Vicarious Reinforcement in Rhesus Macaques (Macaca Mulatta)

What happens to others profoundly influences our own behavior. Such other-regarding outcomes can drive observational learning, as well as motivate cooperation, charity, empathy, and even spite. Vicarious reinforcement may serve as one of the critical mechanisms mediating the influence of other-regarding outcomes on behavior and decision-making in groups. Here we show that rhesus macaques spontaneously derive vicarious reinforcement from observing rewards given to another monkey, and that this reinforcement can motivate them to subsequently deliver or withhold rewards from the other animal. We exploited Pavlovian and instrumental conditioning to associate rewards to self (M1) and/or rewards to another monkey (M2) with visual cues. M1s made more errors in the instrumental trials when cues predicted reward to M2 compared to when cues predicted reward to M1, but made even more errors when cues predicted reward to no one. In subsequent preference tests between pairs of conditioned cues, M1s preferred cues paired with reward to M2 over cues paired with reward to no one. By contrast, M1s preferred cues paired with reward to self over cues paired with reward to both monkeys simultaneously. Rates of attention to M2 strongly predicted the strength and valence of vicarious reinforcement. These patterns of behavior, which were absent in non-social control trials, are consistent with vicarious reinforcement based upon sensitivity to observed, or counterfactual, outcomes with respect to another individual. Vicarious reward may play a critical role in shaping cooperation and competition, as well as motivating observational learning and group coordination in rhesus macaques, much as it does in humans. We propose that vicarious reinforcement signals mediate these behaviors via homologous neural circuits involved in reinforcement learning and decision-making

Emotion and aging: linking neural mechanisms to psychological theory

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Emotion and aging: linking neural mechanisms to psychological theory

No description supplie

Neurobiology of social reward valuation in adults with a history of anorexia nervosa.

ObjectiveAnorexia nervosa (AN) is a disorder characterized by atypical patterns of reward valuation (e.g. positive valuation of hunger). Atypical reward processing may extend into social domains. If so, such findings would be of prognostic significance as impaired social functioning predicts worse outcome. We explore neural circuits implicated in social reward processing in individuals with a history of AN who are weight-restored relative to controls and examine the effects of illness course on the experience of social value.Method20 weight-restored individuals with a history of AN (AN-WR) and 24 healthy control (HC) participants were assessed using fMRI tasks that tapped social reward: smiling faces and full human figures that varied in attractiveness and weight.ResultsAN-WR differed from HC in attractiveness ratings by weight (negatively correlated in AN-WR). While there were no significant differences when viewing smiling faces, viewing full figures resulted in decreased activation in regions implicated in reward valuation (the right caudate) for AN-WR and this region was negatively correlated with a sustained course of the disorder. Exploratory whole brain analyses revealed reduced activation in regions associated with social reward, self-referential processing, and cognitive reappraisal (e.g., medial prefrontal cortex, striatum, and nucleus accumbens) with sustained disorder course.DiscussionThe rewarding value of full body images decreases with a sustained disorder course. This may reflect an extension of atypical reward processing documented in AN-WR, perhaps as a function of starvation dampening visceral motivational signals; the deployment of cognitive strategies that lessen the experience of reward; and/or the nature of the stimuli themselves as provocative of eating disorder symptoms (e.g., thin bodies). These findings did not extend to smiling face stimuli. Advances in technology (e.g., virtual avatars, text messaging) may provide novel means to build relationships, including therapeutic relationships, to support improved social connections without threats to symptom provocation

Mechanisms of nitric oxide-mediated neurogenic,vasodilation in mesenteric resistance arteries of toad, Bufo marinus

This study determined the role of nitric oxide (NO) in neurogenic vasodilation in mesenteric resistance arteries of the toad Bufo marinus. NO synthase (NOS) was anatomically demonstrated in perivascular nerves, but not in the endothelium. ACh and nicotine caused TTX-sensitive neurogenic vasodilation of mesenteric arteries. The ACh-induced vasodilation was endothelium-independent and was mediated by the NO/soluble guanylyl cyclase signaling pathway, inasmuch as the vasodilation was blocked by the soluble guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one and the NOS inhibitors Nω- nitro-L-arginine methyl ester and Nω-nitro-L-arginine. Furthermore, the ACh-induced vasodilation was significantly decreased by the more selective neural NOS inhibitor N5-(1-imino-3-butenyl)-L-ornithine. The nicotine-induced vasodilation was endothelium-independent and mediated by NO and calcitonin gene-related peptide (CGRP), inasmuch as pretreatment of mesenteric arteries with a combination of Nω-nitro-L-arginine and the CGRP receptor antagonist CGRP-(8–37) blocked the vasodilation. Clotrimazole significantly decreased the ACh-induced response, providing evidence that a component of the NO vasodilation involved Ca2+-activated K+ or voltage-gated K+ channels. These data show that NO control of mesenteric resistance arteries of toad is provided by nitrergic nerves, rather than the endothelium, and implicate NO as a potentially important regulator of gut blood flow and peripheral blood pressure