1,721,174 research outputs found
Compositions and methods for prophylaxis and treatment of addictions
The present invention relates to methods of treating or preventing addiction and relapse use of addictive agents, and treating or preventing addictive or compulsive behaviour and relapse practice of an addictive behaviour or compulsion, by administering a peroxisome proliferator-activated receptor gamma (PPAR ) agonist, alone or in combination with another therapeutic agent, such as, for example, an opioid receptor antagonist or an antidepressant, or an addictive agent, such as, for example, an opioid agonist. The present invention also includes pharmaceutical compositions for treating or preventing addiction or relapse that include a PPAR agonist and one or more other therapeutic or addictive agents, as well as unit dosage forms of such pharmaceutical compositions, which contain a dosage effective in treating or preventing addiction or relapse. The methods and compositions of the invention are useful in the treatment or prevention of addiction to any agent, including alcohol, nicotine, marijuana, cocaine, and amphetamines, as well as compulsive and addictive behaviours, including pathological gambling and pathological overeating
Compositions and methods for prophylaxis and treatment of addictions
The present invention relates to methods of treating or preventing addiction and relapse use of addictive agents, and treating or preventing addictive or compulsive behaviour and relapse practice of an addictive behaviour or compulsion, by administering a peroxisome proliferator-activated receptor gamma (PPAR ) agonist, alone or in combination with another therapeutic agent, such as, for example, an opioid receptor antagonist or an antidepressant, or an addictive agent, such as, for example, an opioid agonist. The present invention also includes pharmaceutical compositions for treating or preventing addiction or relapse that include a PPAR agonist and one or more other therapeutic or addictive agents, as well as unit dosage forms of such pharmaceutical compositions, which contain a dosage effective in treating or preventing addiction or relapse. The methods and compositions of the invention are useful in the treatment or prevention of addiction to any agent, including alcohol, nicotine, marijuana, cocaine, and amphetamines, as well as compulsive and addictive behaviours, including pathological gambling and pathological overeating
Grand Challenge in Psychopharmacology: Setting Priorities to Shape a Bright Future
[No abstract available
Genetically selected alcohol preferring rats to model human alcoholism.
Animal models have been successfully developed to mimic and study alcoholism. These models have the unique feature of allowing the researcher to control for the genetic characteristics of the animal, alcohol exposure and environment. Moreover, these animal models allow pharmacological, neurochemical and behavioral manipulations otherwise impossible. Unquestionably, one of the major contributions to the understanding of the neurobiological basis of alcoholism comes from data that have been obtained from the study of genetically selected alcohol preferring rat lines and from the consequences that alcohol drinking and environmental manipulations, (i.e., protracted alcohol drinking, intoxication, exposure to stress, etc.) have on them. In fact, if on the one hand genetic factors may account for about 50-60% of the risk of developing alcohol dependence, on the other hand protracted alcohol exposure is a necessary precondition to actually develop the disease, while environmental vulnerability factors may be crucial for disease progression. The present article will offer an overview of the different genetically selected alcohol preferring rat lines developed and used to study alcoholism. The predictive, face and construct validity of these animal models and the translational significance of findings achieved through their use will be critically discussed
Elementi delle basi neurobiologiche della tossicodipendenza
La tossicodipendenza e’ una patologia cerebrale che scaturisce dalla interazione tra effetti farmacologici delle sostanze d’abuso e fattori predisponenti peculiari del soggetto utilizzatore di essi. Negli anni e’ stata generata una ricca letteratura volta ad identificare, da un lato, i meccanismi neurobiologici che sottendono allo sviluppo della dipendenza da farmaci e d’altro a definire i fattori di vulnerabilità individuale predisponent
Preclinical Animal Studies: Cocaine
Cocaine is the main alkaloid extracted from the Erythroxylon
coca plant, which grows in tropical Andes Mountains
at altitudes between 500 and 1000 m. The use of the
coca leaves by native populations for therapeutic, ritual,
and adaptive (e.g. for attenuation of the perception of
fatigue and hunger) purposes has historical roots, dating
back to over 4000 years ago. Although the European
population had contact with the coca leaf since the
sixteenth century, it was only upon the isolation of
cocaine in 1860 that it turned attention to its pharmacological
effects. At the end of the 1800s, cocaine received
enormous interest in therapeutics, and its use was
proposed for the treatment of many diseases. Of these
uses, the last to disappear was that of local anesthesia.
At the beginning of the twentieth century, the addictive
properties of cocaine began to be investigated and its
toxic profile characterized
Cocaine-predictive stimulus induces drug-seeking behavior and neural activation in limbic brain regions after multiple months of abstinence: reversal by D(1) antagonists
The conditioning of cocaine's subjective actions with environmental stimuli may be a critical factor in long-lasting relapse risk associated with cocaine addiction. To study the significance of learning factors in persistent addictive behavior as well as the neurobiological basis of this phenomenon, rats were trained to associate discriminative stimuli (SD) with the availability of i.v. cocaine vs. nonrewarding saline solution, and then placed on extinction conditions during which the i.v. solutions and SDs were withheld. The effects of reexposure to the SD on the recovery of responding at the previously cocaine-paired lever and on Fos protein expression then were determined in two groups. One group was tested immediately after extinction, whereas rats in the second group were confined to their home cages for an additional 4 months before testing. In both groups, the cocaine SD, but not the non-reward SD, elicited strong recovery of responding and increased Fos immunoreactivity in the basolateral amygdala and medial prefrontal cortex (areas Cg1/Cg3). The response reinstatement and Fos expression induced by the cocaine SD were both reversed by selective dopamine D1 receptor antagonists. The undiminished efficacy of the cocaine SD to elicit drug-seeking behavior after 4 months of abstinence parallels the long-lasting nature of conditioned cue reactivity and cue-induced cocaine craving in humans, and confirms a significant role of learning factors in the long-lasting addictive potential of cocaine. Moreover, the results implicate D1-dependent neural mechanisms within the medial prefrontal cortex and basolateral amygdala as substrates for cocaine-seeking behavior elicited by cocaine-predictive environmental stimuli
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