NERVE GROWTH FACTOR-REGULATED PROPERTIES OF SENSORY NEURONS IN OCT-2 NULL MUTANT MICE
- Author(s)
- NINKINA, NN; BUCHMAN, VL; AKOPIAN, AN; LAWSON, SN; Yamamoto, M; CAMPBELL, E; Corcoran, L; WOOD, JN;
- Details
- Publication Year 1995-11,Volume 33,Issue #2,Page 233-244
- Journal Title
- MOLECULAR BRAIN RESEARCH
- Publication Type
- Journal Article
- Abstract
- The POU-domain transcription factor Oct-2 is expressed in both B lymphocytes and sensory neurones, where its expression is regulated by nerve growth factor (NGF), In order to define a possible role for Oct-2 in neurotrophin signalling, we examined the expression of an NGF-regulated channel (capsaicin-evoked ion fluxes), neuropeptides (substance P, calcitonin gene-related peptide), structural proteins (neurofilaments and peripherin) and receptors (trks) in dorsal root ganglion neurones derived from perinatal transgenic mice containing a defective Oct-2 structural gene. Northern blots show that central nervous tissue contains a larger than normal(> 10 kb) mRNA transcript corresponding in size to an Oct-2 transcript encoding a defective protein. PCR analysis shows the absence of normal Oct-2 transcripts in dorsal root ganglia. In null mutants, capsaicin sensitivity, and neuropeptide and cytoskeletal protein expression were unaffected by the loss of Oct-2 expression. The number of sensory neurones and the gross morphology of CNS tissues that normally express high levels of Oct-2 were also examined and found to be normal in the null mutant. Heterozygous animals show normal thresholds of sensitivity to noxious heat and normal inflammatory responses. Oct-2 does not therefore play an essential role in the NGF responsiveness of sensory neurones in these animals.
- Publisher
- ELSEVIER SCIENCE BV
- Keywords
- TRANSCRIPTION FACTORS; B-CELL; PROTEIN OCT-2; GENE-PRODUCTS; HOMEO DOMAIN; POU-DOMAIN; CGRP GENE; ADULT-RAT; EXPRESSION; DIFFERENTIATION
- Publisher's Version
- https://doi.org/10.1016/0169-328X(95)00128-F
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 1995-11-01 12:00:00