Nitric oxide has a role in attenuating the neuroendocrine response to anaphylactoid stress during lactation

Stress increases nitric oxide (NO) production in the paraventricular nucleus of the hypothalamus (PVH). Lactation diminishes the response to stress and increases basal NO production markers in the PVH of the dam. This study investigated whether lactation modified the anaphylactic reaction to egg white (EW) injection, and if nitric oxide regulates the neuroendocrine response to this stressor. The activational response of PVH to EW was assessed by c-Fos immunohistochemistry, and NO production was determined by histological staining of NADPH-diaphorase and neuronal nitric oxide synthase (nNOS) and by measuring the concentration of total nitrates and nitrites (NOx) in the hypothalamus of lactating and diestrus rats. EW injection significantly increased the number of Fos-positive neurons in the parvocellular subdivision of the PVH in diestrus, but not in lactating rats. Similarly, EW injection increased the number of NADPH-diaphorase- and nNOS-positive cells in the PVH of diestrus rats, but it did not alter the already increased basal number of NO-positive cells in lactating rats. Furthermore, the total concentration of NOx in the hypothalamus, the circulating level of corticosterone and interleukin-6 increased significantly after EW in diestrus, but not in lactating rats, compared to their corresponding controls. Intracerebral administration of L-NAME, a general NOS inhibitor, reversed the attenuation of the activational response to EW in the PVH of lactating rats. The present results show that lactation diminishes the anaphylactoid reaction to EW compared to that in diestrus rats. This attenuation was absent after L-NAME treatment, suggesting that sustained NO production in the PVH during lactation may limit the neuroendocrine response to stress.