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Reward Expectancies (reward + expectancy)

Distribution by Scientific Domains

Life Sciences	75%

Selected Abstracts

Basolateral amygdala inactivation by muscimol, but not ERK/MAPK inhibition, impairs the use of reward expectancies during working memory

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2007
Lisa M. Savage
Abstract Rats were trained on a delayed matching to position (DMTP) task that embedded either a differential outcomes procedure (DOP) or a non-differential outcomes procedure (NOP). The DOP, via Pavlovian conditioning (stimulus,outcome associations), results in the use of unique reward expectancies that facilitate learning and memory performance above subjects trained with a NOP that requires subjects to retain cue information for accurate choice behavior (stimulus,response associations). This enhancement in learning and/or memory produced by the DOP is called the differential outcomes effect (DOE). After being trained on the DMTP task, rats were implanted with two cannulae aimed at the basolateral amygdala (BLA) nuclei. Rats trained with the DOP, relative to those trained with the NOP, displayed enhanced short-term memory (STM) performance under vehicle conditions (i.e. the DOE). However, injections of the ,-aminobutyric acid (GABA)A agonist muscimol into the BLA dose-dependently (0.0625 and 0.125 µg) impaired STM performance only in DOP-trained rats. These results support the role of the BLA in the use of established reward expectancies during a short-term working memory task. Despite the fact that extracellular signal-regulated kinase/mitogen-activated protein kinases (ERK/MAPK) have been shown to be necessary for amygdala-dependent long-term potentiation and some forms of long-term and STM, inhibition of the ERK/MAPK signaling cascade by U0126 (2.0 or 4.0 µg) in the BLA was not critical for updating the STM of either spatial information or reward expectation. [source]

REVIEW: Identifying the neural circuitry of alcohol craving and relapse vulnerability

ADDICTION BIOLOGY, Issue 1 2009
Andreas Heinz
ABSTRACT With no further intervention, relapse rates in detoxified alcoholics are high and usually exceed 80% of all detoxified patients. It has been suggested that stress and exposure to priming doses of alcohol and to alcohol-associated stimuli (cues) contribute to the relapse risk after detoxification. This article focuses on neuronal correlates of cue responses in detoxified alcoholics. Current brain imaging studies indicate that dysfunction of dopaminergic, glutamatergic and opioidergic neurotransmission in the brain reward system (ventral striatum including the nucleus accumbens) can be associated with alcohol craving and functional brain activation in neuronal systems that process attentional relevant stimuli, reward expectancy and experience. Increased functional brain activation elicited by such alcohol-associated cues predicted an increased relapse risk, whereas high brain activity elicited by affectively positive stimuli may represent a protective factor and was correlated with a decreased prospective relapse risk. These findings are discussed with respect to psychotherapeutic and pharmacological treatment options. [source]

Abnormal activity in reward brain circuits in human narcolepsy with cataplexy

ANNALS OF NEUROLOGY, Issue 2 2010
Aurélie Ponz PhD
Objective Hypothalamic hypocretins (or orexins) regulate energy metabolism and arousal maintenance. Recent animal research suggests that hypocretins may also influence reward-related behaviors. In humans, the loss of hypocretin-containing neurons results in a major sleep-wake disorder called narcolepsy-cataplexy, which is associated with emotional disturbances. Here, we aim to test whether narcoleptic patients show an abnormal pattern of brain activity during reward processing. Methods We used functional magnetic resonance imaging in 12 unmedicated patients with narcolepsy-cataplexy to measure the neural responses to expectancy and experience of monetary gains and losses. We statistically compared the patients' data with those obtained in a group of 12 healthy matched controls. Results and Interpretation Our results reveal that activity in the dopaminergic ventral midbrain (ventral tegmental area) was not modulated in narcolepsy-cataplexy patients during high reward expectancy (unlike controls), and that ventral striatum activity was reduced during winning. By contrast, the patients showed abnormal activity increases in the amygdala and in dorsal striatum for positive outcomes. In addition, we found that activity in the nucleus accumbens and the ventral-medial prefrontal cortex correlated with disease duration, suggesting that an alternate neural circuit could be privileged over the years to control affective responses to emotional challenges and compensate for the lack of influence from ventral midbrain regions. Our study offers a detailed picture of the distributed brain network involved during distinct stages of reward processing and shows for the first time, to our knowledge, how this network is affected in hypocretin-deficient narcoleptic patients. ANN NEUROL 2010;67:190,200 [source]