Intracerebroventricular injection of a nitric oxide donor attenuates Fos expression in the paraventricular and supraoptic nuclei of lactating rats

The exact nature of how nitric oxide (NO) acts in the regulation of milk ej ection during lactation is not clearly understood at the moment. In this st udy, we have examined the effect of drugs which spontaneously release NO (s odium nitroprusside, SNP) or inhibit the NO synthase (NOS) enzyme (N-omega- nitro-L-arginine, L-NA) on the activity of some hypothalamic and functional ly associated nuclei using Fos expression as an index of neuronal activatio n. Lactating rats received intracerebroventricular injection of SNP, L-NA o r vehicle (saline) just before they were reunited with their pups after a 1 2-h period of separation and allowed to suckle for 2 h. The difference in t he total pup body weight before and after the period of suckling was used a s a functional end-point of milk transfer. Central injection of SNP in cons cious rats significantly inhibited Fos expression in the paraventricular nu cleus (PVN), supraoptic nucleus (SON), periventricular and preoptic nuclei and also decreased pup body weight compared with saline- or L-NA-injected r ats. Urethane-anesthetized animals, compared with their conscious counterpa rts, showed increased Fos expression in the PVN and SON. However, Fos expre ssion in the PVN of the anesthetized animals was attenuated by L-NA injecti on compared with SNP and saline injection. Taken together with an earlier f inding that SNP disrupts the milk ejection burst of oxytocinergic neurons, these observations suggest: that NO may act within the neuron(s) possibly t o alter the mechanism(s) regulating the periodic neuronal burst activity du ring lactation. (C) 1999 Elsevier Science B.V. All rights reserved.