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The Role of the Amygdala Gaba Receptors and Benzodiazepines in Anxiety

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The Role of the Amygdala Gaba Receptors and Benzodiazepines in Anxiety
Abstract Discussed is some of the research that has been conducted on the role of the amygdala in anxiety, as well as the role of GABA and benzodiazepines in anxiety. Research has indicated through amygdala lesions and stimulation that the amygdala does indeed play a major role in the expression of anxiety. Research has also indicated, through drug infusions to the amygdala, that benzodiazepines cause anxiolysis (by increasing GABA transmission), and that benzodiazepine antagonists increase anxiety (by decreasing GABA transmission). Also discussed are some limitations and problems found with benzodiazepine use.

On the Role of the Amygdala in Anxiety and How Treatment is Effective The functional anatomy of anxiety involves amygdala-based neurocircuits with critical reciprocal connections to the medial prefrontal cortex (i.e. Mailizia, 1999). An understanding of the functional anatomy of anxiety allows for a new perspective on the various anxiety disorders. The neurotransmitters involved in these circuits are reviewed for their relevance to the pharmacologic choices in the treatment of anxiety (i.e. Kang, Wilson & Wilson, 2000). Much research has been conducted on gamma-aminobutyric acid (GABA) as it is the major inhibitory neurotransmitter in the mammalian Central Nervous System (CNS) (i.e. Vekovischeva, Haapalinna & Sarviharju, 1999). GABA participates in the regulation of neuronal excitability through specific membrane proteins (the GABAA receptors). The binding of GABA to these postsynaptic receptor results in an opening of chloride channel integrated in the receptor, which allows the entry of Cl-. As a consequence, this leads to the hyperpolarization of the recipient cell, which is allosterically modulated by a wide variety of chemical entities that interact with distinct binding sites at the GABAA receptor complex. One of the most thoroughly investigated modulatory sites is the benzodiazepine-binding site. The purpose of this paper is to



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