title: Glucocorticoid Induces Incoordination between Glutamatergic and GABAergic Neurons in the Amygdala.
abstract: BACKGROUND
  Stressful life leads to mood disorders. Chronic mild stress is presumably major etiology for depression, and acute severe stress leads to anxiety. These stressful situations may impair hypothalamus-pituitary-adrenal axis and in turn induce synapse dysfunction. However, it remains elusive how the stress hormones mess up subcellular compartments and interactions between excitatory and inhibitory neurons, which we have investigated in mouse amygdala, a structure related to emotional states.
  
  
  RESULTS
  Dexamethasone was chronically given by intraperitoneal injection once a day for one week or was acutely washed into the brain slices. The neuronal spikes and synaptic transmission were recorded by whole-cell patching in amygdala neurons of brain slices. The chronic or acute administration of dexamethasone downregulates glutamate release as well as upregulates GABA release and GABAergic neuron spiking. The chronic administration of dexamethasone also enhances the responsiveness of GABA receptors.
  
  
  CONCLUSIONS
  The upregulation of GABAergic neurons and the downregulation of glutamatergic neurons by glucocorticoid impair their balance in the amygdala, which leads to emotional disorders during stress.
authors.affiliation: Qingdao University, School of Pharmacy, 38 Dengzhou, Shandong, China.
authors.forename: Guang-Yan
authors.initials: GY
authors.lastname: Wang
authors.affiliation: Qingdao University, School of Pharmacy, 38 Dengzhou, Shandong, China.
authors.forename: Zhao-Ming
authors.initials: ZM
authors.lastname: Zhu
authors.affiliation: State Key Lab of Brain and Cognitive Science, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
authors.forename: Shan
authors.initials: S
authors.lastname: Cui
authors.affiliation: Qingdao University, School of Pharmacy, 38 Dengzhou, Shandong, China.|State Key Lab of Brain and Cognitive Science, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.|University of Chinese Academy of Sciences, Beijing, China.
authors.forename: Jin-Hui
authors.initials: JH
authors.lastname: Wang
mesh_terms: D000679:Amygdala / Q000166:cytology* / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D003907:Dexamethasone / Q000494:pharmacology; D059330:GABAergic Neurons / Q000187:drug effects* / Q000502:physiology*; D005938:Glucocorticoids / Q000494:pharmacology*; D018698:Glutamic Acid / Q000378:metabolism*; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D009474:Neurons / Q000187:drug effects* / Q000502:physiology*; D018079:Receptors, GABA / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D005938:Glucocorticoids; D018079:Receptors, GABA; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D003907:Dexamethasone