Diversity and Functions of GABA Receptors: A Tribute to - download pdf or read online

By Uwe Rudolph

This new quantity of Advances in Pharmacology provides the variety and features of GABA Receptors. the quantity seems at study played some time past twenty years which has printed particular physiological and pharmacological services of person GABAA receptor subtypes, delivering novel possibilities for drug development.

  • Contributions from the easiest authors within the field
  • An crucial source for pharmacologists, immunologists, and biochemists

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Additional resources for Diversity and Functions of GABA Receptors: A Tribute to Hanns Möhler, Part A

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Current Opinion in Neurobiology, 20, 262–270. Remick, R. , Keller, F. , Buchanan, R. , Gibson, R. , & Fleming, J. A. (1988). A comparison of the efficacy and safety of alprazolam and desipramine in depressed outpatients. Canadian Journal of Psychiatry, 33, 590–594. Ressler, K. , & Mayberg, H. S. (2007). Targeting abnormal neural circuits in mood and anxiety disorders: From the laboratory to the clinic. Nature Neuroscience, 10, 1116–1121. Richards, J. , & M€ ohler, H. (1987). Resolving GABA/ benzodiazepine receptors: Cellular and subcellular localization in the CNS with monoclonal antibodies.

Neurochemical Research, 15, 199–207. , & Okada, T. (1977a). GABA receptor binding with 3H(+) bicucullinemethiodide in rat CNS. Nature, 267, 65–67. , & Okada, T. (1977b). Demonstration of benzodiazepine receptors in the central nervous system. Science, 198, 849–851. , & Okada, T. (1978). The benzodiazepine receptor in normal and pathological human brain. British Journal of Psychiatry, 133, 261–268. , & Richards, J. G. (1981). Agonist and antagonist benzodiazepine receptor interaction in vitro. Nature, 294, 763–765.

The effectiveness of the extremely low benzodiazepine dose may be due to two factors: the degree of pharmacological inhibition required for rebalancing may be small, as shown in the Rett mouse model (a 30–40% reduction in GABA release is sufficient to induce Rett-like symptoms), or a pathological deficit of GABA neurons may trigger a compensatory upregulation of GABAA receptors, increasing the sensitivity of the system to benzodiazepines. 6. Role of GABAA receptor subtypes It is reassuring that α1 GABAA receptors, which are associated with sedative actions of these drugs, do not appear to be required for reversing the social interaction deficit, as shown by the effectiveness of L-838417, an α2,α3,α5 partial agonist, in the BTBR model.

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