• Anxiety and mood
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• v.1 no.1
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• pp.7-13
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• 2005

Anxiety is one of the basic emotions which human experiences across different cultures in the world and it can be observed in mammals. Our understanding of the neurobiology of this emotion has made some advances, even though it has not been completed, with the development and advance in the investigation method including neuroimaging, neurochemical, and genetic approaches. In this article, the neuroanatomical and neurochemical basis of anxiety is reviewed. The amygdaloid complex has been known to playa key role in processing of anxiety or fear. It has extensive afferent and/or efferent connections with cortical and subcortical structures. The mesial temporal structures including hippocampus appear to be involved in acquisition of anxiety and related behaviors. The prefrontal cortical structures appear to play important roles in conscious awareness of anxiety and in modulating anxiety and related behavior. The bed nucleus of the stria terminalis (BNST) is known to playa critical role in unconditioned fear response. The central noradrenergic system and hypothalamo-pituitary-adrenal axis are known to play important roles in modulating and expressing anxiety-related responses. Anxiety has been gathering attentions from many investigators and numerous preclinical and clinical investigations of anxiety and anxiety disorders have been done. In particular, neural plasticity in critical period and the psychobiological factors related to resilience to extreme stress and anxiety are important issues in this field.

• Korean Journal of Biological Psychiatry
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• v.6 no.1
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• pp.74-80
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• 1999

This study was performed to investigate the mechanism of the clozapine-induced seizures in partially restrained rats by concomitant treatment with drugs affecting monoaminergic systems. Partially restrained rats treated with acute single doses of 10mg/kg clozapine exhibited myoclonic jerks (MJs). Drugs affecting the monoaminergic systems, including 2mg/kg haloperidol, 5mg/kg propranolol, 2mg/kg ritanserin, 20mg/kg fluoxetine, and 20mg/kg imipramine, were concomitantly treated with clozapine to observe the effects of these drugs on the MJs. The drugs were given intraperitoneally either as acute single doses(haloperidol, propranolol, ritanserin, and fluoxetine) or as chronic doses for 21days(haloperidol, imipramine, ritanserin, and fluoxetine). The effects of the concomitant treatment of other drugs on the clozapine-induced MJs were evaluated by comparison of the total numbers of the MJs between the clozapine-treated and concomitantly treated groups. The results were as follows. 1) Concomitant treatment with acute single doses of haloperidol, propranolol, and fluoxetine reduced the total numbers of the clozapine-induced MJs, while concomitant treatment with ritanserin did not. 2) Concomitant treatment with chronic doses of imipramine and ritanserin increased the total numbers of the MJs, while concomitant treatment with fluoxetine reduced them. Concomitant chronic treatment with haloperidol did not affect the numbers of the MJs. These results suggest that dopamine and serotonin, not noradrenalin may be involved in the clozapine-induced MJs in partially restrained rats. Future research needs to study the function of each subtype of monoaminergic receptors on the mechanism of the clozapine-induced seizure.