Publications by authors named "Kevin Zitelli"

Migraine is a debilitating neurological disorder that affects millions worldwide. Elucidating its underlying mechanisms is crucial for developing effective therapeutic interventions. In this editorial, we discuss the potential applications of one-photon miniscopes, which enable minimally invasive, high spatiotemporal resolution fluorescence imaging in freely moving animals.

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The ability to precisely monitor and manipulate neural circuits is essential to understand the brain. Advancements over the last decade in optical techniques such as calcium imaging and optogenetics have empowered researchers to gain insight into brain function by systematically manipulating or monitoring defined neural circuits. Combining these cutting-edge techniques enables a more direct mechanism for ascribing neural dynamics to behavior.

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The identification of distinct cell types in the basal ganglia has been critical to our understanding of basal ganglia function and the treatment of neurological disorders. The external globus pallidus (GPe) is a key contributor to motor suppressing pathways in the basal ganglia, yet its neuronal heterogeneity has remained an untapped resource for therapeutic interventions. Here we demonstrate that optogenetic interventions that dissociate the activity of two neuronal populations in the GPe, elevating the activity of parvalbumin (PV)-expressing GPe neurons over that of Lim homeobox 6 (Lhx6)-expressing GPe neurons, restores movement in dopamine-depleted mice and attenuates pathological activity of basal ganglia output neurons for hours beyond stimulation.

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Unlabelled: In the basal ganglia, focused rhythmicity is an important feature of network activity at certain stages of motor processing. In disease, however, the basal ganglia develop amplified rhythmicity. Here, we demonstrate how the cellular architecture and network dynamics of an inhibitory loop in the basal ganglia yield exaggerated synchrony and locking to β oscillations, specifically in the dopamine-depleted state.

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The molecular mechanisms underlying TBI pathophysiology and recovery are both complex and varied. Further, the pathology underlying many of the clinical sequelae observed in this population evolve over the acute injury period and encompass the subacute and chronic phases of recovery, supporting the contemporary concept that TBI is a chronic disease rather than a static insult from which limited recovery occurs. TBI related complications can also span from acute care to the very chronic stages of recovery that occur years after the initial trauma.

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