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Example sentences for: trkb
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2a), a hallmark of both BDNF and trkB null mutations [ 13 15 ] . In fact, the reduction of fibers seems to be rather uniform throughout a given sensory epithelium with the crista innervation being qualitatively no more reduced than the innervation of the utricle and saccule.
Past research has shown that in BDNF and trkB null mutants this innervation to canal cristae is lost before birth [ 6 13 ] . That even these low levels of expression are significant is clear from the fact that all canal sensory epithelia receive an innervation by both afferents and efferents at birth and later (Figs.
[ 5 ] . BDNF transiently stabilizes silent NM synapses during the period of transition from polyneuronal to mononeuronal innervation of skeletal muscle fibers [ 6 ] . BDNF and CNTF cooperatively affect efficiency of embryonic xenopus neuromuscular synapses in culture [ 7 8 ] . BDNF stimulates transmitter release from neuromuscular synapses [ 9 ] and enhances the efficiency of transmission at the neuromuscular synapse [ 10 ] . BDNF, together with NT-3, can restore neuregulin levels and a normal distribution of AchR at the neuromuscular junction blocked with curare [ 11 ] . BDNF, in conjunction with fibronectin, increases spontaneous synaptic currents in the cultured embryonic xenopus neuromuscular junction [ 12 ] . BDNF down-regulates AchR clustering, most likely by binding to TrkB expressed in myocytes [ 13 ] . BDNF downregulates agrin levels in muscle but increases neuregulin in ventral horn spinal motor neurons at the time when they form neuromuscular synapses [ 14 ] .
1a), but larger than in BDNF or trkB null mutants of the same age [ 13 15 ] . The reduction in apparent size of the vestibular ganglia is in agreement with quantitative data published previously [ 3 13 ] . These data suggest a loss of 80-85% of vestibular sensory neurons in BDNF and trkB null mutants [ 13 ] and of 77% of vestibular sensory neurons in P4 Brn3c null mutants [ 3 ] . Thus, the size reduction in the vestibular sensory ganglion could be compatible with a loss of BDNF production in the immature hair cells.
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