Information capacity and robustness of encoding in the medial prefrontal cortex are modulated by the bioavailability of serotonin and the time elapsed from the cue during a reward-driven task

Pereyra, Armando; Mininni, Camilo J.; Zanutto, B. Silvano

doi:10.1038/s41598-021-93313-6

Cited by 2 publications

(1 citation statement)

References 61 publications

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“…The many functions of the mPFC are mediated by dissociable, heterogeneous populations of projection neurons, which display a wide range of responses to affective stimuli ( Grant et al, 2021 ) and regulate discrete aspects of motivated behavior ( Otis et al, 2017 , 2019 ). Serotonin is well positioned to modulate general cortical synchrony and the balanced activity of output pathways through tuning the activity of both inhibitory microcircuits and projection neurons ( Puig and Gulledge, 2011 ; Dembrow and Johnston, 2014 ), as well as regulating the general cortical response to affective stimuli ( Pereyra et al, 2021a ).…”

Section: The Brake: Contributions Of Inhibitory Control To Impulsivitymentioning

confidence: 99%

A Role for Serotonin in Modulating Opposing Drive and Brake Circuits of Impulsivity

Desrochers

Spring

Nautiyal

2022

Front. Behav. Neurosci.

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Impulsivity generally refers to a deficit in inhibition, with a focus on understanding the neural circuits which constitute the “brake” on actions and gratification. It is likely that increased impulsivity can arise not only from reduced inhibition, but also from a heightened or exaggerated excitatory “drive.” For example, an action which has more vigor, or is fueled by either increased incentive salience or a stronger action-outcome association, may be harder to inhibit. From this perspective, this review focuses on impulse control as a competition over behavioral output between an initially learned response-reward outcome association, and a subsequently acquired opposing inhibitory association. Our goal is to present a synthesis of research from humans and animal models that supports this dual-systems approach to understanding the behavioral and neural substrates that contribute to impulsivity, with a focus on the neuromodulatory role of serotonin. We review evidence for the role of serotonin signaling in mediating the balance of the “drive” and “brake” circuits. Additionally, we consider parallels of these competing instrumental systems in impulsivity within classical conditioning processes (e.g., extinction) in order to point us to potential behavioral and neural mechanisms that may modulate the competing instrumental associations. Finally, we consider how the balance of these competing associations might contribute to, or be extracted from, our experimental assessments of impulsivity. A careful understanding of the underlying behavioral and circuit level contributions to impulsivity is important for understanding the pathogenesis of increased impulsivity present in a number of psychiatric disorders. Pathological levels of impulsivity in such disorders are likely subserved by deficits in the balance of motivational and inhibitory processes.

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