Reward-Seeking Deficits in Major Depression: Unpacking Appetitive Task Performance with Ex-Gaussian Response Time Variability Analysis.
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ABSTRACT:
SUBMITTER: Silvia PJ
PROVIDER: S-EPMC8425250 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Both attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) have been linked to increased reaction time variability (RTV), a marker of attentional fluctuation. Here we test whether specificity to either trait emerges when we examine (1) detailed ex-Gaussian and frequency RTV subcomponents, (2) effects while controlling for the other trait and (3) improvement in the RTV measures following rewards or a faster event rate. 1110 children aged 7-10 years from a population-based sample completed a Go/No-Go task under three conditions (slow, fast and incentives). We measured RTV with standard deviation of RT (SDRT), ex-Gaussian distribution measures (Sigma and Tau), RT fluctuations in cycles of ~14-90 s in all conditions (Slow-4 and Slow-5), and RT fluctuations in cycles of 2-14 s in the fast condition (Slow-2 and Slow-3). Parent-rated ADHD and ASD traits were obtained. All refined RTV components were linked to ADHD traits only and not to ASD traits, while Sigma did not relate to either trait. Although both ADHD and ASD social-communication traits were associated with SDRT, the association with social-communication impairments disappeared when controlling for ADHD traits. A reward-induced improvement in RTV measures, indicating malleability, emerged in relation to ADHD traits but not ASD traits. Under closer inspection, specificity emerges of high RTV to ADHD traits. For the clinician, our findings indicate that attentional fluctuation in children with high ASD traits may be due to co-occurring ADHD traits and emphasise how the effectiveness of rewards does not generalise from ADHD to ASD traits.
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Project description:During olfactory appetitive learning, animals associate an odor, or conditioned stimulus (CS), with an unconditioned stimulus (US), often a sugar reward. This association induces feeding behavior, a conditioned response (CR), upon subsequent exposure to the CS. In this study, we developed a model of this behavior in isolated Drosophila brains. Artificial activation of neurons expressing the Gr5a sugar-responsive gustatory receptor (Gr5a GRNs) induces feeding behavior in starved flies. Consistent with this, we find that in dissected brains, activation of Gr5a GRNs induces Ca2+ transients in motor neurons, MN11?+?12, required for ingestion. Significantly, activation of Gr5a GRNs can substitute for presentation of sugar rewards during olfactory appetitive learning. Similarly, in dissected brains, coincident stimulation of Gr5a GRNs and the antennal lobe (AL), which processes olfactory information, results in increased Ca2+ influx into MN11?+?12 cells upon subsequent AL stimulation. Importantly, olfactory appetitive associations are not formed in satiated flies. Likewise, AL-evoked Ca2+ transients in MN11?+?12 are not produced in ex vivo brains from satiated flies. Our results suggest that a starved/satiated state is maintained in dissected brains, and that this ex vivo system will be useful for identification of neural networks involved in olfactory appetitive learning.
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Project description:ObjectiveThis study examined how two key process-of-care tasks of the collaborative care model (CCM) predict patient depression outcomes.MethodsRegistry data were from a large implementation of the CCM in Washington State and included 5,439 patient-episodes for patients age 18 or older with a baseline Patient Health Questionnaire-9 (PHQ-9) score of ≥10 and at least one follow-up contact with the CCM care manager within 24 weeks of initial contact. Key CCM tasks examined were at least one care manager follow-up contact within four weeks of initial contact and at least one psychiatric consultation between weeks 8 and 12 for patients not responding to treatment by week 8. Clinically significant improvement in depression symptoms was defined as achieving a PHQ-9 score of <10 or a 50% or more reduction in PHQ-9 score compared with baseline. Bivariate and multivariate (logistic and proportional hazard models) analyses were conducted to examine how fidelity with either task predicted outcomes. All analyses were conducted with the original sample and with a propensity score-matched sample.ResultsFour-week follow-up was associated with a greater likelihood of achieving improvement in depression (odds ratio [OR]=1.63, 95% confidence interval [CI]=1.23-2.17) and a shorter time to improvement (hazard ratio=2.06, CI=1.67-2.54). Psychiatric consultation was also associated with a greater likelihood of improvement (OR=1.44, CI=1.13-1.84) but not with a shorter time to improvement. Propensity score-matched analysis yielded very similar results.ConclusionsFindings support efforts to improve fidelity to the two process-of-care tasks and to include these tasks among quality measures for CCM implementation.
