Neural responses accompanying anticipation and experience of monetary gains and losses were monitored by functional magnetic resonance imaging. Trials comprised an initial "prospect" (expectancy) phase, when a set of three monetary amounts was displayed, and a subsequent "outcome" phase, when one of these amounts was awarded. Hemodynamic responses in the sublenticular extended amygdala (SLEA) and orbital gyrus tracked the expected values of the prospects, and responses to the highest value set of outcomes increased monotonically with monetary value in the nucleus accumbens, SLEA, and hypothalamus. Responses to prospects and outcomes were generally, but not always, seen in the same regions. The overlap of the observed activations with those seen previously in response to tactile stimuli, gustatory stimuli, and euphoria-inducing drugs is consistent with a contribution of common circuitry to the processing of diverse rewards.
Leptin, a hormone secreted by fat cells, suppresses food intake and promotes weight loss. To assess the action of this hormone on brain reward circuitry, changes in the rewarding effect of lateral hypothalamic stimulation were measured after leptin administration. At five stimulation sites near the fornix, the effectiveness of the rewarding electrical stimulation was enhanced by chronic food restriction and attenuated by intracerebroventricular infusion of leptin. In contrast, the rewarding effect of stimulating neighboring sites was insensitive to chronic food restriction and was enhanced by leptin in three of four cases. These opposing effects of leptin may mirror complementary changes in the rewarding effects of feeding and of competing behaviors.
Dopamine-containing neurons have been implicated in reward and decision making. One element of the supporting evidence is that cocaine, like other drugs that increase dopaminergic neurotransmission, powerfully potentiates reward seeking. We analyze this phenomenon from a novel perspective, introducing a new conceptual framework and new methodology for determining the stage(s) of neural processing at which drugs, lesions and physiological manipulations act to influence reward-seeking behavior. Cocaine strongly boosts the proclivity of rats to work for rewarding electrical brain stimulation. We show that the conventional conceptual framework and methods do not distinguish between three conflicting accounts of how the drug produces this effect: increased sensitivity of brain reward circuitry, increased gain, or decreased subjective reward costs. Sensitivity determines the stimulation strength required to produce a reward of a given intensity (a measure analogous to the KM of an enzyme) whereas gain determines the maximum intensity attainable (a measure analogous to the vmax of an enzyme-catalyzed reaction). To distinguish sensitivity changes from the other determinants, we measured and modeled reward seeking as a function of both stimulation strength and opportunity cost. The principal effect of cocaine was a two-fourfold increase in willingness to pay for the electrical reward, an effect consistent with increased gain or decreased subjective cost. This finding challenges the long-standing view that cocaine increases the sensitivity of brain reward circuitry. We discuss the implications of the results and the analytic approach for theories of how dopaminergic neurons and other diffuse modulatory brain systems contribute to reward pursuit, and we explore the implications of the conceptual framework for the study of natural rewards, drug reward, and mood.
Quantitative properties of the neural system mediating the rewarding and priming effects of medial forebrain bundle (MFB) stimulation in the rat have been determined by experiments that trade one parameter of the electrical stimulus against another. The first-order neurons in this substrate are for the most part long, thin, myelinated axons, coursing in the MFB and ventral tegmentum, with absolute refractory periods in the range .5-1.2 msec and conduction velocities of 2-8 m/sec. Local potentials in these axons decay with a time constant of about .1 msec. A supernormal period follows the recovery from refractoriness. These axons integrate current over exceptionally long intervals, accommodate slowly, and fire on the break of prolonged anodal pulses. These properties rule out the hypothesis that catecholamine pathways constitute the first-order axons. The second-order (postsynaptic) part of the substrate shows surprisingly simple spatial and temporal integrating characteristics. We examine the logic that permits conclusions of this sort to be derived from behavioral data and the role of these derivations in establishing neurobehavioral linkage hypotheses.In this article we describe properties of the neural tissue whose excitation eventuates in the reinforcing and motivating effects of electrical stimulation of the medial forebrain bundle (MFB) in the rat. The goal of the research is to identify these systems by anatomical and electrophysiological methods, thus providing physiological psychology with a model for studying the neurophysiological bases of learning and motivation in a higher vertebrate.The properties of the substrate for selfstimulation described in this article have been inferred from behavioral trade-off experiments-experiments that determine the value of one parameter of stimulation (e.g., current intensity) required to produce a criterion level of performance at each setting of another parameter (e.g., pulse duration). We review experiments of this kind in selfstimulation while examining two theoretical questions: (a) Why do behavioral trade-off functions have the power to reveal quantitative properties of the substrate for the behavior? and (b) Why must trade-off experiments play a pivotal role in relating anatomical and electrophysiological data to the behavioral phenomenon?Using microelectrodes, physiological psychologists have long been able to examine the response of single neurons to a behaviorally significant stimulus, such as rewarding brain stimulation (Rolls, 1975). The advent of 2-deoxyglucose autoradiography makes it possible to visualize a whole range of neural systems activated by such a stimulus (Figure 1). The existence of powerful techniques for directly revealing nervous activity confronts us with a conceptual problem that physiological psychology shares with other reductionist disciplines: How may one establish that a system defined by observations at one level of analysis explains phe-228
Rats lever pressed for concurrent electrical stimulation of the lateral hypothalamus and ventral tegmentum. The pulse-pair stimulation technique was used, with the first pulse of each pair applied to one electrode and the second to the other electrode; the intrapair interval was varied. The effectiveness of stimulation, measured behaviorally, increased abruptly (within .4 msec) as the intrapair interval was increased in the range from 1.0 to 2.0 msec These results, which do not resemble single-electrode refractory period results, are interpreted as evidence of collision in the directly stimulated, reward-related neurons linking the two sites. We conclude that self-stimulation of the medial forebrain bundle involves the direct activation of long-axon, longitudinal pathways. Estimates of the conduction velocity in the fibers subserving the collision-like effects are consistent with the properties of small myelinated axons but not central monoaminergic fibers.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.