Lactation in the rat activates afferent neuronal pathways that cause marked changes in hormone secretion and maternal behavior. Previously, we used excitatory amino acids (EAAs) to challenge the neuroendocrine axis of the lactating rat and showed altered hypothalamic responsiveness to EAAs. In conducting those studies, we noted that the typical hyperactive behavior associated with NMA (N-methyl-d,l-aspartate) treatment was completely absent in lactating animals. In these studies we have examined the effects of lactation on cortical responsiveness to EAAs by using cFos expression as a marker of neuronal activation. Lactation inhibited hippocampal and cortical cFos induction in response to NMA, which was consistent with the absence of behavioral responses. However, NMA responsiveness was observed in other areas of the brain. Recovery of cortical activation in response to NMA was not observed until 24 h after removal of the suckling stimulus. In contrast, treatment with kainate (an agonist for a different type of glutamate receptor) induced similar patterns of cFos expression and behavioral responses (wet-dog shakes) in cycling and lactating rats. These data demonstrate that lactation, a physiological condition, can inhibit cortical activation that is mediated by NMDA but not kainate receptors. In so doing, lactation represents a novel model system in which to study mechanisms of NMDA receptor inactivation and subsequent consequences on hippocampal and cortical function.
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