Local and target-derived actions of neurotrophins during peripheral nervous system development

Cellular and Molecular Life Sciences

Volumn 58, Issue 8, 2001, Pages 1036-1044

  Ernfors, P ^a  

^a KAROLINSKA INSTITUTE   (Sweden)

Author keywords

Apoptosis; Dorsal root ganglion; Nervous system development; Neurotrophin; Trophic

Indexed keywords

NEUROTROPHIN; TYROSINE KINASE RECEPTOR;

ANIMAL TISSUE; APOPTOSIS; CHICKEN; CONTROLLED STUDY; EMBRYO; EMBRYO DEVELOPMENT; MOUSE; MOUSE STRAIN; NERVE CELL DIFFERENTIATION; NERVOUS SYSTEM DEVELOPMENT; NONHUMAN; PERIPHERAL NERVOUS SYSTEM; REVIEW; SENSORY NERVE CELL; SPINAL GANGLION; STEM CELL; SURVIVAL;

EID: 0034877193     PISSN: 1420682X     EISSN: None     Source Type: Journal    
DOI: 10.1007/PL00000918     Document Type: Review

References (96)

1. Purification of a new neurotrophic factor from mammalian brain
2. Lack of neurotrophin-3 leads to deficiencies in the peripheral nervous system and loss of limb proprioceptive afferents
3. Severe sensory and sympathetic deficits in mice lacking neurotrophin-3
4. Dependence of group Ia afferents on neurotrophin-3
5. A local action of neurotrophin-3 prevents the death of proliferating sensory neuron precursor cells
6. Lack of neurotrophin-3 results in death of spinal sensory neurons and premature differentiation of their precursors
7. Development of mouse dorsal root ganglia: An autoradiographic and quantitative study
8. Synchronous onset of NGF and trkA survival dependence in development of dorsal root ganglia
9. Characterization of neurotrophin and Trk receptor functions in developing sensory ganglia: Direct NT-3 activation of TrkB neurons in vivo
10. Cells expressing mRNA for neurotrophins and their receptors during embryonic rat development
11. Different neurotrophins are expressed and act in a developmental sequence to promote the survival of embryonic sensory neurons
12. Positive and negative interactions of GDNF, NTN and ART in developing sensory neuron subpopulations and their collaboration with neurotrophins
13. Expression and coexpression of trk receptors in subpopulations of adult primary sensory neurons projecting to identified peripheral targets
14. Specific subtypes of cutaneous mechanoreceptors require neurotrophin-3 following peripheral target innervation
15. The duration of neurotrophic factor independence in early sensory neurons is matched to the time course of target field innervation
16. Neurotrophin-3 is a mitogen for cultured neural crest cells
17. Proliferation, differentiation, and survival of rat sensory neuron precursors in vitro require specific trophic factors
18. Neurotrophic factors promote the maturation of developing neurons before they become dependent on these factors
19. Sensory ganglia require neurotrophin-3 early in development
20. Inhibition of the NT-3 receptor TrkC, early in chick embryogenesis, results in severe reductions in multiple neuronal subpopulations in the dorsal root ganglia
21. In vivo effects of neurotrophin-3 during sensory neurogenesis
22. Targeted mutation in the neurotrophin-3 gene results in loss of muscle sensory neurons
23. Requirement of neurotrophin-3 for the survival of proliferating trigeminal ganglion progenitor cells
24. Growth arrest failure, G1-restriction point override, and S-phase death of sensory precursor cells in the absence of neurotrophin-3
25. Apoptosis and the cell cycle
26. Cell cycle: On target with Myc
27. Requirement for the CD95 receptor-ligand pathway in c-Myc-induced apoptosis
28. Defects of embryonic organogenesis resulting from targeted disruption of the N-myc gene in the mouse
29. Embryonic lethality resulting from disruption of both N-myc alleles in mouse zygotes
30. Organization and expression of the chicken N-myc gene
31. Regulation of the neural crest cell fate by N-myc: Promotion of ventral migration and neuronal differentiation
32. Transition of localization of the N-Myc protein from nucleus to cytoplasm in differentiating neurons
33. Expression of trkA cDNA in neuroblastomas mediates differentiation in vitro and in vivo
34. Constitutive N-myc gene expression inhibits trkA mediated neuronal differentiation
35. Expression of Fas ligand in activated T cells is regulated by c-Myc
36. Mechanisms of apoptosis by c-Myc
37. c-Myc-induced sensitization to apoptosis is mediated through cytochrome c release
38. NMR structure of the death domain of the p75 neurotrophin receptor
39. NTR decide?
40. Signalling through the neurotrophin receptor p75(ntr)
41. Death of oligodendrocytes mediated by the interaction of nerve growth factor with its receptor p75
42. Induction of cell death by endogenous nerve growth factor through its p75 receptor
43. Disruption of the neurotrophin-3 receptor gene trkC eliminates Ia muscle afferents and results in abnormal movements
44. Differential effects of combined trk receptor mutations on dorsal root ganglion and inner ear sensory neurons
45. Developmental changes in NT-3 signalling via TrkA and TrkB in embryonic neurons
46. Expression of Trk receptors in the developing mouse trigeminal ganglion: In vivo evidence for NT-3 activation of TrkA and TrkB in addition to TrkC
