Search

We investigated how simultaneous manipulation of suckling and i.c.v. injection of nitric oxide (NO)-related pharmacological agents affect Fos activation in the hippocampus and cortex of lactating rats. Dams received drugs or vehicle injection just prior to reunion with their pups following a 12 h separation and Fos protein activation was examined after 2 h of suckling. In conscious dams, sodium nitroprusside (SNP, an NO donor) significantly activated Fos expression in the hippocampus and cortex compared with vehicle or an NO synthase inhibitor. Urethane anaesthesia abolished Fos expression in the cortex, but not in the hippocampus following simultaneous SNP injection and resumption of suckling. Fos activation in the hippocampus and cortex was significantly attenuated when SNP was injected alone (without dam-pups reunion after separation). Coincident injection of SNP with a NO synthase inhibitor abolished all Fos activation in the hippocampus and cortex. In chronically lactating rats (without any interruption of suckling) SNP injection failed to activate any Fos expression. These observations underscore the importance of stimulus modality in revealing the dynamics of NO-mediated neuronal function within a discrete tissue entity such as the hippocampus or the cortex, which may be relevant to other regions of the brain.

This study examined a possible functional involvement of nitric oxide (NO) in the median eminence (ME) and arcuate nucleus (ARC) after capsaicin treatment in rats. Subcutaneous injection of capsaicin increased nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) activity in the ARC-ME compared with vehicle treatment. Fos expression was increased in the ARC after capsaicin injection compared with vehicle-treated rats. Pretreatment with the NO synthase (NOS) inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME) attenuated the effect of capsaicin on Fos expression and NADPH-d reactivity in the ARC-ME in comparison with rats injected with D-NAME, the inactive stereoisomer of L-NAME. These observations suggest that NO makes a major contribution to the response of the ARC-ME to a stressor such as capsaicin.

Female mice develop a long-lasting olfactory recognition memory of a partner male at the first relay in the vomeronasal system. In this study the synaptic plasticity relevant to this phenomenon was examined at reciprocal dendrodendritic synapses in the accessory olfactory bulb of female mice by electron microscopy. The size of asymmetrical excitatory synapses (mitral/tufted to granule cells) of the reciprocal synapses was significantly larger in the group of female mice which were subjected to a treatment intended to induce olfactory memory formation than in the control group. It is suggested that olfactory memory formation is associated with a conformational change at the level of synaptic structure of the accessory olfactory bulb.

We examined the effect of nitric oxide (NO) on the process of parturition in rats. Subcutaneous injection of the NO donor sodium nitroprusside (SNP) in late pregnancy prolonged the total parturition time. The effect of N omega-nitro-L-arginine was not significantly different from that of saline. Intracerebroventricular injection of SNP in parturient rats delayed the progress of parturition. Both modes of SNP treatment also inhibited expression of maternal behavior. Central injection of oxytocin (OXT) with SNP failed to reduce parturition time significantly, but intrapartum, not postpartum, maternal behaviour was restored. These observations suggest that NO interferes with the release of OXT within the brain, hence affecting the initiation of maternal behaviour, and may also impair oxytocin secretion from the neurohypophysis.