Evidence for an involvement of 5-hydroxytryptaminergic neurones in the maintenance of operant behaviour by positive reinforcement

Abstract

The possible involvement of the ascending 5-hydroxytryptaminergic (5HTergic) pathways in the maintenance of operant behaviour by positive reinforcement was examined using a quantitative paradigm based on Herrnstein's (1970) equation which defines a hyperbolic relationship between steady-state response rate and reinforcement frequency in variable-interval schedules. Nine rats received injections of 5,7-dihydroxytryptamine into the dorsal and median raphe nuclei; 12 rats received sham injections. The rats were trained to steady-state in a series of variable-interval schedules of sucrose reinforcement affording a range of reinforcement frequencies. Herrnstein's equation was fitted to the data obtained from each rat and to the averaged data obtained from the two groups. The value of KH (the parameter expressing the reinforcement frequency needed to obtain the half-maximum response rate) was significantly lower in the lesioned group than in the control group; the values of Rmax (the parameter expressing the maximum response rate) did not differ significantly between the two groups. The levels of 5HT and 5-hydroxyindoleacetic acid in the parietal cortex, hippocampus, nucleus accumbens and hypothalamus were markedly reduced in all four regions in the lesioned group, but the levels of noradrenaline and dopamine were not significantly affected. The results indicate that damage to the central 5HTergic pathways resulted in an increase in the "value" of the sucrose reinforcer, without affecting the animals' response capacity. The results are consistent with the suggestion that the 5HTergic pathways may exert some limiting control on the "values" of certain reinforcers.

Decreased Incentive Motivation Following Knockout or Acute Blockade of the Serotonin Transporter: Role of the 5-HT2C Receptor

“…Treatment with selective serotonin reuptake inhibitors (SSRIs) or the 5-HT releaser dexfenfluramine consistently decreases instrumental responding for primary reinforcers such as food (Thompson, 1977), drugs of abuse (Carroll et al, 1990;Richardson and Roberts, 1991), and brain stimulation reward (Lee and Kornetsky, 1998;McClelland et al, 1989). Conversely, suppression of 5-HT activity can facilitate responding for various primary reinforcers (Lyness et al, 1980;Poschel and Ninteman, 1971;Wogar et al, 1991). These findings suggest that 5-HT broadly inhibits incentive motivation-the process by which motivationally significant stimuli elicit appetitive behaviors.…”

Brain-machine Interface in Robot-assisted Neurorehabilitation for Patients with Stroke and Upper Extremity Weakness – the Therapeutic Turning Point

“…Feature extraction from electroencephalogram, for example ERD or slow cortical potentials, gives the logics that participants have the motor intention, which can be used for driving movement of robot arms. The observation of contingent execution by the robot arm linked to the participant's brain status can give the participant's brain positive feedback [37], which can be associated with favorable outcomes. Selection of adequate brain signal for proper movement and its fine tuning may have favorable influences to the neural plasticity [33,38].…”

“…Appropriate BMIs can give patients the positive feedback [56][57][58]. This operant conditioning associated with the contingent reward via BMI can be linked to the positive feedback [33,37,38,59], which will lead to the increment in motivation of the participants. When the motivation of the patient is high, the chance of reward-based reinforcement learning will also have the chance to be increased [24].…”

Efeitos comportamentais da lesão eletrolítica da região do núcleo mediano da rafe como modelo experimental de mania no rato e no camundongo

“…Estes resultados, somados aos dados descritos em diversas publicações feitas por diferentes grupos de pesquisa nos últimos 40 anos sobre os efeitos da lesão do MnR em animais de laboratório (Albinsson, Andersson, Andersson, Vega-Matuszczyk, & Larsson, 1996;Andrade, 1997;Andrade & Graeff, 2001;Arpa & De Andres, 1993;Asin, Wirtshafter, & Fibiger, 1985;Asin, Wirtshafter, & Kent, 1979aFile, Hyde, & MacLeod, 1979;Jacobs, Wise, & Taylor, 1974;Kostowski, Giacalone, Garattini, & Valzelli, 1968;Le, Harding, Juzytsch, Fletcher, & Shaham, 2002;Wirtshafter & Asin, 1983;Wogar, Bradshaw, & Szabadi, 1991) permitiram identificar inúmeras semelhanças entre o quadro comportamental induzido pela lesão do MnR e o conjunto de comportamentos esperados para atribuição de validade de face em modelos animais do episódio maníaco do transtorno bipolar (Einat, 2006;Lyon, 1991). A avaliação da literatura especializada mostra, como veremos a seguir, que existem vários dados que dão embasamento à hipótese do envolvimento do núcleo mediano da rafe na neurofisiologia da mania e justificam a proposição do objetivo do presente trabalho.…”

“…Em síntese, a inativação desta estrutura por diferentes procedimentos induz: a) hiperatividade (Albinsson et al, 1996;Jacobs et al, 1974); b) estereotipia ; c) facilitação no comportamento sexual (Albinsson et al, 1996); d) agressividade e desrespeito à hierarquia social (File et al, 1979); e) impulsividade (Fletcher, 1995;Le et al, 2002) e exposição ao "risco" (Andrade & Graeff, 2001;Andrade et al, 1999); f) alterações na aprendizagem e controle de estímulos (Asin et al, 1979a(Asin et al, , 1980Wirtshafter & Asin, 1983); g) aumento no valor reforçador dos estímulos incondicionados e condicionados (Fletcher, Korth, & Chambers, 1999;Vollrath-Smith et al, 2012;Wogar et al, 1991); h) irritabilidade (Kostowski et al, 1968) e i) diminuição do tempo total de sono (Arpa & De Andres, 1993;Arpa, Padrino, Rodriguez-Albarino, & de Andres, 1998).…”