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At least 595 records · Page 33Linked to original sources
PubMed2002

Neuronal systems underlying behaviors related to nicotine addiction: neural circuits and molecular genetics.

Nicotine addiction is a complex behavioral phenomenon comprising effects on several neural systems. Recent studies have expanded initial observations that the actions of nicotine on dopaminergic systems increase dopaminergic activity and release, leading to nicotine-induced reinforcement. Indeed, the actions of nicotine on many systems, including brainstem cholinergic, GABAergic, noradrenergic, and serotonergic nuclei, may help to mediate nicotine effects related to addiction. Furthermore, studies of mice lacking nicotinic acetylcholine receptor subunits or expressing supersensitive forms of these subunits have begun to tie together the molecular, neurochemical, and behavioral effects of nicotine. The use of multiple techniques by many laboratories provides optimism that the field is advancing toward elucidating the basic mechanisms of nicotine dependence.

Animals↗
PubMed2000

Alcohol, the brain, and behavior. Mechanisms of addiction.

The actions of alcohol that cause intoxication, initiate and maintain excessive drinking behavior, and promote relapse during abstinence occur primarily in the brain. A thorough understanding of alcohol's effects on the mechanisms underlying brain function is essential to develop and improve alcoholism prevention and treatment strategies. This article is not an exhaustive overview of alcoholism neurobiology, but a sampling of the more significant recent advances in the field.

Alcoholism↗
PubMed1999

Criminal Behavior Associated with Pathological Gambling.

The influence of addictive gambling behavior on criminal behavior was examined in this study. A sample of pathological gamblers from in- and outpatient treatment centers and self-help groups (n = 300) and a sample of high and low frequency gamblers from the general population and army (n = 274) completed a comprehensive questionnaire which assessed social attachment, personality, pathological gambling and criminal behavior variables. The causal analysis of a Lisrel Model leads to the following results: addictive gambling behavior is an important criminogenic factor. This predisposing factor alone cannot sufficiently explain criminal behavior associated with pathological gambling. Personality variables also directly influence the intensity of criminal behavior. Social attachment variables have only an indirect effect. As far as property offenses are concerned, it was found that the direct causal effect of addiction behavior is greater than that of personality.

Journal Article↗
PubMed1999

[Biological addictive drugs--is there a change in drug taking behavior of young drug addicts?].

Abuse of natural products was frequently noticed among young patients with multiple substance abuse. 180 patients of a rehabilitation clinic for young addicts filled out a questionnaire regarding their regularly consumed drugs. Ayahuasca and cactus, the natural drugs of the 70's are rarely found. The patients frequently consumed psilocybin, amanita and datura. We inform about the toxicological basis of the used drugs. A specific exploration of patients with multiple substance abuse in regard to the use of biological drugs is an necessary as random and multicentre follow-up-studies.

Adult↗
PubMed2002

Neural plasticity and addiction: PI3-kinase and cocaine behavioral sensitization.

Drug addiction has been linked to protracted functional changes in neural circuits involved in motivation that can lead to drug dependence, craving and relapse. Here we investigated the role of the phosphatidylinositol 3 kinase (PI3K) signal transduction pathway in long-lasting behavioral sensitization to cocaine in rats, an animal model of the long-lasting functional changes induced by repeated drug use. Our results show that PI3K is required for the expression, but not the induction, of behavioral sensitization to cocaine.

Animals↗
PubMed2000

[Pertinence of the addiction concept in eating behavior disorders].

From a psychodynamic perspective, dependence disorders, irrespective of the object of addiction, can be seen as the expression of the subject's neurobiological, psychopathological, cultural and social vulnerability. Since vulnerability strengthens and reorganizes the personality, it can drive these subjects to perpetuate pathological behaviors. In this light, behavior disorders belong to the field of addiction diseases, especially considering that the underlying psychopathological structures are close to those observed in addiction, that depression plays a central role, and that their development into toxic addictive behavior (drugs, alcohol, psychotrope) is frequent.

Adolescent↗
PubMed1984

Five-year follow-up of opiate addicts with naltrexone and behavior therapy.

A group of 58 heroin addicts were treated with naltrexone and behavior therapy and followed for 5 years. At one-year post-treatment, almost half of the naltrexone-treated subjects were opiate free. Follow-up results at 5 years post-treatment indicate that over 90% of those patients treated with naltrexone became re-addicted for various periods of time. However, naltrexone-treated subjects did feel their treatment with naltrexone had provided them with the ability to remain opiate free for blocks of time. The results suggest that naltrexone is not a "cure" for opiate dependence, but is a medication which can be useful in protecting patients from re-addiction and is a modality patients should be encouraged to return to if they feel vulnerable to re-addiction.

Adult↗
PubMed2005

Stimulant-induced adaptations in neostriatal matrix and striosome systems: transiting from instrumental responding to habitual behavior in drug addiction.

