Physiology of nerve growth factor.

Thoenen, H.; Barde, Yves‐Alain

doi:10.1152/physrev.1980.60.4.1284

Cited by 1,533 publications

(517 citation statements)

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“…During development, availability of neurotrophins in the embryo and neonate govern the survival of neurons during a period of synaptic and neuronal elimination, with exogenously applied neurotrophins reducing normal levels of cell death [75]. The role of neurotrophins in preventing the inappropriate paring of synaptic connections in perinatal animals leaves these neurons much more susceptible to cell death following the removal of a trophic source, either through biochemical manipulations or via de-efferentation by axotomy, than neurons in adult animals [76,77]. Sciatic lesion in neonatal mice results in a loss of approximately two-thirds of the lower motor neurons in the lumbar enlargement, which is completely ameliorated with the application of BDNF, NT-3, or insulin-like growth factor I (IGF-I) [78].…”

Section: Neurotrophins Development and Survivalmentioning

confidence: 99%

Neurotrophins: Potential Therapeutic Tools for the Treatment of Spinal Cord Injury

Hollis

Tuszynski

2011

Neurotherapeutics

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Spinal cord injury permanently disrupts neuroanatomical circuitry and can result in severe functional deficits. These functional deficits, however, are not immutable and spontaneous recovery occurs in some patients. It is highly likely that this recovery is dependent upon spared tissue and the endogenous plasticity of the central nervous system. Neurotrophic factors are mediators of neuronal plasticity throughout development and into adulthood, affecting proliferation of neuronal precursors, neuronal survival, axonal growth, dendritic arborization and synapse formation. Neurotrophic factors are therefore excellent candidates for enhancing axonal plasticity and regeneration after spinal cord injury. Understanding growth factor effects on axonal growth and utilizing them to alter the intrinsic limitations on regenerative growth will provide potent tools for the development of translational therapeutic interventions for spinal cord injury.Keywords Neurotrophin . spinal cord injury . regeneration . axon plasticity . functional recovery Human Spinal Cord InjuryTraumatic injury of the spinal cord can produce a range of debilitating effects and permanently alter the capabilities and quality of life of its surviving victims. Damage to the central nervous system (CNS) in general results in destruction of neuronal circuitry. Contusion, compression, and penetration injuries of the spinal cord can interrupt the flow of sensory and motor information between the brain and periphery [1]. Depending on the location and severity of the injury, deficits can range from weakness of limb movement to total paralysis and ventilator-assisted respiration. Spontaneous functional recovery is limited, but can and often does occur in patients with initial sparing of sensorimotor function [2]. This recovery, which plateaus between 12 to 18 months, is very likely due to sparing and sprouting of axons within the zone of partial preservation, an area where some motor function remains intact, immediately adjacent to the lesion site [2].Approximately 40% of humans that sustain spinal cord injury (SCI) exhibit improvement from their early postinjury baseline, and this spontaneous recovery can range from modest to extensive [2]. Spontaneous recovery primarily appears to depend on the extent of tissue sparing at the injury site, allowing compensatory axonal sprouting and systems reorganization at levels ranging from the spinal cord to the cerebral cortex [3][4][5][6][7][8][9][10]. However, in cases of more severe injuries, means of enhancing endogenous levels of axonal sprouting and inducing true axonal regeneration are required to enhance functional outcomes.Electronic supplementary material The online version of this article

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Section: Neurotrophins Development and Survivalmentioning

confidence: 99%

Neurotrophins: Potential Therapeutic Tools for the Treatment of Spinal Cord Injury

Hollis

Tuszynski

2011

Neurotherapeutics

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“…Conversely, the implantation of an additional extremity anlage resulted in an increase of the number of motoneurons projecting into the augmented target area (31,37). The further extension and evaluation of this concept, replacing the physiological target of motoneurons by sarcoma tissue, resulted-by a cascade of lucky coincidences-in the discovery of nerve growth factor (NGF) (summarized in 48), the molecular incarnation of the retrograde trophic influence of peripheral target cells on sympathetic and subpopulations of sensory (both neural crest and placode derived) neurons (summarized in 4,48,104).…”

Section: Introductionmentioning

confidence: 99%

“…In this context, it should be emphasized that, according to currently available information, there is not a single human or animal degenerative disease of the nervous system which can causally be linked to an insufficient or false (mutated) production of neurotrophic molecule (98). However, neurotrophic molecules have been demonstrated to rescue specific neurons from the consequences of a variety of mechanical (axotomy) or chemical (6-hydroxydopamine, MPTP, excitotoxic amino acids) damages (40,45,50,79,93,96,104,107). Therefore, the use of neurotrophic molecules in the treatment of degenerative diseases ofthe nervous system is a symptomatic one and strongly encourages further investigations aimed at a molecular understanding of the pathogenetic mechanisms of degenerative disorders of the nervous system.…”

Section: Introductionmentioning

confidence: 99%

Trophic Support of Motoneurons: Physiological, Pathophysiological, and Therapeutic Implications

Thoenen¹,

Hughes²,

Sendtner³

1993

Experimental Neurology

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“…NGF is a protein that is required for the development and maintenance of sympathetic and some sensory neurons [ 1,2]. NGF is thought to be synthesized in innervated end organs and retrogradely transported to the neuronal cell body [3,4].…”

Section: Introductionmentioning

confidence: 99%

Stimulation of nerve growth factor synthesis/secretion by 1,4‐benzoquinone and its derivatives in cultured mouse astroglial cells

et al. 1990

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Previously we reported that astroglial cells cultured from mouse brain synthesize and secrete nerve growth factor (NGF) and that, in quiescent cells, catecholamines markedly increase the NGF content in the conditioned medium (CM). We wished to further assess the structural properties required for exhibition of such effect of compounds containing a ring structure analogous to that of catechol on astroglial NGF synthesis. During our study, we found that hydroquinone, which was confirmed not to stimulate .NGF synthesis in mouse fibroblast cells in another of our investigations, is a potent stimulator of NGF synthesis in astroglial cells and that 1,4benzoquinone, an oxidized form of hydroquinone, is a more effective stimulator than hydroquinone itself. In addition, the results of experiments with 1,2benzoquinone derivatives indicated that the presence of a long aliphatic side chain in the molecule eliminates the stimulatory effect of 1,4-benzoquinone on NGF synthesis in astroglial cells.

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Physiology of nerve growth factor.

Cited by 1,533 publications

References 0 publications

Neurotrophins: Potential Therapeutic Tools for the Treatment of Spinal Cord Injury

Neurotrophins: Potential Therapeutic Tools for the Treatment of Spinal Cord Injury

Trophic Support of Motoneurons: Physiological, Pathophysiological, and Therapeutic Implications

Stimulation of nerve growth factor synthesis/secretion by 1,4‐benzoquinone and its derivatives in cultured mouse astroglial cells

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