PMID- 10869711 OWN - NLM STAT- MEDLINE DCOM- 20000929 LR - 20190910 IS - 0165-1838 (Print) IS - 0165-1838 (Linking) VI - 81 IP - 1-3 DP - 2000 Jul 3 TI - Effect of NGF, BDNF, bFGF, aFGF and cell density on NPY expression in cultured rat dorsal root ganglion neurones. PG - 128-38 AB - The effect of neurotrophic factors on neuropeptide Y (NPY) expression was studied in adult rat dispersed dorsal root ganglion (DRG) cultures. Nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), acidic fibroblast growth factor (aFGF) or basic FGF was included in the culture medium during incubation for 72 h. In untreated cultures, around 18% of all neurones (visualized by antibodies to PGP 9.5) expressed NPY-like immunoreactivity (LI). In contrast, in vivo uninjured neurones do not contain detectable levels of NPY-LI. In the immunohistochemical analysis aFGF increased the percentage of NPY-immunoreactive (-IR) neurones 1.8-fold, while NGF, BDNF or bFGF had no significant effect on NPY expression. When the effect of these growth factors was monitored with non-radioactive in situ hybridization, both aFGF and bFGF caused a significant increase (2.25- and 1.8-fold, respectively), whereas, again, NGF and BDNF had no effect. The results also showed an effect of cell density on NPY expression, whereby fewer neurones expressed NPY in high than in low density cultures. This difference was seen in untreated as well as growth factor-treated cultures. The present results support the hypothesis that DRG neurones in culture are in an axotomized state, since they express NPY to about the same extent as axotomized DRG neurones in vivo. Surprisingly, two growth factors of the FGF family enhance NPY expression in DRG neurones, which is in apparent contrast to a published in vivo study [Ji, R.-R., Zhang, Q., Pettersson, R.F., Hokfelt, T., 1996. aFGF, bFGF and NGF differentially regulate neuropeptide expression in dorsal root ganglia after axotomy and induce autotomy. Reg. Pept. 66, 179-189.]. Finally, NPY expression was also influenced by cell density. FAU - Kerekes, N AU - Kerekes N AD - Department of Neuroscience, Karolinska Institutet, S-171 77, Stockholm, Sweden.nora.kerekes@neuro.ki.se FAU - Landry, M AU - Landry M FAU - Lundmark, K AU - Lundmark K FAU - Hokfelt, T AU - Hokfelt T LA - eng GR - DK41301/DK/NIDDK NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - Netherlands TA - J Auton Nerv Syst JT - Journal of the autonomic nervous system JID - 8003419 RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Growth Substances) RN - 0 (Neuropeptide Y) RN - 0 (Oligonucleotide Probes) RN - 0 (RNA, Messenger) RN - 103107-01-3 (Fibroblast Growth Factor 2) RN - 104781-85-3 (Fibroblast Growth Factor 1) RN - 9061-61-4 (Nerve Growth Factor) SB - IM MH - Animals MH - Brain-Derived Neurotrophic Factor/pharmacology MH - Cells, Cultured MH - Fibroblast Growth Factor 1/pharmacology MH - Fibroblast Growth Factor 2/pharmacology MH - Ganglia, Spinal/*cytology/drug effects/*metabolism MH - Growth Substances/*pharmacology MH - Image Processing, Computer-Assisted MH - Immunohistochemistry MH - In Situ Hybridization MH - Male MH - Nerve Growth Factor/pharmacology MH - Neurons/*metabolism MH - Neuropeptide Y/*biosynthesis MH - Oligonucleotide Probes MH - RNA, Messenger/biosynthesis MH - Rats MH - Rats, Sprague-Dawley EDAT- 2000/06/28 11:00 MHDA- 2000/10/07 11:01 CRDT- 2000/06/28 11:00 PHST- 2000/06/28 11:00 [pubmed] PHST- 2000/10/07 11:01 [medline] PHST- 2000/06/28 11:00 [entrez] AID - S0165183800001156 [pii] AID - 10.1016/s0165-1838(00)00115-6 [doi] PST - ppublish SO - J Auton Nerv Syst. 2000 Jul 3;81(1-3):128-38. doi: 10.1016/s0165-1838(00)00115-6.