Effects of Dopamine Receptor Agonist and Antagonists on Cholestasis Induced Anxiolytic-Like Behaviors in Rats.
Effects of dopamine receptor agonist and antagonists on cholestasis induced anxiolytic-like behaviors in rats.
Filed under: Addiction Rehab
Eur J Pharmacol. 2013 Jan 29;
Reza Zarrindast M, Eslimi Esfahani D, Oryan S, Nasehi M, Torabi Nami M
Dysfunctions in dopamine transmission system have been suggested to contribute to the pathogenesis of hepatic encephalopathy. In an experimental animal model, cholestasis induction through bile duct ligation may present several main pathological features of hepatic encephalopathy. Dopaminergic systems are shown to play pivotal roles in regulation of anxiety-like behaviors. The main bile duct in male Wistar rats, weighing 220-240g, was ligated using two ligatures plus duct transection in between. Anxiety-like behaviors were measured using the elevated plus maze task. Cholestasis increased the open arm time percentage (%OAT), 13 but not 10 days after bile duct ligation, indicating an anxiolytic-like effect. Sole intraperitoneal injection of apomorphine (dopamine D(1)/D(2) receptor agonist, 0.25mg/kg), SCH23390 (dopamine D(1) receptor antagonist, 0.005, 0.01 and 0.02mg/kg) or sulpiride (dopamine D(2) receptor antagonist, 0.125, 0.25 and 0.5mg/kg) did not alter %OAT, open arm entries percentage (%OAE) and locomotor activity in the sham-operated rats. Meanwhile, the higher dose apomorphine (0.5mg/kg) induced anxiolytic-like behaviors in this group. The subthreshold dose injection of SCH23390 or sulpiride, partially reversed the anxiolytic-like behaviors induced by cholestasis (13 days after bile duct ligation). On the other hand, subthreshold dose of apomorphine in cholestatic rats (10 days post bile duct ligation) induced anxiolytic-like effects which could be blocked by SCH23390 or sulpiride. The effective doses of above drugs did not alter locomotor activity, number of rearings, groomings and defections. These findings suggested that the dopaminergic system may potentially be involved in the modulation of cholestasis induced anxiolytic-like behaviors in rats.
HubMed – addiction
Instant Transformation of Learned Repulsion into Motivational “Wanting”
Filed under: Addiction Rehab
Curr Biol. 2013 Jan 30;
Robinson MJ, Berridge KC
BACKGROUND: Learned cues for pleasant reward often elicit desire, which, in addicts, may become compulsive. According to the dominant view in addiction neuroscience and reinforcement modeling, such desires are the simple products of learning, coming from a past association with reward outcome. RESULTS: We demonstrate that cravings are more than merely the products of accumulated pleasure memories-even a repulsive learned cue for unpleasantness can become suddenly desired via the activation of mesocorticolimbic circuitry. Rats learned repulsion toward a Pavlovian cue (a briefly-inserted metal lever) that always predicted an unpleasant Dead Sea saltiness sensation. Yet, upon first reencounter in a novel sodium-depletion state to promote mesocorticolimbic reactivity (reflected by elevated Fos activation in ventral tegmentum, nucleus accumbens, ventral pallidum, and the orbitofrontal prefrontal cortex), the learned cue was instantly transformed into an attractive and powerful motivational magnet. Rats jumped and gnawed on the suddenly attractive Pavlovian lever cue, despite never having tasted intense saltiness as anything other than disgusting. CONCLUSIONS: Instant desire transformation of a learned cue contradicts views that Pavlovian desires are essentially based on previously learned values (e.g., prediction error or temporal difference models). Instead desire is recomputed at reencounter by integrating Pavlovian information with the current brain/physiological state. This powerful brain transformation reverses strong learned revulsion into avid attraction. When applied to addiction, related mesocorticolimbic transformations (e.g., drugs or neural sensitization) of cues for already-pleasant drug experiences could create even more intense cravings. This cue/state transformation helps define what it means to say that addiction hijacks brain limbic circuits of natural reward.
HubMed – addiction
Serum levels of brain-derived neurotrophic factor in patients with internet use disorder.
Filed under: Addiction Rehab
Psychiatry Res. 2013 Jan 30;
Geisel O, Banas R, Schneider M, Hellweg R, Müller CA
Internet use disorder (IUD) is characterised by excessive internet gaming use and has temporarily been conceptualised as a behavioural addiction. Since brain-derived neurotrophic factor (BDNF) has been hypothesised to be involved in the development and maintenance of addictive disorders, we investigated BDNF expression in IUD. We measured BDNF serum levels in male patients with IUD (n=11) and individually matched healthy controls (n=10). There was no significant difference in BDNF serum levels of patients with IUD in comparison to control subjects (p=0.451). Serum levels of BDNF were not correlated with severity of IUD or clinical and demographic variables in our study. These preliminary findings possibly suggest a different underlying pathophysiology in IUD compared to addictive disorders. Thus, further studies are needed to clarify, whether IUD represents an addictive spectrum disorder, an impulse control disorder or finally an own entity overlapping both disease categories.
HubMed – addiction
Disordered gambling: a behavioral addiction.
Filed under: Addiction Rehab
Curr Opin Neurobiol. 2013 Jan 31;
Clark L, Limbrick-Oldfield EH
Developments in psychiatry have ratified the existence of behavioral addictions, that certain activities such as gambling or video-game play may be considered addictive in the absence of exogenous (i.e. drug-induced) stimulation of brain reinforcement circuitry. This article describes recent advances in understanding the neurobiological basis of behavioral addiction, with a focus on pathological gambling as the prototypical disorder. We describe positron emission tomography (PET) studies characterizing dopaminergic transmission, and functional imaging studies of reward processing and gambling-related cognitive distortions. The current evidence not only indicates changes in pathological gamblers in core circuitry implicated in drug addiction, but also highlights some subtle differences. Behavioral addictions can also provide experimental traction on distinguishing vulnerability markers for addictions from the active detrimental effects of chronic drug use.
HubMed – addiction
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