Acute withdrawal from nicotine involves reduced activity and may be due to temporary disruption of a brain reward pathway
Grade Level at Time of Presentation
Sophomore
Major
Neuroscience
Minor
-
Institution
Morehead State University
KY House District #
49
KY Senate District #
38
Faculty Advisor/ Mentor
Wesley White, PhD; Ilsun White, PhD
Department
Department of Psychology
Abstract
Acute withdrawal from nicotine involves reduced activity and may be due to temporary disruption of a brain reward pathway.
Terra E. Riggs, Samuel L. Case, Brandi C. Carey, Ilsun M. White, Wesley White
Neuroscience Program, Department of Psychology, Morehead State University, Morehead, KY 40351.
The present study was part of a research program that uses an animal model approach to identify the motivational deficits arising from intermittent drug use and the brain circuits involved in these deficits. In prior research, administration of amphetamine or morphine reduced activity, in most rats, 15-24 hours later. This reduction appeared to be a sign of acute withdrawal. When administered 30 minutes after amphetamine or morphine, a dopamine D1 antagonist prevented the reduction in activity. A dopamine D1 antagonist is a drug that blocks the brain circuit that produces the rewarding effects of drugs. The current study looked at whether nicotine also produced a reduction in activity that could be prevented by a D1 antagonist. Two groups of rats each underwent a series of five-day tests. Groups received a control treatment on Day 1 of a test, and on Day 3 groups received the experimental treatment. The experimental treatment for tests 1-4 included only nicotine, whereas for tests 5-8 the experimental treatment included nicotine followed 30 minutes later by a D1 antagonist. One group received a moderate dose of nicotine (0.3 mg/kg), and the second group received a high dose (1.0 mg/kg). Treatments were administered subcutaneously. Following treatments, rats were placed in individual open fields, and their activity was monitored for 24 hours. In the moderate dose group, half of the subjects had reduced activity 15-24 hours following nicotine, and the D1 antagonist prevented this reduction. In the high dose group, all of the subjects had reduced activity 15-24 hours following nicotine, and the D1 antagonist partially blocked this reduction. Nicotine, amphetamine, and morphine may all produce signs of acute withdrawal by disrupting the reward pathway. Supported by NIH grant DA015351.
Acute withdrawal from nicotine involves reduced activity and may be due to temporary disruption of a brain reward pathway
Acute withdrawal from nicotine involves reduced activity and may be due to temporary disruption of a brain reward pathway.
Terra E. Riggs, Samuel L. Case, Brandi C. Carey, Ilsun M. White, Wesley White
Neuroscience Program, Department of Psychology, Morehead State University, Morehead, KY 40351.
The present study was part of a research program that uses an animal model approach to identify the motivational deficits arising from intermittent drug use and the brain circuits involved in these deficits. In prior research, administration of amphetamine or morphine reduced activity, in most rats, 15-24 hours later. This reduction appeared to be a sign of acute withdrawal. When administered 30 minutes after amphetamine or morphine, a dopamine D1 antagonist prevented the reduction in activity. A dopamine D1 antagonist is a drug that blocks the brain circuit that produces the rewarding effects of drugs. The current study looked at whether nicotine also produced a reduction in activity that could be prevented by a D1 antagonist. Two groups of rats each underwent a series of five-day tests. Groups received a control treatment on Day 1 of a test, and on Day 3 groups received the experimental treatment. The experimental treatment for tests 1-4 included only nicotine, whereas for tests 5-8 the experimental treatment included nicotine followed 30 minutes later by a D1 antagonist. One group received a moderate dose of nicotine (0.3 mg/kg), and the second group received a high dose (1.0 mg/kg). Treatments were administered subcutaneously. Following treatments, rats were placed in individual open fields, and their activity was monitored for 24 hours. In the moderate dose group, half of the subjects had reduced activity 15-24 hours following nicotine, and the D1 antagonist prevented this reduction. In the high dose group, all of the subjects had reduced activity 15-24 hours following nicotine, and the D1 antagonist partially blocked this reduction. Nicotine, amphetamine, and morphine may all produce signs of acute withdrawal by disrupting the reward pathway. Supported by NIH grant DA015351.