摘要: Anxiety/fear is a normal reaction to threatening situations and it represents physiologically protective function. often manifested as avoidance also characterized by overt sympathetic reactions. Pathological anxiety level of that disproportionate the threat can be even in absence threat. In clinical practice, categorical systems set boundary at which particular becomes an disorder. Although genetic contribution disorders has long been suspected, only recently polymorphisms various neurotransmitter neuromodulatory have linked disorders. Still, these factors relatively small overall disease phenotype complex interaction between environment will ultimately explain development susceptibility anxiety. Genetic biochemical studies, combined with analysis mouse strains induced mutations implicate multiple neurobiological processes Although association neurotransmitters their receptors anxiety-like behavior not surprising, cytokines cell adhesion molecules were identified modulators anxiety. Furthermore, intracellular signaling pathways target genes allowing assembly specific “anxiety” pathways. It apparent anxiety-related involve communication neurons that, via pathways, eventually converge onto regulation transcription and/or translation. The proper function especially crucial during early postnatal one hypothesize abnormalities any lead to, altered gene expression, changes neuronal morphology Importantly, all commonly used anxiolytic drugs integrated into this model implying modulate molecular cellular establish control anxiety. Keywords: anxiety; fear; anxiety disorders; neurotransmitters; receptors; signaling pathways; neuronal circuits; knockout mice; association studies