Regular ArticleNeurotrophin Receptor TrkB Activation Is Not Required for the Postnatal Survival of Retinal Ganglion Cells in Vivo
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Cited by (54)
The molecular basis of retinal ganglion cell death in glaucoma
2012, Progress in Retinal and Eye ResearchCitation Excerpt :Both exogenous BDNF administration and strategies that result in TrkB activation lead to enhanced RGC survival in acute and chronic models of optic nerve damage (Chen and Weber, 2001; Cheng et al., 2002; Di Polo et al., 1998; Hu et al., 2010b; Klöcker et al., 2000; Leaver et al., 2006; Mansour-Robaey et al., 1994; Mey and Thanos, 1993; Parrilla-Reverter et al., 2009; Peinado-Ramon et al., 1996). Paradoxically, the number of RGCs in BDNF or TrkB knockout mice have been shown to be similar to those found in wild-type animals (Cellerino et al., 1997; Pollock et al., 2003; Rohrer et al., 2001), suggesting that other neurotrophic factors compensate for the lack of BDNF or that BDNF signaling through TrkB is not required for RGC survival during development. Of interest, however, RGCs from BDNF null mice displayed hypomyelinated axons (Cellerino et al., 1997) which correlated with marked functional deficits (Rothe et al., 1999), a phenotype that might increase the vulnerability of these neurons to die following glaucomatous optic nerve damage.
Neurotrophic factors and the regeneration of adult retinal ganglion cell axons
2012, International Review of NeurobiologyOlfactory ensheathing glia: Repairing injury to the mammalian visual system
2011, Experimental NeurologyCitation Excerpt :Similar to the rest of the CNS, it has been suggested that appropriate therapeutic manipulation of neurotrophic signaling pathways will promote the survival of injured RGCs (for reviews see Chierzi and Fawcett, 2001; Zhi et al., 2005; Harvey et al., 2006; Johnson et al., 2009). Among the neurotrophic factors known to promote survival of RGCs include BDNF (Rohrer et al., 2001; Leaver et al., 2006b; Peinado-Ramón et al., 1996), neurotrophin 4/5 (Cui et al., 2003; Peinado-Ramón et al., 1996), glial cell-derived neurotrophic factor (GDNF; Jiang et al., 2007) and ciliary neurotrophic factor (CNTF; Cui et al., 2003; Ji et al., 2004; Parrilla-Reverter et al., 2009). Numerous laboratories have tried to improve the efficacy of neurotrophic treatments to the injured optic nerve with varying success (Mey and Thanos, 1993; Chierzi and Fawcett, 2001; Harvey et al., 2006; Berry et al., 2008).
Heterozygous NTF4 Mutations Impairing Neurotrophin-4 Signaling in Patients with Primary Open-Angle Glaucoma
2009, American Journal of Human GeneticsNeurotrophin roles in retinal ganglion cell survival: Lessons from rat glaucoma models
2009, Experimental Eye ResearchCitation Excerpt :NT have important survival properties for adult neurons as well. The application of exogenous NT, especially BDNF, to isolated RGC prolongs their survival in culture (Johnson et al., 1986; Rodriguez-Tebar et al., 1989; Cohen-Cory and Fraser, 1994; Meyer-Franke et al., 1995; Rohrer et al., 2001). Importantly, multiple studies indicate that the intravitreal injection of BDNF prolongs injured, adult RGC survival in vivo (Mey and Thanos, 1993; Mansour-Robaey et al., 1994; Peinado-Ramon et al., 1996; Di Polo et al., 1998; Chen and Weber, 2001).
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To whom correspondence should be addressed at the Storm Eye Institute, Room 707, Medical University of South Carolina, 167 Ashley Avenue, Charleston, SC 29425. Fax: (843) 792-1723. E-mail: [email protected].