PMID- 11717365 OWN - NLM STAT- MEDLINE DCOM- 20020111 LR - 20220309 IS - 1529-2401 (Electronic) IS - 0270-6474 (Print) IS - 0270-6474 (Linking) VI - 21 IP - 23 DP - 2001 Dec 1 TI - Regional differences in neurotrophin availability regulate selective expression of VGF in the developing limbic cortex. PG - 9315-24 AB - Gene and protein expression patterns in the cerebral cortex are complex and often change spatially and temporally through development. The signals that regulate these patterns are primarily unknown. In the present study, we focus on the regulation of VGF expression, which is limited to limbic cortical areas early in development but later expands into sensory and motor areas. We isolated neurons from embryonic day 17 rat cortex and demonstrate that the profile of VGF expression in perirhinal (expressing) and occipital (nonexpressing) populations in vitro is similar to that in the perinatal cortex in vivo. The addition of neutralizing neurotrophin antibodies indicates that endogenous brain-derived neurotrophic factor (BDNF) is necessary for the normal complement of VGF-expressing neurons in the perirhinal cortex, although endogenous neurotrophin-3 (NT-3) regulates the expression of VGF in a subpopulation of cells. ELISA analysis demonstrates that there is significantly more BDNF present in the perirhinal cortex compared with the occipital cortex in the perinatal period. However, the total amount of NT-3 is similar between the two regions and, moreover, there is considerably more NT-3 than BDNF in both areas, a finding seemingly in conflict with regional VGF expression. Quantification of the extracellular levels of neurotrophins in perirhinal and occipital cultures using ELISA in situ analysis indicates that perirhinal neurons release significantly more BDNF than the occipital population. Furthermore, the amount of NT-3 released by the perirhinal neurons is significantly less than the amount of BDNF. Local injection of BDNF in vivo into a normally negative VGF region results in robust ectopic expression of VGF. These data suggest that the local availability of specific neurotrophins for receptor occupation, rather than the total amount of neurotrophin, is a critical parameter in determining the selective expression of VGF in the developing limbic cortex. FAU - Eagleson, K L AU - Eagleson KL AD - Department of Neurobiology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261, USA. keagle+@pitt.edu FAU - Fairfull, L D AU - Fairfull LD FAU - Salton, S R AU - Salton SR FAU - Levitt, P AU - Levitt P LA - eng GR - AG 10676/AG/NIA NIH HHS/United States GR - MH 45507/MH/NIMH 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 - United States TA - J Neurosci JT - The Journal of neuroscience : the official journal of the Society for Neuroscience JID - 8102140 RN - 0 (Antibodies) RN - 0 (Brain-Derived Neurotrophic Factor) RN - 0 (Nerve Growth Factors) RN - 0 (Neuropeptides) RN - 0 (Neurotrophin 3) RN - 0 (Proteins) RN - 0 (RNA, Messenger) RN - 0 (Vgf protein, rat) SB - IM MH - Animals MH - Antibodies/pharmacology MH - Brain-Derived Neurotrophic Factor/administration & dosage/metabolism MH - Cells, Cultured MH - Cerebral Cortex/cytology/embryology/*metabolism MH - Enzyme-Linked Immunosorbent Assay MH - Gene Expression Regulation, Developmental/drug effects/physiology MH - Immunohistochemistry MH - In Situ Hybridization MH - Limbic System/cytology/embryology/*metabolism MH - Microinjections MH - Nerve Growth Factors/antagonists & inhibitors/*metabolism/pharmacology MH - Neurons/cytology/drug effects/metabolism MH - Neuropeptides MH - Neurotrophin 3/metabolism MH - Occipital Lobe/cytology/embryology/metabolism MH - Parahippocampal Gyrus/cytology/embryology/metabolism MH - Proteins/genetics/*metabolism MH - RNA, Messenger/metabolism MH - Rats MH - Rats, Sprague-Dawley MH - Signal Transduction/drug effects MH - Tissue Distribution PMC - PMC6763919 EDAT- 2001/11/22 10:00 MHDA- 2002/01/12 10:01 PMCR- 2002/06/01 CRDT- 2001/11/22 10:00 PHST- 2001/11/22 10:00 [pubmed] PHST- 2002/01/12 10:01 [medline] PHST- 2001/11/22 10:00 [entrez] PHST- 2002/06/01 00:00 [pmc-release] AID - 21/23/9315 [pii] AID - 5850 [pii] AID - 10.1523/JNEUROSCI.21-23-09315.2001 [doi] PST - ppublish SO - J Neurosci. 2001 Dec 1;21(23):9315-24. doi: 10.1523/JNEUROSCI.21-23-09315.2001.