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Faculty
Nigel Atkinson
Professor in Neurobiology

Email: nigela@mail.utexas.edu
Website
Main Office: PAT 228
Phone: 232-3404

Alternate Office: PAT 230
Alt. Phone: (512) 471-1629

Mailing Address
The University of Texas at Austin
Neurobiology, Section of
1 University Station C0920
Austin ,TX 78712-0248
Nigel Atkinson

Research Summary

The fundamental question that drives us is: How are ion channel genes regulated and what are the consequences of this regulation? To address this question we have been using the slowpoke gene of Drosophila as a model. The slowpoke gene encodes the BK-type Ca2+-activated K+ channel. In insects and mammals these channels are used in both nervous tissue and muscle. In humans this channel plays a central role in controlling blood pressure. Our work shows that slowpoke is homeostatically regulated. Treatments that reduce neural excitability enhance slowpoke expression while treatments that increase activity reduce slowpoke expression. Both of these changes are postulated to shift the nervous system back towards a more normal level of excitability. In this vein, we have developed a Drosophila model of tolerance to drugs of abuse. In this model, flies sedated one time with either ethanol or an organic solvent acquire tolerance to solvent sedation. Tolerance is reduced drug response responsiveness caused by prior drug exposure and is a factor that leads one to addiction. We have shown that sedation also induces slowpoke expression and that slowpoke is absolutely required for the production of behavioral tolerance. Electrophysiological assays show that increased slowpoke enhances neural excitability in a manner postulated to resist sedation and to produce tolerance. At this time, we are identifying the transcriptional mechanisms that slowpoke uses to monitor and respond to state of neural activity. We have observed that drug sedation causes changes in chromatin remodeling and how that these changes leads to increased channel expression.