Anxiety and Brain Noradrenaline System(Bases and Clinical Practice of Anxiety and Depression)

Tanaka masatoshi

doi:10.15064/jjpm.37.3_231

We examined the role of rat brain noradrenaline (NA) system in the provocation of anxiety by measuring levels of 3-methoxy-4-hydroxyphenylethyleneglycol sulfate (MHPG-S0_<4>) , the major metabolite of noradrenaline (NA) , and NA Ievels in the perfusates obtained by intracerebral microdialysis. Diazepam, an anxiolytic drug of benzodiazepines (BDZs) , significantly reduced both increases in NA release caused by immobilization stress in the hypothalamus, amygdala and locus coeruleus (LC)region and emotional responses exposed to stress. These changes were reversed by flumazenil, an antagonist of BDZs, which suggested that the actions of diazepam were mediated via BDZ receptors. Stresses, wherein the emotional factor was predominantly involved, caused increases in NA release in these brain regions and these increases were also attenuated by diazepam in a flumazenil reversible manner. Yohimbine, which caused significant increases in NA release in these regions, enhanced anxiety-related behavior in the animals and β-carboline 3-carboxylate ethyl ester, an anxiogenic drug, caused increases in NA release in these regions. From these findings, it is suggested that increases in NA release in the hypothalamus, amygdala and LC are, in part, involved in the provocation of anxiety and/or fear.

Anxiety and Brain Noradrenaline System(Bases and Clinical Practice of Anxiety and Depression)

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