Koloski, M. F. | Search bioRxiv

bioRxiv2023

Cognitive rehabilitation can improve brain injury-induced deficits in behavioral flexibility and impulsivity linked to impaired reward-feedback activity.

Traumatic brain injury (TBI) affects a large population, resulting in severe cognitive impairments. Although cognitive rehabilitation is an accepted treatment for some deficits, studies in patients are limited in ability to probe physiological and behavioral mechanisms. Therefore, animal models are needed to optimize strategies. Frontal TBI in a rat model results in robust and replicable cognitive deficits, making this an ideal candidate for investigating cognitive rehabilitation. In this study, we report three distinct frontal TBI experiments assessing behavior well into the chronic post-injury period using male Long-Evans rats. First, we evaluated the impact of frontal injury on local field potentials recorded simultaneously from 12 brain regions during a probabilistic reversal learning task (PbR). Next, rats were tested on reversal learning (PbR) or impulsivity (differential reinforcement of low-rate behavior: DRL) and half received salient cues associated with reinforcement contingencies as a form of "cognitive rehabilitation". After rehabilitation on the PbR task, brains were stained for markers of activity. On the DRL, cues were devalued to determine if beneficial effects persisted on impulsive behavior. TBI resulted in outcome salience deficits evident in task performance and reward-feedback signals occurring at beta frequencies in orbitofrontal cortex (OFC) and associated frontostriatal regions. Cognitive rehabilitation improved flexibility and increased OFC activity. Rehabilitation also reduced impulsivity, even after cues were degraded, which was partially mediated by improvements in timing behavior. The current study established a robust platform for investigating cognitive rehabilitation in animals and identified a strong role for dysfunctional OFC signaling after frontal TBI.

neuroscience↗

bioRxiv2022

Cortico-Striatal Beta-Oscillations as a Marker of Learned Reward Value

Single neuron correlates of reward value have been observed in brain regions along the cortico-striatal pathway including ventral striatum, orbital, and medial prefrontal cortex. Brain imaging studies in humans further validate these findings and suggest that value is represented in a network of brain regions opposed to a particular area. Neural activity oscillates at periodic frequencies to coordinate long-range communication in widespread, dynamic networks. To explore how oscillatory dynamics across brain regions may represent reward value, we measured local field potentials of male Long-Evans rats during three distinct behavioral tasks, each probing a different aspect of reward processing. Our goal was to use a data-driven approach to identify a common electrophysiology property associated with reward value. We found that reward-locked oscillations at beta frequencies, in both single units and local field potentials, were markers of positive reward valence. More importantly, Reward-locked beta-oscillations scaled with expected reward value on specific trial types and in a behaviorally relevant way across tasks. Oscillatory signatures of reward processing were observed throughout the cortico-striatal network including electrodes placed in orbitofrontal cortex, anterior insula, medial prefrontal cortex, ventral striatum, and amygdala. These data suggests that beta-oscillations reflect learned reward value in a distributed network, and this may serve as a stable and robust bio-marker for future studies.

animal behavior and cognition↗