Abstract: The embodiments disclosed herein provide methods for inhibiting, reducing and/or treating pain in a subject by administering to a subject in need thereof a pharmaceutical formulation that includes a pharmacologically active compound that is adapted to disrupt PRL signaling in pain neurons. In certain embodiments, the compound is a PRL-R antagonist. In certain embodiments, the compound is adapted to alter the expression of one or more components involved in PRL signaling. Also provided for herein are methods to diagnose a pain disorder in a subject, comprising obtaining a measure of the amount of PRL or PRL mRNA in a biological sample.

Abstract: Disclosed are cDNA expression libraries enriched for cDNAs that encode, for example, secretory and membrane-bound proteins and to methods for making such libraries. Also disclosed are methods for using the cDNA expression libraries disclosed herein to screen for proteins, nucleic acids, and agents that modulate the function and/or expression of proteins.

Abstract: The embodiments disclosed herein provide methods for inhibiting, reducing and/or treating pain in a subject by administering to a subject in need thereof a pharmaceutical formulation that includes a pharmacologically active compound that is adapted to disrupt PRL signaling in pain neurons. In certain embodiments, the compound is a PRL-R antagonist. In certain embodiments, the compound is adapted to alter the expression of one or more components involved in PRL signaling. Also provided for herein are methods to diagnose a pain disorder in a subject, comprising obtaining a measure of the amount of PRL or PRL mRNA in a biological sample.

Abstract: The present invention relates to a novel 1,957 amino acid tetrodotoxin-insensitive voltage-gated sodium channel specifically located in mammalian sensory neurons. Nucleic acid sequences coding for the novel sodium channel, vectors, host cells and methods of identifying modulators of the novel sodium channel for use in treatment of pain are also provided.