Differential sensitivity to stress in rats of OFA hr/hr strain, compared with Wistar and Sprague Dawley strains, may contribute to their lactation failure

VALDEZ, SUSANA; BONAFEDE, MELISA; CARREÑO, NORMA; DEIS, RICARDO; JAHN, GRACIELA

STRESS

TAYLOR & FRANCIS LTD

Año: 2011

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, measured by radioimmunoassay) responses to stress (room change and 2 min. ether, n=8-10, bled by venipuncture during the ether exposure and 5 min after ) with those of Wistar and Sprague Dawley (SD) rats during the cycle, pregnancy, lactation, after ovariectomy and ovarian steroid hormone impregnation and on suckling response. We also studied the hypothalamic expression of prolactin (PRLRlong), progesterone (PR) and estrogen (ER) 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. Estrogen impregnantion (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 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.