Estrogen regulation of brain vasotocin secretion in the catfish Heteropneustes fossilis: An interaction with catecholaminergic system

Vasotocin (VT) is a basic neurohypophysial nonapeptide in non-mammalian vertebrates and is involved in diverse functions like osmoregulation, reproduction, metabolism and behavior. In this study, we report that estradiol-17 beta (E-2) regulates brain and plasma VT secretion through the involvement of the catechol-aminergic (CA) system. To demonstrate this, E-2 level was altered through ovariectomy (OVX, 3 weeks) and replacement study with low and high E-2 doses (0.1 and 0.5 mu g/g body weight). CA activity was inhibited by treatment with alpha-methylparatyrosine (alpha-MPT; 250 mu g/g body weight), a competitive inhibitor of tyrosine hydroxylase. VT was assayed by an enzyme immunoassay method. In the sham group, the low E-2 dose produced 82% and 104% increase, respectively, in brain and plasma VT levels. The high E-2 dose decreased the VT levels significantly. The low E-2 dose decreased brain E-2 but elevated plasma E-2. In the high E-2 group, the E-2 level increased further in both brain and plasma. OVX resulted in a significant inhibition (69% and 25%, respectively) of both brain and plasma VT, which was correlated with low E-2 levels. The low E-2 dose not only reversed the inhibition, but increased the VT level in both brain and plasma in comparison to the sham groups. The high E-2 replacement inhibited VT levels further low in both brain and plasma. The alpha-MPT treatment inhibited VT levels significantly in both sham and OVX groups. The drug treatment abolished partially the restorative effect of the low E-2 dose in the ovariectomized fish. In the high E-2 dose group, alpha-MPT decreased brain and plasma VT levels further low compared to the sham + 0.5 mu g E-2 group or OVX + 0.5 mu g E-2 group except the brain VT level, which increased in the OVX + 0.5 mu g E-2 group. It is inferred that E-2 may exert biphasic effects on VT through the mediation of the CA system. (C) 2011 Elsevier Inc. All rights reserved.