title: Transient suppression of resting corticosterone levels induces sustained increase of AVP stores in hypothalamic CRH-neurons of rats.
abstract: Previous studies showed that various stressors can induce delayed (days) and long-lasting (weeks) increases of vasopressin (AVP) stores in terminals of CRH neurons in the external zone of the median eminence (ZEME) in adult rats. Here we tested whether this long-lasting neuroplastic change can be induced by mechanisms other than stressor provoked transsynaptic activation of CRH neurons. Single i.v. administration of a CRH antibody to adult rats causes a delayed (at least 1 day) and long-lasting (3 weeks) increase (2-3 fold) of AVP stores in the ZEME without affecting CRH stores. It suppresses ether-induced ACTH-responses for at least 8 days. In contrast, resting pm levels of ACTH and corticosterone (CORT) were suppressed only during the first 2 days. Suppletion of CORT levels on day 1 and 2, attenuates the antibody induced AVP-increase by 57%. CRH-immunoneutralization did not affect the AVP stores in CORT supplemented ADX rats. Thus, long-term increases of AVP stores induced by CRH-immunoneutralization largely depend on short-term suppression of pm CORT levels. Accordingly, single administration of metyrapone, which causes a transient suppression of pm CORT levels, increases AVP (1.5 fold) but not CRH stores one week later. We conclude that transient activation of hypothalamic CRH neurons results in long-lasting increases in AVP co-expression irrespective of the nature of the activating stimulus.
authors.affiliation: Graduate School Neurosciences Amsterdam, Research Institute Neurosciences Vrije Universiteit, Faculty of Medicine, Department of Pharmacology, The Netherlands.
authors.forename: E D
authors.initials: ED
authors.lastname: Schmidt
authors.forename: A W
authors.initials: AW
authors.lastname: Janszen
authors.forename: R
authors.initials: R
authors.lastname: Binnekade
authors.forename: F J
authors.initials: FJ
authors.lastname: Tilders
mesh_terms: D000315:Adrenalectomy; D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D001127:Arginine Vasopressin / Q000032:analysis / Q000378:metabolism*; D003345:Corticosterone / Q000097:blood* / Q000494:pharmacology; D003346:Corticotropin-Releasing Hormone / Q000032:analysis / Q000276:immunology / Q000502:physiology*; D004986:Ether; D007031:Hypothalamus / Q000166:cytology*; D007116:Immunization, Passive; D008297:Male; D008473:Median Eminence / Q000737:chemistry; D008797:Metyrapone / Q000494:pharmacology; D009474:Neurons / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D013312:Stress, Physiological / Q000097:blood / Q000139:chemically induced
chemical_list: D004986:Ether; D001127:Arginine Vasopressin; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; D003345:Corticosterone; D008797:Metyrapone