Neurobiological mechanisms in human anxiety. Evidence supporting central noradrenergic hyperactivity.
Preclinical studies in laboratory rodents and non-human primates have led to the hypothesis that noradrenergic hyperactivity is associated with some human anxiety states. This hypothesis has recently received support from a variety of clinical investigations. Drugs which increase noradrenergic function induce anxiety in human subjects. Increased turnover of norepinephrine has been shown to occur with naturally occurring anxiety conditions. The mechanism of action clonidine and tricyclic antidepressants as antianxiety agents may be due to their ability to reduce central noradrenergic function. Future studies will need to evaluate, in addition to central noradrenergic function, other neuronal systems in brain involving endogenous opioids, benzodiazepine receptors, purines and gamma-aminobutyric acid in human anxiety disorders.
D000818:Animals; D014151:Anti-Anxiety Agents / Q000494:pharmacology; D001007:Anxiety / Q000209:etiology* / Q000503:physiopathology; D001921:Brain / Q000503:physiopathology*; D006801:Humans; D008125:Locus Coeruleus / Q000503:physiopathology; D008734:Methoxyhydroxyphenylglycol / Q000378:metabolism; D009638:Norepinephrine / Q000502:physiology*; D051381:Rats; D013375:Substance Withdrawal Syndrome / Q000503:physiopathology
D014151:Anti-Anxiety Agents; D008734:Methoxyhydroxyphenylglycol; D009638:Norepinephrine