Biology subjects

Koloski, M. F.

Publications and source records attributed to Koloski, M. F..

4 recordsLinked to original sources

bioRxiv2026

Cortical oscillations reflect opponent ensemble dynamics through coordinated multifrequency activity

Neural oscillations are widely used as proxies for neuronal activity, where power in individual frequency bands is commonly interpreted as functionally indexing neural circuit engagement. However, power in individual frequency bands shows heterogeneous and sometimes opposing relationships with neuronal activity across regions and behavioral contexts, challenging the assumption of a stable frequency-to-circuit mapping. Here we show that glutamatergic population activity in rat medial prefrontal cortex is not stably linked with power in isolated frequency bands, but rather with dynamically recurring multi-frequency amplitude co-fluctuations. These multi-frequency patterns, termed spectral motifs, occurred in opponent pairs with nearly identical frequency composition but inverted relationships to population calcium activity. This opponent motif structure, observed across cortical regions and species, provides a key component for understanding how oscillations are linked to neuronal activity. We found that shifts in motif opponency balance explained changes in glutamatergic activity that occur during brain-computer interface learning better than models based on frequency band power alone. Furthermore, opponent motifs map selectively onto opponent cell ensembles and enable bidirectional mapping between local field potentials and ensemble activity. These findings identify multi-frequency opponent motifs as a conserved organizational principle linking oscillatory dynamics to population-level circuit states and challenge the notion that individual frequency bands can serve as interpretable functional units mapping onto neural circuit activity.

neuroscience↗

bioRxiv2025

Methylphenidate-induced reductions in choice impulsivity are associated with alterations in cortico-striatal beta oscillations.

Impulsive choice- preferring small, immediate rewards over larger, delayed reward- is a hallmark of many psychiatric disorders. Methylphenidate, a dopamine and noradrenaline transporter inhibitor, reduces impulsivity, but the neural mechanisms underlying this effect remain unclear. Identifying a neurophysiological signature of methylphenidates action could be used clinically to predict treatment response and guide drug development. To this end, we recorded local field potentials (LFP) from 32 electrodes spanning cortico-striatal circuits in rats performing a temporal discounting task, under saline or methylphenidate treatment conditions. Methylphenidate decreased beta frequency (15-30 Hz) power and connectivity for small, immediate rewards while simultaneously increasing beta power for large, delayed rewards. Reduced connectivity in cortico-striatal networks during small rewards predicted increased preference for delayed rewards. These findings suggest that methylphenidate influences discounting behavior by modulating reward-evoked beta oscillations in cortico-striatal networks. Thus, beta oscillations may serve as a translational biomarker of treatment responsivity to monoaminergic drugs, providing a circuit-level assay to measure and predict changes in impulsive behavior.

neuroscience↗

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↗