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.
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.
Disease: Central Nervous System