Biochemistry of anxiety.
The identification of a biochemical (cellular, molecular) basis of anxiety has not only a heuristic value but also considerable consequences for any kind of prophylaxis and therapy of anxiety. An abnormally high activity of noradrenergic and/or serotoninergic neuronal pathways, all originating in the lower brainstem has been proposed by various authors to be critical for the activation of neuronal networks generating anxiety. Recent progress in the understanding of the mechanism of action of anxiolytic drugs and of a variety of anxiogenic agents suggests the possibility that an abnormal neuronal activity of the nonconvulsive type in the limbic system generates the emotion of anxiety and the accompanying behavioral, autonomic and motor symptoms. A central role is suggested for gamma-aminobutyric acid (GABA), which normally prevents those types of neurones possessing the inherent properties for paroxysmal activity to respond with epileptiform activity to normal or excessive stimuli. The GABA receptor/chloride channel complex with its regulatory sites may be the site of a primary biochemical functional lesion.
Haefely
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D001007:Anxiety / Q000503:physiopathology*; D004827:Epilepsy / Q000503:physiopathology; D006801:Humans; D008125:Locus Coeruleus / Q000503:physiopathology; D009474:Neurons / Q000502:physiology; D009638:Norepinephrine / Q000502:physiology; D011963:Receptors, GABA-A / Q000502:physiology; D012701:Serotonin / Q000502:physiology
D011963:Receptors, GABA-A; D012701:Serotonin; D009638:Norepinephrine