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Are Glutamatergic Pathways Involved in the Pathophysiology of Anxiety?

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New Concepts in Anxiety

Abstract

During the last two decades, several neurotransmitter systems have been implicated in the pathophysiology of anxiety. The evidence implicating these systems assumes that an understanding of the molecular events resulting in an anxiolytic action will lead to an understanding of anxiety. While pharmacological studies have demonstrated that both anxiolytic and anxiogenic effects can be obtained with agents acting through a variety of neurotransmitter receptors (see Dorow and Duka, 1986, for review), the physiological mechanisms responsible for anxiety remain uncertain. None the less, these pharmacological studies indicate that anxiety (like other neuropsychiatric disorders) is not mediated by a single neurotransmitter system, suggesting that disruption of a homeostatic balance among neurochemical systems may result in the development and expression of anxiety. Our laboratory is investigating the mechanisms involved in the maintenance of homeostatic balance among neurotransmitter systems in limbic areas, with the hypothesis that agents which selectively modulate this balance may exhibit specific anxiolytic properties. One of the mechanisms that may be involved in maintaining this homeostatic balance is the interaction between fast-acting, ligand-gated ion channels mediating excitatory and inhibitory transmission.

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Trullas, R., Winslow, J.T., Insel, T.R., Skolnick, P. (1991). Are Glutamatergic Pathways Involved in the Pathophysiology of Anxiety?. In: Briley, M., File, S.E. (eds) New Concepts in Anxiety. Palgrave, London. https://doi.org/10.1007/978-1-349-11847-2_30

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  • DOI: https://doi.org/10.1007/978-1-349-11847-2_30

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