TY - JOUR
T1 - Nicotine-conditioned locomotor activity in rats
T2 - Dopaminergic and GABAergic influences on conditioned expression
AU - Bevins, Rick A.
AU - Besheer, Joyce
AU - Pickett, Katherine S.
N1 - Funding Information:
Grants from the National Institute on Drug Abuse (DA-11893), the Nebraska Cancer and Smoking Disease Research Program, and the University of Nebraska-Lincoln Research Council supported the research in the present report. The Vigabatrin (GVG) was a gift from Hoechst Marion Roussel. We thank Roger Dooley for designing and constructing the automated infrared emitter/detector system used to collect the activity data. We are also grateful to Todd Hinze for his technical assistance, to Michael Bardo and Matthew Palmatier for their thoughtful comments on an earlier version of this report, and to Eliot Hearst for donating the white noise generator.
PY - 2001
Y1 - 2001
N2 - Little is known about the processes that mediate acquisition and expression of conditioned associations between contextual cues and psychomotor effects of nicotine. In four separate experiments using rats, an environment repeatedly paired with nicotine acquired the ability to elicit increases in activity even in the absence of drug. This conditioned effect was sensitive to nicotine dose. Rats that had 0.6 or 1.2 mg/kg nicotine, but not 0.3 mg/kg, paired with the environment were more active than an unpaired control group (Experiment 1). In Experiment 2, control groups eliminated accounts based on nonspecific effects of nicotine and inhibitory conditioning decreasing activity in the unpaired controls of Experiment 1. Pretreatment on the test day with 100 mg/kg of gamma vinyl-GABA (GVG), a compound that inhibits the enzyme required to breakdown GABA, partially blocked the expression of locomotor conditioning without impairing activity in controls (Experiment 3). In Experiment 4, pretreatment on the test day with the dopamine D1 receptor antagonist SCH-23390 (0.03 mg/kg) blocked expression of nicotine-conditioned locomotor activity; the D2/D3 receptor antagonist eticlopride did not. Thus, the dopamine D1 receptor subtype appears to play a role in context-elicited increases in activity conditioned by nicotine; GABA may also modulate the expression of this conditioned effect.
AB - Little is known about the processes that mediate acquisition and expression of conditioned associations between contextual cues and psychomotor effects of nicotine. In four separate experiments using rats, an environment repeatedly paired with nicotine acquired the ability to elicit increases in activity even in the absence of drug. This conditioned effect was sensitive to nicotine dose. Rats that had 0.6 or 1.2 mg/kg nicotine, but not 0.3 mg/kg, paired with the environment were more active than an unpaired control group (Experiment 1). In Experiment 2, control groups eliminated accounts based on nonspecific effects of nicotine and inhibitory conditioning decreasing activity in the unpaired controls of Experiment 1. Pretreatment on the test day with 100 mg/kg of gamma vinyl-GABA (GVG), a compound that inhibits the enzyme required to breakdown GABA, partially blocked the expression of locomotor conditioning without impairing activity in controls (Experiment 3). In Experiment 4, pretreatment on the test day with the dopamine D1 receptor antagonist SCH-23390 (0.03 mg/kg) blocked expression of nicotine-conditioned locomotor activity; the D2/D3 receptor antagonist eticlopride did not. Thus, the dopamine D1 receptor subtype appears to play a role in context-elicited increases in activity conditioned by nicotine; GABA may also modulate the expression of this conditioned effect.
KW - Dopamine
KW - Eticlopride
KW - GVG
KW - Locomotor sensitization
KW - Pavlovian conditioning
KW - SCH-23390
KW - Vigabatrin
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U2 - 10.1016/S0091-3057(00)00451-2
DO - 10.1016/S0091-3057(00)00451-2
M3 - Article
C2 - 11274718
AN - SCOPUS:0035085698
SN - 0091-3057
VL - 68
SP - 135
EP - 145
JO - Pharmacology Biochemistry and Behavior
JF - Pharmacology Biochemistry and Behavior
IS - 1
ER -