Morphological effects of ciliary neurotrophic factor treatment during neuromuscular synapse elimination

Jordan, Cynthia L.

doi:10.1002/(sici)1097-4695(199609)31:1<29::aid-neu3>3.0.co;2-h

Cited by 12 publications

(1 citation statement)

References 43 publications

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“…In vivo, exogenously administered CNTF reduces motor neuron death during development (Oppenheim et al, 1991;Forger et al, 1993), following early postnatal axotomy (Sendtner et al, 1990) and in motor neuron disease models (Sendtner et al, 1992;Ikeda et al, 1995;Sagot et al, 1995). It also reduces the developmentally associated loss of axon terminals (Jordan, 1996), increases the size of neuromuscular junctions after peripheral nerve lesion (Huang et al, 2002) and maintains motor neuron terminals in genetically defined ALS models (Pun et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Muscle and motor neuron ciliary neurotrophic factor receptor α together maintain adult motor neuron axons in vivo

Lee

Serbinski

Braunlin

et al. 2016

Eur J of Neuroscience

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The molecular mechanisms maintaining adult motor innervation are comparatively unexplored relative to those involved during development. In addition to the fundamental neuroscience question, this area has important clinical ramifications given that loss of neuromuscular contact is thought to underlie several adult onset human neuromuscular diseases including amyotrophic lateral sclerosis. Indirect evidence suggests that ciliary neurotrophic factor (CNTF) receptors may contribute to adult motor neuron axon maintenance. To directly address this in vivo, we used adult onset mouse genetic disruption techniques to deplete motor neuron and muscle CNTF receptor α (CNTFRα), the essential ligand binding subunit of the receptor, and incorporated reporters labelling affected motor neuron axons and terminals. The combined depletion of motor neuron and muscle CNTFRα produced a large loss of motor neuron terminals and retrograde labelling of motor neurons with FluoroGold indicated axon die-back well beyond muscle, together revealing an essential role for CNTFRα in adult motor axon maintenance. In contrast, selective depletion of motor neuron CNTFRα did not affect motor innervation. These data, along with our previous work indicating no effect of muscle specific CNTFRα depletion on motor innervation, suggest that motor neuron and muscle CNTFRα function in concert to maintain motor neuron axons. The data also raise the possibility of motor neuron and/or muscle CNTFRα as therapeutic targets for adult neuromuscular denervating diseases.

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Section: Introductionmentioning

confidence: 99%

Muscle and motor neuron ciliary neurotrophic factor receptor α together maintain adult motor neuron axons in vivo

Lee

Serbinski

Braunlin

et al. 2016

Eur J of Neuroscience

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Glia as mediators of steroid hormone action on the nervous system: An overview

Jordan

1999

J. Neurobiol.

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This special issue on steroids and glia represents the intersection of two emerging themes in the neurosciences: (a) Glia actively modulate and participate in brain function throughout life, and (b) glia are sensitive to steroid hormones. This overview begins by reviewing some of the basic principles of steroid hormone action on the brain and introducing the various glia that inhabit the peripheral and central nervous system. A prominent theme among the articles that follow is that glia may be direct targets for steroid hormones since they possess steroid receptors and the promoter region of glial‐specific genes such as glutamine synthetase contain hormone‐responsive elements. The articles in this special issue discuss evidence that glia may mediate steroid action on the nervous system in the context of (a) steroid metabolism, which may control the hormonal microenvironment of neurons both in the normal and injured brain; (b) brain development including sexual differentiation; (c) synaptic plasticity which may underlie the cyclic release of luteinizing hormone releasing hormone in the female rodent brain; (d) neural repair and aging; and (e) brain immune function. Another theme among these articles is that glia influence neurons via specific secreted and cell‐surface molecules, and that steroids affect this mode of communication by altering the level of glial production of these signaling molecules and/or the sensitivity of neurons to such signals. © 1999 John Wiley & Sons, Inc. J Neurobiol 40: 434–445, 1999

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CNTF and Related Neurokines

Halvorsen¹,

Kaur²

2006

Handbook of Neurochemistry and Molecular Neurobiology

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Morphological effects of ciliary neurotrophic factor treatment during neuromuscular synapse elimination

Cited by 12 publications

References 43 publications

Muscle and motor neuron ciliary neurotrophic factor receptor α together maintain adult motor neuron axons in vivo

Muscle and motor neuron ciliary neurotrophic factor receptor α together maintain adult motor neuron axons in vivo

Glia as mediators of steroid hormone action on the nervous system: An overview

CNTF and Related Neurokines

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