COEXPRESSION OF PREPROTACHYKININ-A, ALPHA-CALCITONIN GENE-RELATED PEPTIDE, SOMATOSTATIN, AND NEUROTROPHIN RECEPTOR FAMILY MESSENGER-RNAS INRAT DORSAL-ROOT GANGLION NEURONS

Syntheses of substance P, somatostatin, and calcitonin gene-related pe ptide in sensory neurons have been suggested to be regulated by neurot rophic factors retrogradely transported from target tissues. In this s tudy, we re-examined this idea by investigating the coexpression of ne urotrophin receptor (trk family proto-oncogene) messenger RNAs, and pr eprotachykinin-A (a precursor peptide of substance P), alpha-calcitoni n gene-related peptide and somatostatin messenger RNAs in lumbar dorsa l root ganglion neurons by means of in situ hybridization histochemist ry in rats. Approximately 35-40%, 5% and 15-20% of sensory neurons dis played signals for trkA, trkB, and trkC messenger RNAs, respectively. Approximately 28% of dorsal root ganglion neurons were positive for pr eprotachykinin-A messenger RNA, and were divided into two groups; thos e labeled strongly and those labeled weakly by in situ hybridization. All the strongly-labeled neurons (78% of preprotachykinin-A-positive c ells) expressed trkA messenger RNA at the same time, while the weakly- labeled neurons did not. Thirty-seven per cent of dorsal root ganglion neurons expressed alpha-calcitonin gene-related peptide messenger RNA , and most of these neurons (84%) also expressed trkA messenger RNA. N o or few preprotachykinin-A messenger RNA- and/or alpha-calcitonin gen e-related peptide messenger RNA-expressing neurons were also positive for trkB or trkC messenger RNAs. Nine per cent of dorsal root ganglion neurons expressed somatostatin messenger RNA, and these neurons lacke d all three trk messenger RNAs. Furthermore, most of these neurons (ab out 90%) showed positive, albeit weak, signals for preprotachykinin-A and alpha-calcitonin gene-related peptide messenger RNAs. The results suggest that expression of preprotachykinin-A and alpha-calcitonin gen e-related peptide messenger RNAs is mediated by nerve growth factor vi a trkA receptor but not by brain-derived neurotrophic factor or neurot rophin-3, and that somatostatin gene transcription is not regulated by any member of the neurotrophin family in rat sensory neurons.