Prolactin-derived vasoinhibins increase anxiety- and depression-related behaviors.

摘要: Summary The hormone prolactin (PRL) regulates neuroendocrine and emotional stress responses. It is found in the hypothalamus, where protein partially cleaved to vasoinhibins, a family of N-terminal antiangiogenic PRL fragments ranging from 14 18 kDa molecular masses, with unknown effects on response. Here, we show that intracerebroventricular administration recombinant vasoinhibin, containing first 123 amino acids human correspond 14 kDa PRL, exerts anxiogenic depressive-like detected elevated plus-maze, open field, forced swimming tests. To investigate whether stressor exposure affects generation vasoinhibins concentrations mRNA, were evaluated hypothalamic extracts virgin female rats immobilized for 30 min at different time points after onset. levels mRNA higher 60 min but declined 360 min seen non-stressed animals. elevation did not correlate stress-induced increase circulating levels, nor was it modified by blocking adenohypophyseal secretion bromocriptine. A vasoinhibin having an electrophoretic migration rate corresponding 17 kDa hypothalamus. Despite this similar stressed rats. Stress reduced cleavage as shown incubation These results suggest are potent depressive factors increases hypothalamus partly reducing its conversion vasoinhibins. reciprocal interplay between may represent effective mechanism regulate anxiety depression.