Publication | Closed Access
Differential Regulation of Calcitonin Gene‐related Peptide (CGRP) in Regenerating Rat Facial Nucleus and Dorsal Root Ganglion
104
Citations
39
References
1991
Year
Peripheral Nerve InjuryPeripheral NervePeripheral NervesSynaptic SignalingCellular PhysiologyCalcitonin Gene‐related PeptideSocial SciencesPeripheral Nervous SystemGanglion CellDorsal Root GanglionMolecular NeuroscienceMolecular PhysiologyRat Facial NucleusNervous SystemCell BiologySignal TransductionNeuroanatomyPhysiologyCgrp MrnaNeuropeptide ReceptorCalcitonin Gene-related PeptideNeuroscienceCentral Nervous SystemSciatic Nerve SectionMedicineNeuropeptides
The content of calcitonin gene-related peptide (CGRP) and CGRP-mRNA were determined in axotomized rat facial motor nucleus and sensory fifth lumbar dorsal root ganglion (L5 DRG) using radioimmunoassay and Northern blot analysis. After facial nerve transection CGRP levels in the facial nucleus showed a biphasic, approximately five-fold increase. A first peak occurred at postoperative day 3 and, after a transient decrease to normal levels at day 9, another increase was observed reaching a peak around the time of reinnervation (postoperative day 21). CGRP-mRNA showed a similar, biphasic increase. The first peak in CGRP mRNA preceded the peptide peak by 2 days, the second peak was approximately day 21. In contrast, a decrease in CGRP levels is seen in L5 DRG after sciatic nerve section, reaching minimal levels of 45% of control during the second postoperative week. CGRP-mRNA in axotomized DRG also decreases preceding the decrease in peptide levels. No recovery to normal levels is seen for either peptide or mRNA levels in regenerating DRG up to 45 days after injury. Thus, axotomy leads to a differential regulation of both CGRP and CGRP-mRNA in regenerating facial motor nucleus and sensory L5 DRG. This difference may be due to different regulating factors present in both the respective target tissues and the CNS regions and could reflect different functions of CGRP in regenerating motor and sensory neurons.
| Year | Citations | |
|---|---|---|
Page 1
Page 1