Neural Information Laboratory -
Alan Dorval, Ph.D.

Lab Contact Information

Sorenson Molecular Biotechnology Building (SMBB), 4th Floor
36 South Wasatch Drive
Salt Lake City, UT  84112
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Phone:
801.587.3868 (lab)
801.587.7631 (office)

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Goal: To apply what we learn about how brain processing differs between healthy individuals and those with Parkinson's disease (PD) toward devising new approaches for alleviating symptoms of PD and other neurological disorders.

Dorval Lab

We use electrophysiological recordings, computational neuroscience and neuronal information theory to decipher the symbols used by brain cells to process information, interpret the world, retain and retrieve memories, and command coordinated muscle activity. Through these techniques and clinical research, we learn how diseases and disorders of the nervous system impair the generation, storage, transmission, and interpretation of those physiologically meaningful symbols. With this knowledge, we aim to improve existing neuromodulatory therapies and devise novel neural engineering interventions to enhance the quality of life in patients with neurological disorders.

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Dedicated equipment to accelerate neural processing research

Six interdisciplinary research groups that focus on neural information processing - Dorval, Rabbitt, Taha, Wachowiak, White, and Wilcox Labs - received matching funds from the U of U to purchase an integrated system for optical and electrophysiological studies in vivo. “These diverse, systems neuroscience groups will utilize the shared equipment to develop new techniques, tools, and software for intracellular recordings, optical stimulation, and intracellular recordings,” explains John White, Ph.D., Director, Neuronal Dynamics Laboratory. READ MORE

Deep brain stimulation alleviates parkinsonian bradykinesia by regularizing pallidal activity

Deep brain stimulation (DBS) can alleviate the motor symptoms of Parkinson's disease, although the therapeutic mechanisms are unclear. Here, Dorval demonstrates that DBS relieves symptoms by minimizing pathologically disordered neuronal activity in the basal ganglia. READ THE PAPER

 
Last Updated: 6/5/14