Lactation deficit in OFA hr/hr rats may be caused by differential sensitivity to stress compared with Wistar and Sprague Dawley rats

VALDEZ SR; BONAFEDE MM; CARREÑO NB; DEIS RP; JAHN GA

STRESS

TAYLOR & FRANCIS LTD

Lugar: Amsterdam; Año: 2012 vol. 15 p. 361 - 377

1025-3890

OFA hr/hr (OFA) rats present lactation deficit. To explore whether abnormal stress responsiveness causes this deficit, we compared their hormonal (prolactin, progesterone and corticosterone) responses to stress (room change and 2 min. ether) with those of Wistar and Sprague Dawley (SD) rats during the cycle, pregnancy, lactation, after ovariectomy and ovarian steroid hormone priming and on suckling response. We also studied the hypothalamic expression of prolactin (PRLRlong) and the isoforms of progesterone (PR A and B) and estrogen (ERα and β) receptors in late pregnancy and the capacity of anxiolytic (diazepam) administration to improve lactation. Ether exposure increased circulating hormones in the three strains on cycling and ovariectomized rats, but was less effective in pregnancy and lactation. Elevated estrogen (estrus and estradiol-treated ovariectomized rats) potentiated prolactin response more in SD and OFA than in Wistar rats. Elevated progesterone (late pregnancy, lactation, ovariectomized-progesterone-treated rats) inhibited the response less in OFA than in SD or Wistar rats. Ether exposure inhibited the suckling response only in OFA rats. Diazepam treatment increased pup survival rate and suckling response. Hypothalamic total PR mRNA content, assayed by RT-PCR, was higher in pregnant OFA rats compared with SD and Wistar, but PRB/PRA protein ratio, determined by Western blot was low in Wistar rats, intermediate in OFA and highest in SD rats. The heightened sensitivity to stress of lactating OFA rats may contribute to their lactational deficit and be caused by a combination of hypoprolactinemia and reduced inhibitory capacity of progesterone.