PubMed Health⌕ Search

PubMed · 2648975

Brain dopamine and reward.

Abstract

While the evidence is strong that dopamine plays some fundamental and special role in the rewarding effects of brain stimulation, psychomotor stimulants, opiates, and food, the exact nature of that role is not clear. One thing is clear: Dopamine is not the only reward transmitter, and dopaminergic neurons are not the final common path for all rewards. Dopamine antagonists and lesions of the dopamine systems appear to spare the rewarding effects of nucleus accumbens and frontal cortex brain stimulation (Simon et al 1979) and certainly spare the rewarding effects of apomorphine (Roberts & Vickers 1988). It is clear that reward circuitry is multisynaptic, and since dopamine cells do not send axons to each other or receive axons from each other, dopamine can at best serve as but a single link in this circuitry. If dopamine is not a final common path for all rewards, could it be an intermediate common path for most rewards? Some workers have argued against such a view, but at present they must do so on incomplete evidence. For example, Phillips (1984) has argued that there must be multiple reward systems, functionally independent and organized in parallel with one another. His primary evidence, however, is the fact that brain stimulation is rewarding at different levels of the nervous system. As we have seen in the case of midline mesencephalic stimulation, the location of the electrode tip in relation to the dopamine cells and fibers tells us little about the role of dopamine in brain stimulation reward. It seems clear that the ventral tegmental dopamine system plays a critical role in midline mesencephalic reward, despite the distance from the electrode tip to the dopamine cells where morphine causes its dopamine-dependent facilitory effects or to the dopamine terminals where low-dose neuroleptics presumably cause theirs. Until pharmacological challenge has been extended to the cases discussed by Phillips, we can only speculate as to the role of dopamine in each of those cases. In the cases where pharmacological challenge has been examined, only nucleus accumbens and frontal cortex have been found to have dopamine-independent reward sites. It is not consistent with the dopamine hypothesis that dopamine-independent reward sites should exist in these areas, since any reward signals carried to nucleus accumbens or frontal cortex by dopamine fibers would-unless we are to believe that reward "happens" at these sites-have to be carried to the next stage of the circuit by nondopaminergic fibers (there are no dopaminergic cell bodies in any of the dopamine terminal areas).(ABSTRACT TRUNCATED AT 400 WORDS)

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

R A Wise, P P Rompre. 1989. Brain dopamine and reward.. https://doi.org/10.1146/annurev.ps.40.020189.001203

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Protocol for Detecting and Sequencing Chikungunya Virus from Field-Collected Mosquitoes.

Arboviral diseases represent a major public health challenge, especially in tropical regions where environmental conditions may favor the proliferation and spread of mosquito vectors. Thus, early and accurate detection of chikungunya virus (CHIKV) in mosquito populations can be a valuable tool for effective surveillance of circulating variants and for identifying new viral introductions. Given the challenges of detecting arboviruses in field-captured mosquitoes, we describe an integrated workflow for CHIKV molecular detection and whole-genome sequencing. This protocol includes mosquito homogenization using a bead-based mechanical disruptor, RNA extraction using TRIzol reagent with minor modifications, molecular screening using CHIKV-specific RT-qPCR, and whole-genome amplification followed by sequencing on Illumina platforms. Despite the protocol being optimized for individual mosquitoes, it results in high-quality RNA suitable for both entomological surveillance and genomic analysis. As this protocol allows recovery of complete CHIKV genomes from mosquito specimens, it can serve as a basis for genomic epidemiology studies, enabling monitoring of viral diversity and lineage dynamics, and facilitating early detection of emerging variants to support timely and targeted public health interventions in endemic and at-risk regions.

Animals↗

Genomic Profiling of Chromatin State Using CUT&Tag.

Alterations in chromatin state, mediated through histone modifications and the incorporation of histone variants, are fundamental to establishing transcriptional networks and cell identity. Recent advances in low-input epigenome profiling methods, such as CUT&Tag and CUT&RUN, have enabled the study of chromatin states from very limited starting materials. In this chapter, we describe procedures for generating CUT&Tag libraries to profile histone modifications and histone variants in early-developing zebrafish embryos.

Animals↗

Relaxin-2: Shaping the Proteomic Landscape of Skeletal Muscle Physiology, Glucose Trafficking, and Mitochondrial Function in Rat.

Relaxin-2 is a hormone with robust beneficial effects on the heart and blood vessels and potential as a therapy for cardiovascular (CV) disease. Considering the interorgan communication between skeletal muscle and heart, and the relation between muscle quality/composition and CV events, we hypothesize that relaxin-2 may regulate skeletal muscle physiology and metabolism. We aim to evaluate the impact of relaxin-2 on the proteome of skeletal muscle from healthy Sprague-Dawley rats. Animals were treated with 0.4 mg/kg/day of serelaxin (recombinant form of human relaxin-2) or vehicle (PBS) for 2 weeks employing subcutaneous osmotic minipumps. Skeletal muscle protein identification and quantification were performed by LC-MS/MS using a Data-Independent Acquisition (DIA)-Sequential Window Acquisition of All Theoretical Fragment Ion Spectra (SWATH) method. SWATH/MS quantitative analysis identified that relaxin-2 significantly decreased 95 proteins and significantly increased 32 proteins in rat skeletal muscle when compared to control rats. From these, 34 proteins were associated with muscle function, myogenesis, muscle differentiation and/or regeneration, 20 are mitochondrial proteins (six from the complexes of the electron transport chain), and 10 proteins participate in glucose metabolism. Qualitative data-dependent workflow analysis identified 35 proteins exclusive to the skeletal muscle of the relaxin-2-treated group: eight proteins related to processes of skeletal muscle function (size, ion homeostasis or organization of caveolae structures and cytoskeleton) and myogenesis, and two proteins involved in muscle differentiation. Our work highlighted for the first time the role of relaxin-2 in crucial processes of muscle physiology and energetic metabolism, which could influence several processes involved in myopathy and CV.

Animals↗