Mike Beckstead, PhD
- Research Program: Geroscience
- Position: Associate Member, Physiology
Biography
The Beckstead lab studies communication between dopamine neurons and other cell types in the brain in the context of motivated behavior and dopamine-related diseases. Dopamine neurons are a prominent cell type in the ventral midbrain that are necessary for both reward learning and the initiation of voluntary movement. Their dysfunction is linked to several debilitating diseases observed throughout life, including Parkinson’s disease, addiction, and schizophrenia. In the clinic, these disorders tend to have poor treatment options, in part because we lack a basic understanding of how the relevant neurocircuitry is modulated in disease states. The Beckstead lab explores the function of dopamine neurons at the cellular, circuit, and systems-level with an eye toward preserving normal dopamine function. Prominent techniques include single-cell electrophysiology (in rodent brain slices and in vivo), operant self-administration paradigms, optogenetics, locomotor behavior, immunohistochemistry, and brain site-specific pharmacology. By combining electrophysiological, behavioral, and other approaches the lab is able to investigate the cellular, synaptic, and circuit bases of neuronal function in the normal and diseased brain.
Dr. Beckstead received his Ph.D. in Pharmacology from Wake Forest University School of Medicine in 2002. He pursued postdoctoral training at the Vollum Institute in Portland, OR where he began to explore the neurophysiological mechanisms underlying motivated behavior. In 2009 he joined the Department of Physiology at the University of Texas Health Science Center at San Antonio, and in 2016 was promoted with tenure. In 2017 he moved his lab to the Oklahoma Medical Research Foundation, where he is currently an Associate Member in the Aging & Metabolism Research Program and the Hille Family Foundation Chair in Neurodegenerative Disease Research.
Publications
- Graduate School
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Neurophysiology
Volume Institute
Portland, OR -
Pharmacology
Wake Forest University
Winston-Salem, NC
- Undergraduate School
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Pharmacy
Ohio Northern University
Ada, OH
- Dopamine
- Brain Aging
- Neurodegeneration
- Drug Abuse
- Neurophysiology
- Progressive parkinsonism due to mitochondrial impairment: lessons from the MitoPark mouse model 2021
- Neurotensin receptor 1 deletion decreases methamphetamine self-administration and the associated reduction in dopamine cell firing 2021
- Female mice are resilient to age-related decline of substantia nigra dopamine neuron firing parameters 2020
- Inducible cell-specific mouse models for paired epigenetic and transcriptomic studies of microglia and astroglia 2020
- A history of ethanol drinking increases locomotor stimulation and blunts enhancement of dendritic dopamine transmission by methamphetamine 2020
- Progressively disrupted somatodendritic morphology in dopamine neurons in a mouse Parkinson's model 2018
- Dopaminergic neurons exhibit an age-dependent decline in electrophysiological parameters in the MitoPark mouse model of Parkinson's disease 2016
- Aging decreases L-type calcium currents and pacemaker firing fidelity in substantia nigra dopamine neurons 2014
- Vesicular dopamine release elicits an inhibitory postsynaptic current in midbrain dopamine neurons 2004