Abstract
Anxiety stems from and perpetuates dysregulation of neurobiological systems, but the exact mechanisms of anxiety disorders are still only partially understood. Gamma-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter known to counterbalance the action of the excitatory neurotransmitter glutamate. Several pharmacologic agents target the GABA system and modulate the overall effect of GABA. This article highlights multiple neurobiological interactions that play a role in anxiety and reviews selected studies of plasma neurosteroid levels, plasma GABA levels, and benzodiazepine binding site sensitivity and density in patients with anxiety disorders. The article concludes with further support for the role of the GABA system in anxiety by summarizing the current evidence supporting the use of novel GABAergic agents including tiagabine in the treatment of anxiety disorders.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Acetates / pharmacology
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Acetates / therapeutic use
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Amines*
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Anxiety Disorders / blood
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Anxiety Disorders / drug therapy
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Anxiety Disorders / physiopathology*
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Benzodiazepines / pharmacology
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Benzodiazepines / therapeutic use
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Cyclohexanecarboxylic Acids*
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GABA Agents / pharmacology
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GABA Agents / therapeutic use
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Gabapentin
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Glutamic Acid / physiology
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Humans
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Nipecotic Acids / pharmacology
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Nipecotic Acids / therapeutic use
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Receptors, GABA-A / drug effects
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Receptors, GABA-A / metabolism
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Receptors, GABA-A / physiology
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Synaptic Transmission / drug effects
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Synaptic Transmission / physiology
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Tiagabine
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gamma-Aminobutyric Acid / blood
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gamma-Aminobutyric Acid / physiology*
Substances
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Acetates
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Amines
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Cyclohexanecarboxylic Acids
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GABA Agents
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Nipecotic Acids
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Receptors, GABA-A
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Benzodiazepines
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Glutamic Acid
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gamma-Aminobutyric Acid
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Gabapentin
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Tiagabine