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1.
Neural Comput ; 22(9): 2334-68, 2010 Sep 01.
Artigo em Inglês | MEDLINE | ID: mdl-20569176

RESUMO

Clinical and experimental observations show individual differences in the development of addiction. Increasing evidence supports the hypothesis that dopamine receptor availability in the nucleus accumbens (NAc) predisposes drug reinforcement. Here, modeling striatal-midbrain dopaminergic circuit, we propose a reinforcement learning model for addiction based on the actor-critic model of striatum. Modeling dopamine receptors in the NAc as modulators of learning rate for appetitive--but not aversive--stimuli in the critic--but not the actor--we define vulnerability to addiction as a relatively lower learning rate for the appetitive stimuli, compared to aversive stimuli, in the critic. We hypothesize that an imbalance in this learning parameter used by appetitive and aversive learning systems can result in addiction. We elucidate that the interaction between the degree of individual vulnerability and the duration of exposure to drug has two progressive consequences: deterioration of the imbalance and establishment of an abnormal habitual response in the actor. Using computational language, the proposed model describes how development of compulsive behavior can be a function of both degree of drug exposure and individual vulnerability. Moreover, the model describes how involvement of the dorsal striatum in addiction can be augmented progressively. The model also interprets other forms of addiction, such as obesity and pathological gambling, in a common mechanism with drug addiction. Finally, the model provides an answer for the question of why behavioral addictions are triggered in Parkinson's disease patients by D2 dopamine agonist treatments.


Assuntos
Comportamento Aditivo/fisiopatologia , Individualidade , Núcleo Accumbens/fisiopatologia , Receptores Dopaminérgicos/fisiologia , Reforço Psicológico , Simulação por Computador , Humanos , Modelos Neurológicos , Rede Nervosa/fisiopatologia
2.
Neural Comput ; 21(10): 2869-93, 2009 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-19635010

RESUMO

Based on the dopamine hypotheses of cocaine addiction and the assumption of decrement of brain reward system sensitivity after long-term drug exposure, we propose a computational model for cocaine addiction. Utilizing average reward temporal difference reinforcement learning, we incorporate the elevation of basal reward threshold after long-term drug exposure into the model of drug addiction proposed by Redish. Our model is consistent with the animal models of drug seeking under punishment. In the case of nondrug reward, the model explains increased impulsivity after long-term drug exposure. Furthermore, the existence of a blocking effect for cocaine is predicted by our model.


Assuntos
Encéfalo/efeitos dos fármacos , Encéfalo/fisiopatologia , Transtornos Relacionados ao Uso de Cocaína/fisiopatologia , Cocaína/farmacologia , Simulação por Computador , Recompensa , Algoritmos , Animais , Química Encefálica/efeitos dos fármacos , Química Encefálica/fisiologia , Tomada de Decisões/efeitos dos fármacos , Tomada de Decisões/fisiologia , Modelos Animais de Doenças , Dopamina/metabolismo , Inibidores da Captação de Dopamina/farmacologia , Humanos , Comportamento Impulsivo/induzido quimicamente , Comportamento Impulsivo/fisiopatologia , Aprendizagem/efeitos dos fármacos , Aprendizagem/fisiologia , Reforço Psicológico
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