Studies on Normal and Inflamed Dental Pulp, NPY Regulation of Peripheral Human Nociceptors, Peripheral Mechanisms of Opioid Analgesia, Cannabinoid-induced Desensitization of TRPV1 Receptors Adrenergic Modulation of Trigeminal Nociceptors
Studies on Normal and Inflamed Dental Pulp, NPY Regulation of Peripheral Human Nociceptors, Peripheral Mechanisms of Opioid Analgesia, Cannabinoid-induced Desensitization of TRPV1 Receptors Adrenergic Modulation of Trigeminal Nociceptors
This protocol is for a number of in vitro studies using human surgical biopsies and evaluating the pharmacology and genetics of human nociceptors ("pain detecting") neurons
Purpose/Objectives
a. Specific Aims Specific Aim 1: Characterize in humans the effects of inflammation and neuronal degeneration on peripheral levels of NPY, and related Y receptors (Y1, Y2, Y5) in periradicular tissue.
Specific Aim 2: Determine whether NPY inhibits neurosecretion from peripheral terminals of capsaicin-sensitive neurons innervating normal versus inflamed tissue.
Specific Aim 3: Determine whether peripheral administration of NPY is analgesic and/or anti-allodynic in patients experiencing spontaneous pain and mechanical allodynia in a clinical model of inflammation with associated neuronal degeneration.
Specific Aim 4: Evaluate whether population characteristics are associated with altered pain reports. First, we will determine whether patients with the C1128 single nucleotide polymorphism (SNP) of the PreProNPY gene, whose phenotype confers substantially augmented peripheral NPY neurosecretion, report less pain compared with patients without this genetic polymorphism. Second, we will determine whether ethnic/cultural factors associated with an underserved minority population (Hispanics in the San Antonio area) are associated with altered pain reports.
Inclusion Criteria:
Exclusion Criteria: