reward circuitry
Recently Published Documents


TOTAL DOCUMENTS

269
(FIVE YEARS 90)

H-INDEX

54
(FIVE YEARS 5)

2022 ◽  
Author(s):  
Caroline Wyatt

Bipolar disorder, like many neuropsychiatric conditions, can be studied from a number of perspectives; from observation of behaviour, to study of cognitive dysfunction, through to changes at the molecular and genetic level. A consequence of this way of working is that there is inadequate communication between different levels of analysis, such that insufficient thought is given to whether a theoretical model derived from behavioural work fits with neurobiological data, and vice versa. Such limitations represent a key limiting factor in successful translation. Therefore, this paper takes a dominant theoretical model of bipolar disorder, based on that by Gray (1994) and developed by Alloy et al., (2015) as a basis to propose that the foundational pathology in bipolar is reward hypersensitivity, and to review how recent diverse neurobiological, cognitive and behavioural findings fit with this understanding. Executive Function deficits, partially derived from heritable structural changes are suggested as a foundation through which reward hypersensitivity develops to disorder, and CANA1C polymorphism-induced hyperactivity, further serves to drive the system towards reward seeking goals, through interaction with dopaminergic systems. This action is supplemented by a genetic predisposition for cognitive regulatory dysfunction, leading to improper modulation of emotive and reward networks. Specifically, deficits in top-down limbic modulation leads to behaviours disproportionally driven by limbic and reward circuitry; this pathology strengths over time through use. This therefore eventually results in substantial regional disconnect, reflected in epigenetic changes to neurotransmitters and observable histological changes.


2021 ◽  
Author(s):  
Yuri Imaizumi ◽  
Agnieszka Tymula ◽  
Yasuhiro Tsubo ◽  
Masayuki Matsumoto ◽  
Hiroshi Yamada

Prospect theory, arguably the most prominent theory of choice, is an obvious candidate for neural valuation models. How the activity of individual neurons, a possible computational unit, reflects prospect theory remains unknown. Here, we show with theoretical accuracy equivalent to that of human neuroimaging studies that single-neuron activity in four core reward-related cortical and subcortical regions represents the subjective valuation of risky gambles in monkeys. The activity of individual neurons in monkeys passively viewing a lottery reflects the desirability of probabilistic rewards, parameterized as a multiplicative combination of a utility and probability weighting functions in the prospect theory framework. The diverse patterns of valuation signals were not localized but distributed throughout most parts of the reward circuitry. A network model aggregating these signals reliably reconstructed risk preferences and subjective probability perceptions revealed by the animals' choices. Thus, distributed neural coding explains the computation of subjective valuations under risk.


2021 ◽  
Vol 13 ◽  
Author(s):  
Marie-Charlotte Allichon ◽  
Vanesa Ortiz ◽  
Paula Pousinha ◽  
Andry Andrianarivelo ◽  
Anna Petitbon ◽  
...  

Drug addiction is defined as a compulsive pattern of drug-seeking- and taking- behavior, with recurrent episodes of abstinence and relapse, and a loss of control despite negative consequences. Addictive drugs promote reinforcement by increasing dopamine in the mesocorticolimbic system, which alters excitatory glutamate transmission within the reward circuitry, thereby hijacking reward processing. Within the reward circuitry, the striatum is a key target structure of drugs of abuse since it is at the crossroad of converging glutamate inputs from limbic, thalamic and cortical regions, encoding components of drug-associated stimuli and environment, and dopamine that mediates reward prediction error and incentive values. These signals are integrated by medium-sized spiny neurons (MSN), which receive glutamate and dopamine axons converging onto their dendritic spines. MSN primarily form two mostly distinct populations based on the expression of either DA-D1 (D1R) or DA-D2 (D2R) receptors. While a classical view is that the two MSN populations act in parallel, playing antagonistic functional roles, the picture seems much more complex. Herein, we review recent studies, based on the use of cell-type-specific manipulations, demonstrating that dopamine differentially modulates dendritic spine density and synapse formation, as well as glutamate transmission, at specific inputs projecting onto D1R-MSN and D2R-MSN to shape persistent pathological behavioral in response to drugs of abuse. We also discuss the identification of distinct molecular events underlying the detrimental interplay between dopamine and glutamate signaling in D1R-MSN and D2R-MSN and highlight the relevance of such cell-type-specific molecular studies for the development of innovative strategies with potential therapeutic value for addiction. Because drug addiction is highly prevalent in patients with other psychiatric disorders when compared to the general population, we last discuss the hypothesis that shared cellular and molecular adaptations within common circuits could explain the co-occurrence of addiction and depression. We will therefore conclude this review by examining how the nucleus accumbens (NAc) could constitute a key interface between addiction and depression.


