title: Reorganization of synaptic inputs to the hypothalamic paraventricular nucleus during chronic psychogenic stress in rats.
abstract: BACKGROUND
  Chronic stress in humans precipitates hyper-reactivity of the hypothalamic-pituitary-adrenocortical (HPA) axis and triggers symptoms associated with certain forms of depression. Reorganization of neuronal networks has been implicated in development of depression, however it remained unknown how chronic exposure to psychogenic challenges affects excitatory and inhibitory inputs to corticotropin-releasing hormone (CRH) neurons in the hypothalamic paraventricular nucleus that govern neuroendocrine stress response.
  
  
  METHODS
  Rats (n = 32) were exposed for 21 days to chronic variable stress and their behavioral (sucrose preference) and hormonal (corticosterone) responses were followed together with electron microscopic stereologic analysis of excitatory and gamma-aminobutyric acid (GABA)-containing, inhibitory synapses on the CRH synthesizing neurons.
  
  
  RESULTS
  Chronic stress in rats resulted in weight loss, anhedonia, and hyperactivity of hypothalamic-pituitary-adrenocortical axis. Following 3 weeks' exposure to variable psychologic stressors the number of synapses has been doubled in the paraventricular nucleus. Asymmetrical excitatory as well as GABAergic inhibitory synaptic contacts were increased on CRH neurons; however, the excitatory/inhibitory input ratio remained constant. In response to chronic stress, we found rearrangement of inhibitory GABA-containing inputs with the increase of contacts on dendrites and decrease at the soma region of CRH neurons.
  
  
  CONCLUSIONS
  Significant remodeling of synaptic contacts was found on CRH neurons in response to chronic stress. This morphologic plasticity might be related to the hyperactivity of the HPA axis and to development of stress-related psychopathologies such as depression.
authors.affiliation: Laboratory of Molecular Neuroendocrinology, Institute of Experimental Medicine, Szigony u. 43, Budapest, Hungary.
authors.forename: Ildikó H
authors.initials: IH
authors.lastname: Miklós
authors.forename: Krisztina J
authors.initials: KJ
authors.lastname: Kovács
mesh_terms: D000818:Animals; D001526:Behavioral Symptoms / Q000378:metabolism / Q000503:physiopathology; D002908:Chronic Disease; D003345:Corticosterone / Q000378:metabolism*; D003346:Corticotropin-Releasing Hormone / Q000378:metabolism; D003863:Depression / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D023421:Models, Animal; D009434:Neural Pathways / Q000378:metabolism / Q000503:physiopathology; D010286:Paraventricular Hypothalamic Nucleus / Q000378:metabolism / Q000503:physiopathology; D010913:Pituitary-Adrenal System / Q000378:metabolism / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D013312:Stress, Physiological; D013315:Stress, Psychological / Q000150:complications / Q000378:metabolism / Q000503:physiopathology; D009435:Synaptic Transmission; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
chemical_list: D005680:gamma-Aminobutyric Acid; D003346:Corticotropin-Releasing Hormone; D003345:Corticosterone