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Brain Stress Systems and Addiction

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Air date: Monday, May 4, 2009, 12:00:00 PM
Time displayed is Eastern Time, Washington DC Local
Views: Total views: 182 * This only includes stats from October 2011 and forward.
Category: Neuroscience
Runtime: 01:16:44
Description: Studies on the neurobiology of addiction continue to be focused on how the multiple neurochemical systems within the extended amygdala basal forebrain neurocircuitry change with the development of addiction and retain those changes to convey vulnerability to relapse. Animal models of the longterm changes in the brain produced by patterns of drug use associated with addiction and associated with vulnerability to relapse continue to be developed and refined. Recent developments include establishment of changes in the pattern of intravenous self-administration of heroin and nicotine with continuous access. Animals allowed continuous daily access to heroin compared to those with limited 2hour access showed a dramatic escalation in heroin intake such that responding moves into the normally inactive phase of the light-dark cycle. These studies suggest that prolonged exposure to drugs of abuse increase drug taking behavior. The brain circuit responsible for the aversive effects of opiate withdrawal hypothesized to be changed in the development of dependence is the same extended amygdala circuit hypothesized previously to be responsible for acute positive reinforcing effects of opiates. Opiate withdrawal-induced Fos immunoreactivity in the rat extended amygdala paralleled the development of conditioned place aversion. Functional interaction between opioid and cannabinoid receptors in drug self-administration have also been demonstrated. The neurochemical basis for the escalation in drug intake associated with dependence is under current investigation with a focus on neuropeptidergic mechanisms.

Previous studies of alcohol dependent, opiate dependent and cocaine dependent animals during acute withdrawal have shown enhanced stress-like responses that are reversed by selective competitive corticotropin-releasing factor (CRF) antagonists. Studies with animals exposed to chronic administration of cocaine, alcohol and cannabinoids have shown increases in CRF activity in the amygdala as measured by in vivo microdialysis. Even more exciting are results showing that CRF antagonists gain the ability to reduce alcohol drinking in animals with a history of dependence, but are inactive in animals with no history of dependence. These results suggest that the increased drug intake associated with drug dependence may involve not only decreases in the function of transmitter systems that are associated with the acute reinforcing (rewarding) effects of drugs of abuse (previous work from our group), but also with the recruitment of the brain neuropeptide systems associated with behavioral and neurobiological responses to stressors.

NIH Neuroscience Seminar Series
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NLM Title: Brain stress systems and addiction [electronic resource] / George Koob.
Series: NIH neuroscience seminar series
Author: Koob, George F.
National Institutes of Health (U.S.)
Publisher:
Other Title(s): NIH neuroscience seminar series
Abstract: (CIT): Studies on the neurobiology of addiction continue to be focused on how the multiple neurochemical systems within the extended amygdala basal forebrain neurocircuitry change with the development of addiction and retain those changes to convey vulnerability to relapse. Animal models of the longterm changes in the brain produced by patterns of drug use associated with addiction and associated with vulnerability to relapse continue to be developed and refined. Recent developments include establishment of changes in the pattern of intravenous self-administration of heroin and nicotine with continuous access. Animals allowed continuous daily access to heroin compared to those with limited 2 hour access showed a dramatic escalation in heroin intake such that responding moves into the normally inactive phase of the light-dark cycle. These studies suggest that prolonged exposure to drugs of abuse increase drug taking behavior. The brain circuit responsible for the aversive effects of opiate withdrawal hypothesized to be changed in the development of dependence is the same extended amygdala circuit hypothesized previously to be responsible for acute positive reinforcing effects of opiates. Opiate withdrawal-induced Fos immunoreactivity in the rat extended amygdala paralleled the development of conditioned place aversion. Functional interaction between opioid and cannabinoid receptors in drug self-administration have also been demonstrated. The neurochemical basis for the escalation in drug intake associated with dependence is under current investigation with a focus on neuropeptidergic mechanisms. Previous studies of alcohol dependent, opiate dependent and cocaine dependent animals during acute withdrawal have shown enhanced stress-like responses that are reversed by selective competitive corticotropin-releasing factor (CRF) antagonists. Studies with animals exposed to chronic administration of cocaine, alcohol and cannabinoids have shown increases in CRF activity in the amygdala as measured by in vivo microdialysis. Even more exciting are results showing that CRF antagonists gain the ability to reduce alcohol drinking in animals with a history of dependence, but are inactive in animals with no history of dependence. These results suggest that the increased drug intake associated with drug dependence may involve not only decreases in the function of transmitter systems that are associated with the acute reinforcing (rewarding) effects of drugs of abuse (previous work from our group), but also with the recruitment of the brain neuropeptide systems associated with behavioral and neurobiological responses to stressors. NIH Neuroscience Seminar Series.
Subjects: Brain--pathology
Brain--physiopathology
Stress, Physiological
Substance-Related Disorders--pathology
Publication Types: Lectures
Webcasts
Download: To download this event, select one of the available bitrates:
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NLM Classification: WM 270
NLM ID: 101507185
CIT Live ID: 7147
Permanent link: https://videocast.nih.gov/launch.asp?15084

 

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