Converging evidence indicates that repeated exposure to motor stimulants such as cocaine and amphetamine produces marked alterations in network responsiveness of striatal neurons to subsequent challenge with the same stimulant drug. Such alterations, which correlate with persistent patterns of repetitive behavior, associate with distinct compartmental changes in the neostriatum. Striatal matrix system neurons undergo "silencing" following repeated drug challenges, allowing striosome system neurons to exhibit preferential activation. Matrix neurons are innervated by sensory and motor areas of neocortex and are activated in the course of on-going, adaptive behavior. Inactivation of matrix neurons by chronic stimulant exposure may therefore constrain sensorimotor and cognitive processing. In turn, the striosomes are anatomically connected through re-entrant loops with limbic prefrontal and allocortical structures, such as anterior cingulate cortex, orbital frontal cortex, and basolateral amygdala, all of which play a part in stimulant-induced reinforcement and relapse to drug-taking. Moreover, functional evidence links striosome system neurons, which are responsible for providing inhibitory regulatory feedback to midbrain dopamine neurons, with reinforcement-based processes. In considering such evidence, we postulate that recurrent matrix inactivation and recruitment of striosome-based pathways by chronic stimulant exposure represent neural end-points of the transit from action-outcome associative behavior to conditioned habitual responding. Within this theoretical framework, habitual behavior can be elicited by both interoceptive cues and exteroceptive conditioned stimuli to promote the automatic execution of learned responses.

Amphetamine↗
PubMed2003

Does drug abuse beget drug abuse? Behavioral analysis of addiction liability in animal models of prenatal drug exposure.

Prenatal exposure to drugs of abuse is the single largest preventable cause of developmental compromise of American children today. In the clinical population, it is difficult to determine the independent effects of gestational exposure to a single drug on brain development, in part due to the confounding effects of additional risk factors that are encountered in the substance-abusing population. The enormous clinical and societal problem of gestational toxicity of drugs of abuse, both legal and illegal, has driven the need to develop and investigate animal models of gestational drug exposure in which these variables can be controlled. More specifically, as clinical data are gathered suggesting an increased liability to substance abuse among children of drug-abusing mothers, a mechanistic understanding of the lasting effects of early drug exposure on the developing brain and the behavioral repertoire of the developing animal is crucial. In this review we summarize experimental animal research that investigates the role of drug exposure in utero on the functional development of specific brain circuits that are involved in the reinforcing effects of drugs of abuse, and on the behaviors that are mediated by these brain reward systems.

Adult↗
PubMed2006

Genetic dissociation of two behaviors associated with nicotine addiction: beta-2 containing nicotinic receptors are involved in nicotine reinforcement but not in withdrawal syndrome.

RATIONALE: Nicotine addiction is characterized by two distinct behaviors, chronic compulsive self-administration and the induction of a withdrawal syndrome upon cessation of nicotine consumption. OBJECTIVE: To examine if these two processes rely on beta2-containing nicotinic receptors--beta2*nAChRs--we analyzed the behavior of mice lacking these receptors in the two situations. RESULTS: First, we showed that, in contrast to wild-type (WT) mice, beta2-knockout (beta2-/-) mice exhibit no intra-ventral tegmental area (VTA) nicotine self-administration, whereas their ability to self-administer morphine is intact. However, beta2-/- mice showed some sensitivity to locomotor effects of nicotine, implying an effect of the drug on other nicotinic subtypes. Then, we observed that beta2-/- mice exhibited a normal nicotine withdrawal syndrome, i.e., increased levels of rearing and jumping upon precipitated withdrawal. Thus, the beta2*nAChRs are not involved in the behaviors induced by cessation of nicotine consumption. CONCLUSION: Taken together, the present data demonstrated a genetic dissociation of two distinct behavioral patterns associated with nicotine addiction. They further suggested that independent molecular mechanisms underlie these two aspects, offering the possibility of controlling them separately.

Animals↗
PubMed1990

Maternal cocaine addiction and fetal behavioral state. I: A human model for the study of sudden infant death syndrome.

Abnormalities of respiratory regulation, such as apnea and abnormal hypoxic arousal during sleep, are mechanistic in the pathophysiology of SIDS. In utero cocaine exposure is associated with poor head growth, abnormal neurodevelopment, and an increased incidence of sudden, unexplained death, suggesting that in utero cocaine exposure disrupts the central regulation of breathing. It is likely that this disruption is due to altered CNS maturation. Indeed, cocaine alters norepinephrine metabolism within the locus coeruleus, important in arousal from sleep, suggesting that the increased incidence of SIDS in cocaine exposed infants may be secondary to sleep-related deficits in arousal. Since components of fetal behavioural state organization reflect the successful integration of the Central Nervous System, have a specific developmental timetable, and can be studied by fetal ultrasound techniques, we developed a strategy for assessing the state organization of the fetus by ultrasound techniques. We hypothesize that fetal evaluation of state will be a marker of abnormal CNS maturation and a predictor of risk, i.e. abnormal neurodevelopment and/or state related arousal deficits predisposing the cocaine exposed neonate to SIDS. We propose that the study of in utero cocaine exposed fetuses will provide a human model for examining the pathophysiology of SIDS.

Behavior↗
PubMed1996

Network-level changes in expression of inducible Fos-Jun proteins in the striatum during chronic cocaine treatment and withdrawal.

Repeated exposure to psychomotor stimulants produce long-term changes in behavior ranging from addiction to behavioral sensitization. Many of these behaviors depend on the nigrostriatal system of the basal ganglia. We show here that chronic cocaine exposure not only leads to time-varying alterations in the inducibility of bZIP transcription factors in individual striatal neurons, but also to long-lasting network changes in which ensembles of striatal neurons express these proteins. These network-level adaptations suggest that the behavioral sensitization induced by repeated psychomotor stimulant exposure may reflect an enduring functional reorganization of basal ganglia circuits.

Animals↗