Transient suppression of resting corticosterone levels induces sustained increase of AVP stores in hypothalamic CRH-neurons of rats.

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.