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Effects of brain‐derived neurotrophic factor on the development of NADPH‐diaphorase/nitric oxide synthase‐positive amacrine cells in the rodent retina
Author(s) -
Cellerino Alessandro,
ArangoGonzález Blanca Aurora,
Kohler Konrad
Publication year - 1999
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.1999.00690.x
Subject(s) - nitric oxide synthase , retina , inner nuclear layer , endocrinology , brain derived neurotrophic factor , ganglion cell layer , medicine , neurotrophic factors , biology , inner plexiform layer , amacrine cell , nadph dehydrogenase , nitric oxide , neuroscience , microbiology and biotechnology , chemistry , receptor
Amacrine neurons expressing nitric oxide synthase (NOS) contain brain‐derived neurotrophic factor (BDNF) receptors and respond to exogenous BDNF [Klöcker, N., Cellerino, A. & Bähr, M. (1998) J. Neurosci., 18, 1038–1046]. We analysed the effects of BDNF on the development of neurons which express NOS in the mouse and rat retina. Rat pups received a total of three intraocular injections of BDNF at intervals of 48 h, starting at postnatal day 16 (P16), and were killed at P22. The retinas were stained for NADPH‐diaphorase, a histological marker of NOS. NOS‐expressing neurons were found in both the inner nuclear layer (INL) and the ganglion cell layer (GCL). Two classes of NOS‐expressing neurons, type I and type II, had already been distinguished in the INL [Koistinaho, J. & Sagar, S.M. (1995) In Osborne, N.N. & Chader, G.J. (eds), Progress in Retinal and Eye Research, Vol. 15. Oxford University Press, pp. 69–87] and a third one in the GCL. Up‐regulation of NADPH‐diaphorase activity was observed after BDNF treatment. The number of type I neurons remained stable, whereas the number of type II neurons and NOS‐positive neurons in the GCL increased significantly (P < 0.001). Type I and type II neurons were significantly larger in BDNF‐treated retinas. Double‐labelling experiments revealed that BDNF induces NADPH‐diaphorase in dopaminergic neurons and amacrine cells displaced to the GCL, but not in retinal ganglion cells. In mice homozygous for a null mutation of the bdnf gene, the intensity of NADPH‐diaphorase labelling in both somata and processes was reduced, but the number of labelled neurons was not dramatically reduced. These findings indicate that BDNF regulates the neurotransmitter phenotype of NOS‐expressing amacrine neurons under physiological conditions, but is not required for their survival.