title: Neurotrophin sensitivity of prevertebral and paravertebral rat sympathetic autonomic ganglia.
abstract: Prevertebral and paravertebral sympathetic autonomic ganglia respond differently to a large number of experimental and clinical insults. The selective involvement of subpopulations of sympathetic neurons may reflect differences in their response to neurotrophic substances. To test this hypothesis, we investigated the response of prevertebral and paravertebral rat sympathetic ganglia to selected neurotrophic substances in vivo and in vitro and identified the ganglionic distribution of neurons expressing high affinity neurotrophin receptor mRNAs. Dissociated cultures of embryonic prevertebral and paravertebral ganglionic neurons showed comparable responses to NGF deprivation and only small differences in their response to rescue with other trophic substances. In situ hybridization studies of adult rat sympathetic ganglia using probes specific for the high-affinity neurotrophin receptor transcripts trks A, B, and C demonstrated that neurons in both prevertebral and paravertebral sympathetic ganglia express predominantly trkA receptors in vivo. In addition, increased tyrosine hydroxylase (TOH) activity was induced only by doses of neurotrophic substances that activate trkA and showed only small differences between neonatal prevertebral and paravertebral ganglia. Although small differences in the sensitivity of pre- and paravertebral sympathetic neurons to various neurotrophins have been identified in our studies, they are unlikely, in isolation, to explain major differences in the sensitivity of these ganglia to neuropathologic processes.
authors.affiliation: Department of Pathology, Washington University School of Medicine, Saint Louis, MO, USA.
authors.forename: R E
authors.initials: RE
authors.lastname: Schmidt
authors.forename: D A
authors.initials: DA
authors.lastname: Dorsey
authors.forename: L A
authors.initials: LA
authors.lastname: Selznick
authors.forename: P S
authors.initials: PS
authors.lastname: DiStefano
authors.forename: S L
authors.initials: SL
authors.lastname: Carroll
authors.forename: L N
authors.initials: LN
authors.lastname: Beaudet
authors.forename: K A
authors.initials: KA
authors.lastname: Roth
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D000831:Animals, Newborn; D019208:Brain-Derived Neurotrophic Factor / Q000494:pharmacology; D002478:Cells, Cultured; D020934:Ciliary Neurotrophic Factor; D004622:Embryo, Mammalian; D004790:Enzyme Induction; D005728:Ganglia, Sympathetic / Q000166:cytology / Q000254:growth & development / Q000502:physiology*; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects; D009414:Nerve Growth Factors / Q000494:pharmacology*; D009419:Nerve Tissue Proteins / Q000494:pharmacology; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D020933:Neurotrophin 3; D011518:Proto-Oncogene Proteins / Q000032:analysis / Q000096:biosynthesis; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D020794:Receptor Protein-Tyrosine Kinases / Q000032:analysis / Q000096:biosynthesis; D020801:Receptor, Ciliary Neurotrophic Factor; D020917:Receptor, trkA; D020812:Receptor, trkC; D017475:Receptors, Nerve Growth Factor / Q000032:analysis / Q000096:biosynthesis*; D014158:Transcription, Genetic / Q000187:drug effects; D014446:Tyrosine 3-Monooxygenase / Q000096:biosynthesis
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D020934:Ciliary Neurotrophic Factor; D009414:Nerve Growth Factors; D009419:Nerve Tissue Proteins; D020933:Neurotrophin 3; D011518:Proto-Oncogene Proteins; D012333:RNA, Messenger; D020801:Receptor, Ciliary Neurotrophic Factor; D017475:Receptors, Nerve Growth Factor; C071951:neurotrophin 5; D014446:Tyrosine 3-Monooxygenase; D020794:Receptor Protein-Tyrosine Kinases; D020917:Receptor, trkA; D020812:Receptor, trkC; C073922:neurotrophin 4