2021 ◽  
Author(s):  
Marta Cano ◽  
Erik Lee ◽  
Alexis Worthley ◽  
Kristen Ellard ◽  
Tracy Barbour ◽  
...  

Anhedonia is a core symptom of major depressive disorder (MDD) resulting from maladaptive reward processing. Electroconvulsive therapy (ECT) appears to be an effective treatment for patients with treatment-resistant depression (TRD). However, no previous neuroimaging studies have taken a dimensional approach to assess whether ECT-induced gray matter (GM) volume changes are specifically related to improvements in anhedonia and positive valence emotional constructs. Here we aimed to assess the relationship between right unilateral (RUL) ECT-induced brain volumetric changes and improvement in anhedonia and reward processing in patients with TRD. We evaluated 15 patients at two time points (before the first ECT session and after acute ECT completion) using magnetic resonance imaging (MRI), clinical scales (i.e., Quick Inventory of Depressive Symptomatology [QIDS] for syndromal depression severity and Snaith-Hamilton Pleasure Scale [SHAPS] for anhedonia) and the Temporal Experience of Pleasure Scale (TEPS) for anticipatory and consummatory experiences of pleasure. Patients with TRD showed a significant improvement in anhedonia symptoms and both anticipatory and consummatory pleasure after RUL ECT completion. Moreover, GM volume increases within the right reward system were related to anhedonia responders and, specifically, improvement in anticipatory (but not consummatory) reward. We highlight the importance of a dimensional and circuit-based approach to understanding target engagement and the mechanism of action of ECT, with the goal to define symptom- and circuit-specific response biomarkers for device neuromodulation therapies.


2021 ◽  
pp. 112-116
Author(s):  
Simon Lacey ◽  
K. Sathian

The “art infusion effect” suggests that people evaluate products more positively when they are associated with art images than non-art images. Using functional magnetic resonance imaging during viewing of art and non-art images matched for content, the authors investigated whether artistic status alone could activate the reward circuit. Relative to non-art images, art images indeed activated reward-related regions including the ventral striatum. This activity was uncorrelated with response times, ratings of familiarity, or aesthetic preference for art images, suggesting that these variables were unrelated to the art-selective activations. Effective connectivity analyses showed that the ventral striatum was driven by visual cortical regions when viewing art images but not non-art images and was not driven by regions that correlated with aesthetic preference for either art or non-art images. These findings suggest that visual art involves activation of reward circuitry based on artistic status alone and independently of its aesthetic value.


2021 ◽  
pp. 43-47
Author(s):  
John P. O’Doherty ◽  
Raymond J. Dolan

Faces are a highly privileged class of stimuli in humans, and facial attractiveness is a particularly salient attribute of faces that can exert considerable influence on the behavior of others. In the 2003 paper discussed in this chapter, the authors aimed to investigate the neural correlates of facial attractiveness in the brain, hypothesizing that attractive faces would recruit basic reward circuits, especially the orbitofrontal cortex. Consistent with their hypothesis, they found robust engagement of the orbitofrontal cortex to attractive faces and, moreover, that this response was enhanced if a face exhibited a smiling expression. Taken together, these results suggest that facial attractiveness and cues signaling positive social feedback can robustly recruit the brain’s reward circuitry, positioning attractive faces alongside other basic rewards while also aligning attractive faces with other aesthetically pleasing stimuli that engage similar circuits such as works of art.


2021 ◽  
Vol 10 (21) ◽  
pp. 5133
Author(s):  
Ingrid Caroline van Nieuwpoort ◽  
Tessa N. A. Slagboom ◽  
Sigridur Jakobsdóttir ◽  
Jan Berend Deijen ◽  
Dick J. Veltman ◽  
...  