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Project description:Hemodynamic recordings from visual cortex contain powerful endogenous task-related responses that may reflect task-related arousal, or "task engagement" distinct from attention. We tested this hypothesis with hemodynamic measurements (intrinsic-signal optical imaging) from monkey primary visual cortex (V1) while the animals' engagement in a periodic fixation task over several hours was varied through reward size and as animals took breaks. With higher rewards, animals appeared more task-engaged; task-related responses were more temporally precise at the task period (approximately 10-20 seconds) and modestly stronger. The 2-5 minute blocks of high-reward trials led to ramp-like decreases in mean local blood volume; these reversed with ramp-like increases during low reward. The blood volume increased even more sharply when the animal shut his eyes and disengaged completely from the task (5-10 minutes). We propose a mechanism that controls vascular tone, likely along with local neural responses in a manner that reflects task engagement over the full range of timescales tested.
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Project description:Resource-seeking behaviours are ordinarily constrained by physiological needs and threats of danger, and the loss of these controls is associated with pathological reward seeking1. Although dysfunction of the dopaminergic valuation system of the brain is known to contribute towards unconstrained reward seeking2,3, the underlying reasons for this behaviour are unclear. Here we describe dopaminergic neural mechanisms that produce reward seeking despite adverse consequences in Drosophila melanogaster. Odours paired with optogenetic activation of a defined subset of reward-encoding dopaminergic neurons become cues that starved flies seek while neglecting food and enduring electric shock punishment. Unconstrained seeking of reward is not observed after learning with sugar or synthetic engagement of other dopaminergic neuron populations. Antagonism between reward-encoding and punishment-encoding dopaminergic neurons accounts for the perseverance of reward seeking despite punishment, whereas synthetic engagement of the reward-encoding dopaminergic neurons also impairs the ordinary need-dependent dopaminergic valuation of available food. Connectome analyses reveal that the population of reward-encoding dopaminergic neurons receives highly heterogeneous input, consistent with parallel representation of diverse rewards, and recordings demonstrate state-specific gating and satiety-related signals. We propose that a similar dopaminergic valuation system dysfunction is likely to contribute to maladaptive seeking of rewards by mammals.
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Project description:Whilst reward pathologies e.g., anhedonia and apathy, are major and common in stress-related neuropsychiatric disorders, their neurobiological bases and therefore treatment are poorly understood. Functional imaging studies in humans with reward pathology indicate that attenuated BOLD activity in nucleus accumbens (NAc) occurs during reward anticipation/expectancy but not reinforcement; potentially, this is dopamine (DA) related. In mice, chronic social stress (CSS) leads to reduced reward learning and effortful motivation and, here, DA-sensor fibre photometry was used to investigate whether these behavioural deficits co-occur with altered NAc DA activity during reward anticipation and/or reinforcement. In CSS mice relative to controls: (1) Reduced discriminative learning of the sequence, tone-on + appetitive behaviour = tone-on + sucrose reinforcement, co-occurred with attenuated NAc DA activity throughout tone-on and sucrose reinforcement. (2) Reduced effortful motivation during the sequence, operant behaviour = tone-on + sucrose delivery + tone-off / appetitive behaviour = sucrose reinforcement, co-occurred with attenuated NAc DA activity at tone-on and typical activity at sucrose reinforcement. (3) Reduced effortful motivation during the sequence, operant behaviour = appetitive behaviour + sociosexual reinforcement co-occurred with typical NAc DA activity at female reinforcement. Therefore, in CSS mice attenuated NAc DA activity is specific to reward anticipation and as such potentially causal to deficits in learning and motivation. CSS did not impact on the transcriptome of ventral tegmentum DA neurons, suggesting that its stimulus-specific effects on NAc DA activity originate elsewhere in the neural circuitry of reward processing.
2024-07-31 | GSE268460 | GEO