PMID- 10662837 OWN - NLM STAT- MEDLINE DCOM- 20000225 LR - 20191023 IS - 0270-6474 (Print) IS - 1529-2401 (Electronic) IS - 0270-6474 (Linking) VI - 20 IP - 4 DP - 2000 Feb 15 TI - Rapid regulation of brain-derived neurotrophic factor mRNA within eye-specific circuits during ocular dominance column formation. PG - 1470-83 AB - The neurotrophin brain-derived neurotrophic factor (BDNF) has emerged as a candidate retrograde signaling molecule for geniculocortical axons during the formation of ocular dominance columns. Here we examined whether neuronal activity can regulate BDNF mRNA in eye-specific circuits in the developing cat visual system. Dark-rearing throughout the critical period for ocular dominance column formation decreases levels of BDNF mRNA within primary visual cortex, whereas short-term (2 d) binocular blockade of retinal activity with tetrodotoxin (TTX) downregulates BDNF mRNA within the lateral geniculate nucleus (LGN) and visual cortical areas. Brief (6 hr to 2 d) monocular TTX blockade during the critical period and also in adulthood causes downregulation in appropriate eye-specific laminae in the LGN and ocular dominance columns within primary visual cortex. Monocular TTX blockade at postnatal day 23 also downregulates BDNF mRNA in a periodic fashion, consistent with recent observations that ocular dominance columns can be detected at these early ages by physiological methods. In contrast, 10 d monocular TTX during the critical period does not cause a lasting decrease in BDNF mRNA expression in columns pertaining to the treated eye, consistent with the nearly complete shift in physiological response properties of cortical neurons in favor of the unmanipulated eye known to result from long-term monocular deprivation. These observations demonstrate that BDNF mRNA levels can provide an accurate "molecular readout" of the activity levels of cortical neurons and are consistent with a highly local action of BDNF in strengthening and maintaining active synapses during ocular dominance column formation. FAU - Lein, E S AU - Lein ES AD - Howard Hughes Medical Institute, Department of Molecular Biology, Berkeley, California 94720, USA. FAU - Shatz, C J AU - Shatz CJ LA - eng GR - R01 EY002858/EY/NEI NIH HHS/United States GR - R37 EY002858/EY/NEI NIH HHS/United States GR - EY 02858/EY/NEI NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, Non-P.H.S. 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 (Brain-Derived Neurotrophic Factor) RN - 0 (RNA, Messenger) RN - 4368-28-9 (Tetrodotoxin) SB - IM MH - Aging MH - Animals MH - Brain-Derived Neurotrophic Factor/*genetics MH - Cats MH - Darkness MH - Dominance, Cerebral/*genetics MH - *Gene Expression Regulation, Developmental/drug effects MH - Geniculate Bodies/metabolism/physiology MH - RNA, Messenger/genetics MH - Superior Colliculi/metabolism/physiology MH - Tetrodotoxin/pharmacology MH - *Transcription, Genetic MH - Vision, Binocular MH - Vision, Monocular MH - Visual Cortex/growth & development/metabolism/*physiology MH - Visual Pathways/growth & development/metabolism/*physiology PMC - PMC6772351 EDAT- 2000/02/09 09:00 MHDA- 2000/03/04 09:00 PMCR- 2000/08/15 CRDT- 2000/02/09 09:00 PHST- 2000/02/09 09:00 [pubmed] PHST- 2000/03/04 09:00 [medline] PHST- 2000/02/09 09:00 [entrez] PHST- 2000/08/15 00:00 [pmc-release] AID - 3916 [pii] AID - 10.1523/JNEUROSCI.20-04-01470.2000 [doi] PST - ppublish SO - J Neurosci. 2000 Feb 15;20(4):1470-83. doi: 10.1523/JNEUROSCI.20-04-01470.2000.