Innovation

Chloride-dependent steroid effects at alpha4-beta2-delta GABA-A receptors increase anxiety

The Research Foundation of the State University of New York
posted on 07/16/2009

A stress responsive mechanism for anxiety behavior using the GABA-A receptor molecule which leads to excitability in the central nervous system.

Advantages

The technology defines a mechanism for the anxiety response to stress that is specific for a stress hormone, but would not produce sedation, as do current therapies.

Innovation Details
 

Detailed Description

The onset of puberty is associated with increases in emotional reactivity and anxiety. Responses to stressful events are amplified, and anxiety and panic disorder first emerge at this time. Few studies have addressed the biological basis of this important issue, although suicide rise increases in adolescence, despite the use of adult-based medical strategies. A brain molecule known as the GABAA receptor plays a pivotal role in the generation of anxiety. This receptor is the target for endogenous steroids such as THP, which increase GABA-gated currents at physiological concentration of the steroid. This is a mechanism for anxiety behavior, especially in response to stress. Our researchers have identified the site on a brain molecule (the GABA-A receptor) which leads to excitability in the central nervous system. This technology could then be used to devise strategies to reduce the anxiety response to stress. This discovery has special relevance for fluctuations in naturally occurring steroids, including puberty, premenstrual syndrome, menopause and post-partum periods, as well as chronic stress.

File Number: R1609-100 

Disease: Central Nervous System

Other Information: Principal Investigator: Sheryl S. Smith


IP Protection

Patent Number(s): 60/906,165

License Online

This innovation currently is not available for online licensing. Please contact Dr. Yalcintas at The Research Foundation of the State University of New York for more information.

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February 11, 2009

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