Prolactin (PRL) is secreted not only to support reproductive functions and lactation but also to maintain homeostatic functions under stress. Consequently, PRL release is known to be regulated not only by endogenous releasing factors but also by exogenous chemical substances with anti-stress activities. Prominent among these is nicotine which causes the release of PRL by acting CNS sites, in particular the nucleus tractus solitarius (NTS). The mechanism by which nicotine modulates PRL release is poorly understood. Recently, a 3 I-amino acid peptide, named the Prolactin Releasing Peptide (PrRP), was isolated which potently induced prolactin release from primary pituitary cells. Our preliminary data indicate that the PrRP mRNA is present in the NTS while its receptor is found in the hypothalamus. These data suggest that PrRP may be another important mediator of nicotine-induced PRL release. Upon nicotine stimulation, PrRP may be released from the NTS to act either on the hypothalamus and induce the release of other prolactin-releasing peptides or by being secreted in the potal blood and acting directly on the pituitary. We therefore propose to test the hypothesis of a direct link between PrRP and nicotine, by showing that PrRP is present in the nicotine sensitive (~ positive) NTS neurons and that nicotine induces PrRP release in the cerebrospinal fluid.
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