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Reward and anti-reward circuits in health and disease
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Both animals and humans are motivated to seek natural rewards to feel pleasure but also avoid unpleasant and aversive stimuli that predict pain, loss and danger. Disruption of reward-related neural circuits, specifically mesocorticolimbic dopaminergic pathways, is believed to contribute to the development of psychiatric illnesses and drug addiction. Increasing evidence also reports the contribution of non-dopamine reward and anti-reward brain circuits in maladaptive motivated behaviors associated with affective disorders and addiction.
In this Collection, the editors at Communications Biology, Nature Neuroscience, Nature Communications and Scientific Reports welcome original research Articles presenting novel reward and anti-reward mechanisms recruited by neural circuits and neuromodulatory systems that can drive adaptive motivated behaviors under normal conditions or pathologically reinforce maladaptive behaviors. We specifically encourage studies employing a multidisciplinary approach and a combination of traditional and modern neuroscience techniques such as genomic, transcriptomic, and proteomic tools, viral strategies, optogenetics, chemogenetics, miniscope imaging, electrophysiology and behavioral assays of motivation. This call for papers invites both basic and preclinical studies in animal models, as well as studies involving human tissue.
Mouse behavioral assays sheds light on the impact of adolescent exposure to vaping and the unique changes that occur in brain regions related to reward and reinforcement.
The functional connectivity patterns in cocaine use disorder and their spatial link to neurotransmitter receptor densities are characterized. Findings suggest dopamine D2/3 receptor densities may underlie the functional architecture of cocaine use.
A preclinical study in mice suggests important roles for a scaffold protein, A-kinase anchoring protein 150 (AKAP150) in regulation of synaptic function, glutamatergic plasticity and intrinsic excitability of lateral habenula (LHb) neurons.
The role of dopaminergic neurons in modulating striatal dynamics on subsecond timescales remains unclear. Long, Lee et al. show that only potentially supra-physiological dopamine levels are capable of strongly and rapidly altering striatal spiking activity.
Mohebi et al. report that dopamine (DA) pulses in different rat striatal subregions signal prediction errors across different timescales. In this way, one learning process may achieve a range of adaptive behaviors.
Monosynaptic cerebellar projections to the substantia nigra pars compacta (SNc) increase the activity of SNc neurons and striatal dopamine levels. These projections may convey information related to movement initiation, vigor and reward processing.
A widely accepted assumption in addiction research is that overvaluation of drug cues is caused by enhanced dopaminergic response to these cues. Here, the authors show similar dopamine neuronal responses to cues predicting opioids vs. natural rewards.
The nucleus accumbens is a key region in rewarding and aversive behaviors. Here, authors show that nucleus accumbens shell D1- and D2-MSNs were similarly co-recruited during appetitive and aversive conditioning, yet D2-MSNs appeared to be more relevant for the extinction of aversive associations.
The evolutionary origin of habenular asymmetries is elusive. Here they show morphological and molecular conservations indicative of an ancient origin in vertebrates and identify Wnt signaling as a core mechanism underlying their formation and diversification.