title: Vasopressin administration into the paraventricular nucleus normalizes plasma oxytocin and corticosterone levels in Brattleboro rats.
abstract: Adult male rats of the Brattleboro strain were used to investigate the impact of the congenital absence of vasopressin on plasma adrenocorticotropin, corticosterone, and oxytocin concentrations as well as the release pattern of oxytocin within the hypothalamic paraventricular nucleus (PVN), in response to a 10-min forced swimming session. Measurement of adrenocorticotropin in plasma samples collected via chronically implanted jugular venous catheters revealed virtually identical stress responses for vasopressin-lacking Brattleboro (KO) and intact control animals. In contrast, plasma corticosterone and oxytocin levels were found to be significantly elevated 105 min after onset of the stressor in KO animals only. Microdialysis samples collected from the extracellular fluid of the PVN showed significantly higher levels of oxytocin both under basal conditions and in response to stressor exposure in KO vs. intact control animals accompanied by elevated oxytocin mRNA levels in the PVN of KO rats. These findings suggest that the increased oxytocin levels in the PVN caused by the congenital absence of vasopressin may contribute to normal adrenocorticotropin stress responses in KO animals. However, whereas the stressor-induced elevation of plasma oxytocin in KO rats may be responsible for their maintained corticosterone levels, oxytocin seems unable to fully compensate for the lack of vasopressin. This hypothesis was tested by retrodialyzing synthetic vasopressin into the PVN area concomitantly with blood sampling in KO animals. Indeed, this treatment normalized plasma oxytocin and corticosterone levels 105 min after forced swimming. Thus, endogenous vasopressin released within the PVN is likely to act as a paracrine signal to facilitate the return of plasma oxytocin and corticosterone to basal levels after acute stressor exposure.
authors.affiliation: Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary.
authors.forename: Dóra
authors.initials: D
authors.lastname: Zelena
authors.forename: Kristina
authors.initials: K
authors.lastname: Langnaese
authors.forename: Agnes
authors.initials: A
authors.lastname: Domokos
authors.forename: Ottó
authors.initials: O
authors.lastname: Pintér
authors.forename: Rainer
authors.initials: R
authors.lastname: Landgraf
authors.forename: Gábor B
authors.initials: GB
authors.lastname: Makara
authors.forename: Mario
authors.initials: M
authors.lastname: Engelmann
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D001127:Arginine Vasopressin / Q000008:administration & dosage / Q000378:metabolism / Q000494:pharmacology*; D003345:Corticosterone / Q000097:blood*; D007262:Infusions, Intravenous; D008297:Male; D023421:Models, Animal; D010121:Oxytocin / Q000097:blood*; D010286:Paraventricular Hypothalamic Nucleus / Q000187:drug effects* / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D011910:Rats, Brattleboro; D015398:Signal Transduction / Q000502:physiology; D013312:Stress, Physiological / Q000502:physiology; D014662:Vasoconstrictor Agents / Q000008:administration & dosage / Q000494:pharmacology*
chemical_list: D012333:RNA, Messenger; D014662:Vasoconstrictor Agents; D001127:Arginine Vasopressin; D010121:Oxytocin; D000324:Adrenocorticotropic Hormone; D003345:Corticosterone