental approaches has been necessary to reach current knowledge of these subtypes, including in situ hybridization, agonist and antagonist binding, function measured by neurotransmitter release from synaptosomal preparations, and immunoprecipitation by selective antibodies. Early developments that facilitated this effort include the radioactive labeling of selective binding agents, such as [ 125 I]-α-bungarotoxin and [ 3 H]-nicotine, advances in cloning the subunits, and expression and evaluation of function of combinations of subunits in Xenopus oocytes. The discovery of epibatidine and α-conotoxin MII (α-CtxMII), and the development of nAChR subunit null mutant mice have been invaluable in determining which nAChR subunits are important for expression and function in mice, as well as allowing validation of the specificity of subunit specific antibodies. These approaches have identified five nAChR subtypes of nAChR that are expressed on dopaminergic nerve terminals. Three of these contain the α6 subunit (α4α6β2β3, α6β2β3, α6β2) and bind α-CtxMII with high affinity. One of these three subtypes (α4α6β2β3) also has the highest sensitivity to nicotine of any native nAChR that has been studied, to date. The two subtypes that do not have high affinity for α-CtxMII (α4β2, α4α5β2) are somewhat more numerous than the α6* subtypes, but do bind nicotine with high affinity. Given that our first studies detected readily measured differences in sensitivity to agonists and antagonists among these five nAChR subtypes, it seems likely that subtype selective compounds could be developed that would allow therapeutic manipulation of diverse nAChRs that have been implicated in a number of human conditions. Alterations in nicotinic cholinergic receptor (nAChRs) number or function have been implicated in psychopathologies such as anxiety, attention deficit hyperactivity disorder, depression, schizophrenia (reviewed in [1,2,3]), at least one form of familial epilepsy [4], and Parkinson's and Alzheimer's diseases [5]. It is not particularly surprising that nAChRs might play important roles in modulating several human diseases given that binding sites for nicotinic ligands such as [ 125 I]-α-bungarotoxin [6,7,8], [ 3 H]-nicotine [7,8] Corresponding author: Sharon R Grady e-mail: sharon.grady@colorado.edu phone: 303-492-9677 fax: 303-492-8063 mailing address: Institute for Behavioral Genetics University of Colorado 447UCB Boulder, CO 80309. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered w...

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Nicotine enhancement of contextual fear conditioning

Cited by 147 publications

References 40 publications

β2 subunit containing acetylcholine receptors mediate nicotine withdrawal deficits in the acquisition of contextual fear conditioning

β2 subunit containing acetylcholine receptors mediate nicotine withdrawal deficits in the acquisition of contextual fear conditioning

Bupropion dose-dependently reverses nicotine withdrawal deficits in contextual fear conditioning

The subtypes of nicotinic acetylcholine receptors on dopaminergic terminals of mouse striatum

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