47. High specificity of neurotrophins in the embryonic chicken trigeminal system
48. Neurotrophin-3 is a survival factor in vivo for early mouse trigeminal neurons
49. Timing of neuronal death in trkA, trkB and trkC mutant embryos reveals developmental changes in sensory neuron dependence on Trk signalling
50. trkC-mediated NT-3 signaling is required for the early development of a subpopulation of neurogenic neural crest cells
51. trkC, a receptor for neurotrophin-3, is widely expressed in the developing nervous system and in non-neuronal tissues
52. Expression of trk and neurotrophin mRNA in dorsal root and sympathetic ganglia of the quail during development
53. Immunocytochemical localization of trkA receptors in chemically identified subgroups of adult rat sensory neurons
54. Dorsal root ganglion neurons are destroyed by exposure in utero to maternal antibody to nerve growth factor
55. On the role of nerve growth factor in the development of myelinated nociceptors
56. Requirement for nerve growth factor in the development of myelinated nociceptors in vivo
57. Selective dependence of mammalian dorsal root ganglion neurons on nerve growth factor during embryonic development
58. Nerve growth factor and nociception
59. Dorsal root ganglion neurons expressing trk are selectively sensitive to NGF deprivation in utero
60. Mice lacking nerve growth factor display perinatal loss of sensory and sympathetic neurons yet develop basal forebrain cholinergic neurons
61. Severe sensory and sympathetic neuropathies in mice carrying a disrupted trk/NGF receptor gene
62. Non-TrkA-expressing small DRG neurons are lost in TrkA deficient mice
63. Neurotrophin receptor genes are expressed in distinct patterns in developing dorsal root ganglia
64. Nerve growth factor receptor TrkA is down-regulated during postnatal development by a subset of dorsal root ganglion neurons
65. Timing of neuronal death in trkA, trkB and trkC mutant embryos reveals developmental changes in sensory neuron dependence on Trk signalling
66. A distinct subgroup of small DRG cells express GDNF receptor components and GDNF is protective for these neurons after nerve injury
67. IB4-binding DRG neurons switch from NGF to GDNF dependence in early postnatal life
68. Endogenous nerve growth factor regulates the sensitivity of nociceptors in the adult rat
69. Evidence that endogenous nerve growth factor is responsible for the collateral sprouting, but not the regeneration, of nociceptive axons in adult rats
70. Endogenous NGF and nerve impulses regulate the collateral sprouting of sensory axons in the skin of the adult rat
71. Direct evidence for neurogenic inflammation and its prevention by denervation and by pretreatment with capsaicin
72. The role of sensory nerve endings in neurogenic inflammation induced in human skin and in the eye and paw of the rat
73. The effect of a sciatic nerve block on the development of inflammation in carrageenan injected rats
74. Primary afferent tachykinins are required to experience moderate to intense pain
75. Tachykinin receptors and tachykinin receptor antagonists
76. Nerve growth factor contributes to the generation of inflammatory sensory hypersensitivity
77. Nerve growth factor-induced hyperalgesia in the neonatal and adult rat
78. Neutralization of endogenous NGF prevents the sensitization of nociceptors supplying inflamed skin
79. Nerve growth factor and sensory function
80. Placode and neural crest-derived sensory neurons are responsive at early developmental stages to brain- derived neurotrophic factor
81. A BDNF autocrine loop in adult sensory neurons prevents cell death
82. Mice lacking brain-derived neurotrophic factor develop with sensory deficits
83. A role for BDNF in mechanosensation
84. Neurotrophin-4/5 is a mammalian-specific survival factor for distinct populations of sensory neurons
85. Mice lacking brain-derived neurotrophic factor exhibit visceral sensory neuron losses distinct from mice lacking NT-4 and display a severe developmental deficit in control of breathing
86. Point mutation in trkB causes loss of NT-4-dependent neurons without major effects on diverse BDNF responses
87. Neurotrophin 4 is required for the survival of a subclass of hair follicle receptors
88. LNGFR
89. Cutaneous overexpression of neurotrophin-3 selectively restores sensory innervation in NT-3 gene knockout mice
90. Endogenous neurotrophin-3 supports the survival of a subpopulation of sensory neurons in the neonatal rat
91. Superfluousness of motor innervation for the formation of muscle spindles in neonatal rat
92. Reduction in the number of spinal motor neurons in neurotrophin-3-deficient mice
93. Selective expression of neurotrophin-3 messenger RNA in muscle spindles of the rat
94. Introduction of a neurotrophin-3 transgene into muscle selectively rescues proprioceptive neurons in mice lacking endogenous neurotrophin-3
95. Muscle sensory neurons require neurotrophin-3 from peripheral tissues during the period of normal cell death
96. Neurotrophin-3 promotes the differentiation of muscle spindle afferents in the absence of peripheral targets