Neuron
ArticleThe duration of neurotrophic factor independence in early sensory neurons is matched to the time course of target field innervation
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Regulation of Neuronal Survival by Neurotrophins in the Developing Peripheral Nervous System
2013, Comprehensive Developmental Neuroscience: Patterning and Cell Type Specification in the Developing CNS and PNSThe life, death and regenerative ability of immature and mature rat retinal ganglion cells are influenced by their birthdate
2010, Experimental NeurologyCitation Excerpt :There are, however, clues from the peripheral nervous system (PNS) where there is an established correlation between the timing of neurogenesis, length of the pathway and the timing of the trophic dependency switch. Studies on cranial sensory neurons and lower motor neurons show that the further the axon has to grow, the longer it takes for the axons to switch on their trophic dependency (Davies, 1989; Vogel and Davies, 1991; Mettling et al., 1995). In placode-derived sensory neurons this switch is driven by an “intrinsic timing program specified in the progenitors” (Davies, 2003).
BDNF is required for the survival of differentiated geniculate ganglion neurons
2010, Developmental BiologyRetinoid signaling is involved in governing the waiting period for axons in chick hindlimb
2008, Developmental BiologyRegulation of intrinsic neuronal properties for axon growth and regeneration
2007, Progress in NeurobiologyThe role of neurotrophins in the maintenance of the spinal cord motor neurons and the dorsal root ganglia proprioceptive sensory neurons
2005, International Journal of Developmental NeuroscienceCitation Excerpt :As previously mentioned in Section 1, relationship between different skeletal muscle-associated neurons, non-muscle innervating neurons and target-derived neurotrophins can be studied in different ways. In vitro studies suggest that survival of many populations of cranial sensory neurons firstly depends on BDNF or NT-3, followed by a switch to another neurotrophin at a later developmental stage (Vogel and Davies, 1991; Buchman and Davies, 1993). Alternatively, the neurotrophins, the receptor tyrosine kinases and the p75 receptor component can be targeted in null mutation experiments, as extensively reported (Lee et al., 1992; Snider, 1994; Farinas and Reichardt, 1996; Snider and Silos-Santiago, 1996).