(1) Background: Prader–Willi syndrome (PWS) is characterized by hyperphagia, resulting in morbid obesity if not controlled. The primary aim of this study was to investigate whether PWS patients show altered activation of brain areas involved in hunger. As a secondary objective, we assessed whether there is an association between these brain areas and several endocrine and metabolic factors in the fasting state. (2) Methods: 12 PWS adults and 14 healthy controls (siblings) performed a food-related experimental task after an overnight fast while brain activation in regions of interest was measured by functional MRI. (3) Results: In controls, significantly more activation was found in the left insula (p = 0.004) and the bilateral fusiform gyrus (p = 0.003 and 0.013) when the individuals were watching food as compared to non-food pictures, which was absent in PWS patients. Moreover, in PWS adults watching food versus non-food pictures a significant negative correlation for glucose and right amygdala activation (p_fwe = 0.007) as well as a positive correlation for leptin and right anterior hippocampus/amygdala activation (p_fwe = 0.028) was demonstrated. No significant associations for the other hormonal and metabolic factors were found. (4) Conclusions: PWS individuals show aberrant food-related brain activation in the fasting state. Leptin is associated with activation within the neural motivation/reward circuitry, while the opposite is true for glucose.


2021 ◽  
Vol 14 ◽  
Author(s):  
Loreto S. San Martin ◽  
Lorena Armijo-Weingart ◽  
Anibal Araya ◽  
Gonzalo E. Yévenes ◽  
Robert J. Harvey ◽  
...  

The glycine receptor (GlyR), a ligand-gated ion channel, is critical for inhibitory neurotransmission in brainstem, spinal cord, and in supraspinal regions. Recent data from several laboratories have shown that GlyRs are expressed in the brain reward circuitry and that α1 and α2 are the principal subunits expressed in the nucleus accumbens (nAc). In the present study, we studied the sensitivity to ethanol of homomeric and heteromeric α3 GlyR subunits in HEK293 cells and dissociated neurons from the nAc. Finally, we explored ethanol-related behaviors in a Glra3 knockout mouse (Glra3–/–). Studies in HEK293 cells showed that while homomeric α3 GlyR subunits were insensitive to ethanol, heteromeric α3β GlyR subunits showed higher sensitivity to ethanol. Additionally, using electrophysiological recordings in dissociated accumbal neurons, we found that the glycine current density increased in Glra3–/– mice and the GlyRs were less affected by ethanol and picrotoxin. We also examined the effect of ethanol on sedation and drinking behavior in Glra3–/– mice and found that the duration in the loss of righting reflex (LORR) was unchanged compared to wild-type (WT) mice. On the other hand, using the drinking in the dark (DID) paradigm, we found that Glra3–/– mice have a larger ethanol consumption compared to WT mice, and that this was already high during the first days of exposure to ethanol. Our results support the conclusion that heteromeric α3β, but not homomeric α3, GlyRs are potentiated by ethanol. Also, the increase in GlyR and GABAAR mediated current densities in accumbal neurons in the KO mice support the presence of compensatory changes to α3 knock out. The increase in ethanol drinking in the Glra3–/– mice might be associated to the reduction in β and compensatory changes in other subunits in the receptor arrangement.


2021 ◽  
Author(s):  
Leah Middleton ◽  
Melanie Schaffler ◽  
Isabella Succi ◽  
William Foster ◽  
Mark Gradwell ◽  
...  

AbstractPleasurable touch during social behavior is the key to building familial bonds and meaningful connections. One form of social touch occurs during sex. Although sexual behavior is initiated in part by touch, and touch is ongoing throughout copulation, the identity and role of sensory neurons that transduce sexual touch remain unknown. A population of sensory neurons labeled by the G-protein coupled receptor Mrgprb4 detect stroking touch in mice1,2. Here, we study the social relevance of this population by genetically engineering mice to allow activation or ablation of Mrgprb4-lineage neurons and reveal that these neurons are required for sexual receptivity and sufficient to activate reward circuitry. Even in social isolation, optogenetic stimulation of Mrgprb4-lineage neurons through the back skin is sufficient to induce a conditioned place preference and a striking dorsoflexion resembling the lordotic copulatory posture in females. In the absence of Mrgprb4-lineage neurons, female mice no longer find male mounts rewarding: sexual receptivity is supplanted by aggression and a coincident decline in dopaminergic release in the mesolimbic reward pathway. In addition to sexual behavior, Mrgprb4-lineage neurons are also required for social postures induced by female-to-female back touch. Together, these findings establish that Mrgprb4-lineage neurons are the first neurons of a skin-to-brain circuit encoding the rewarding quality of social touch.


Sign in / Sign up

Export Citation Format

Share Document