Capsaicin-evoked release of immunoreactive calcitonin gene-related peptide from rat trigeminal ganglion: evidence for intraganglionic neurotransmission.
Chemically-mediated cross-excitation has been described between neurons within sensory ganglia. However, the identity and source of the chemical mediators is not known. Ca(2+)-dependent release of neurotransmitters from cultured sensory neurons in vitro has been observed, although neurite outgrowth may confound the ability to extrapolate findings from culture systems to in vivo conditions. Thus, the present studies evaluate the hypothesis of capsaicin-sensitive intraganglionic neuropeptide release from freshly prepared slices of rat sensory ganglia. The ganglionic slice preparation provides an advantage over neuronal cultures, because release may be assessed within minutes after tissue collection (minimizing phenotypic changes) and while maintaining gross anatomical relationships. Trigeminal ganglia (TGG) were quickly removed from male, Sprague--Dawley rats (175--200 g), chopped into 200 microm slices and placed into chambers within 3 min of collection. Chambers were perfused with buffer, and superfusates were collected and assayed for immunoreactive calcitonin gene-related peptide (iCGRP) release via radioimmunoassay. After about 90 min of baseline collection, tissue was treated with capsaicin followed by a washout period. Capsaicin (1--100 microM) evoked concentration-dependent increases in iCGRP release. A competitive capsaicin receptor antagonist, capsazepine, significantly inhibited capsaicin-evoked release of iCGRP. In addition, capsaicin-evoked release of iCGRP was dependent on the presence of extracellular calcium. Furthermore, capsaicin-evoked release from TGG slices was significantly greater than that from slices of equivalent weights of adjacent trigeminal nerve shown histologically to be free of neuronal somata. These data support the hypothesis that Ca(2+)-dependent exocytosis of neuropeptides may occur within the TGG in vivo and that the majority of this release derives from neuronal somata.
Department of Restorative Sciences, University of Minnesota, Box 120 UMHC, 516 Delaware St. SE Minneapolis, MN 55455, USA Departments of Endodontics and Pharmacology, University of Texas Health Science Center, Mail Code 7892, 7703 Floyd Curl Drive, San Antonio 78229-3900, TX, USA Division of Endodontics, University of California, P.O. Box 758, San Francisco, CA 94143, USA.
Yvonne M
YM
Ulrich-Lai
Christopher M
CM
Flores
Catherine A
CA
Harding-Rose
Harold E
HE
Goodis
Kenneth M
KM
Hargreaves
D000818:Animals; D000906:Antibodies; D015740:Calcitonin Gene-Related Peptide / Q000032:analysis / Q000276:immunology / Q000378:metabolism*; D002211:Capsaicin / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005089:Exocytosis / Q000187:drug effects / Q000502:physiology; D066298:In Vitro Techniques; D008297:Male; D010146:Pain / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D009435:Synaptic Transmission / Q000187:drug effects* / Q000502:physiology*; D012668:Trigeminal Ganglion / Q000378:metabolism*; D014276:Trigeminal Nerve / Q000378:metabolism
D000906:Antibodies; D015740:Calcitonin Gene-Related Peptide; D002211:Capsaicin