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Stathmin , a gene regulating neural plasticity, affects fear and anxiety processing in humans
Author(s) -
Brocke Burkhard,
Lesch KlausPeter,
Armbruster Diana,
Moser Dirk A.,
Müller Anett,
Strobel Alexander,
Kirschbaum Clemens
Publication year - 2010
Publication title -
american journal of medical genetics part b: neuropsychiatric genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.393
H-Index - 126
eISSN - 1552-485X
pISSN - 1552-4841
DOI - 10.1002/ajmg.b.30989
Subject(s) - amygdala , stathmin , anxiety , psychology , neuroscience , fear conditioning , long term potentiation , startle response , neuroplasticity , fear potentiated startle , biology , genetics , gene , psychiatry , receptor
Abstract The identification of biological mechanisms underlying emotional behavior is crucial for our understanding of the pathogenesis of mental disorders. Besides genes modulating neural transmission and influencing amygdala reactivity and anxiety‐related temperamental traits a different plasticity regulating genes affect interindividual differences in emotional regulation. Recently it has been demonstrated that stathmin , a regulator of microtubule formation which affects long‐term potentiation (LTP), controls learned and innate fear responses in rodents, but its role in human emotion regulation is unknown. We hypothesized that in humans the gene coding for stathmin ( STMN1 ), which is highly expressed in the lateral nucleus of the amygdala and associated thalamic and cortical structures, influences behavioral responses to fear and anxiety stimuli by way of two common single nucleotide polymorphisms (rs182455, SNP1; rs213641, SNP2). These polymorphisms are located within or close to the putative transcriptional control region. We used the acoustic startle paradigm and a standardized laboratory protocol for the induction of fear and psychosocial stress in 106 healthy volunteers to investigate the impact of stathmin gene variation on two fear‐ and anxiety‐controlling effector‐systems of the amygdala. We found that STMN1 genotype interacting with individuals' gender significantly impacts fear and anxiety responses as measured with the startle and cortisol stress response. We therefore conclude that STMN1 genotype has functional relevance for the acquisition and expression of basic fear and anxiety responses also in humans. © 2009 Wiley‐Liss, Inc.