Nodal and terminal sprouting from motor nerves in fast and slow muscles of the mouse.

Brown, Michael C.; Holland, R. L.; Ironton, R

doi:10.1113/jphysiol.1980.sp013410

Cited by 141 publications

(78 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the cat (Steinbach, 1981), interruption of the sciatic nerve in one hindlimb was followed by an increase in synaptic size in fast twitch muscles (peroneus tertius and extensor digitorum longus) but not in slow twitch muscles (soleus) situated in the contralateral intact hindlimb. A similar observation also has been made in mice (Brown et al, 1980), where after cutting the innervation to one hindlimb, there was an increase, although small, in the incidence of sprouting in the contralateral fast twitch peroneus tertius muscle but not in the slow twitch soleus muscle.…”

Section: Supernumerary Innervation Produced By Low Doses Of Colchicinesupporting

confidence: 52%

Transneuronal and peripheral mechanisms for the induction of motor neuron sprouting

Rotshenker¹

1982

J. Neurosci.

View full text Add to dashboard Cite

After injury to the nerve to one cutaneous pectoris muscle of the frog, the intact nerve to the contralateral muscle sprouts and forms additional synaptic connections with already innervated muscle fibers. It has been suggested (Rotshenker, S. (1979) J. Physiol. (Lond.) 292: 535-547; Rotshenker, S., and F. Reichert (1980) J. ) that axotomy initiates a signal for sprouting in the injured neurons that is transferred transneuronally across the spinal cord to intact motor neurons. The present study was designed to test the hypothesis that axotomy initiates the signal for sprouting by interfering with some trophic signaling between the injured neurons and denervated muscle. Colchicine therefore was applied to the nerve to the left muscles to inhibit axonal transport on whose integrity trophic interactions depend. Consequently, supernumerary innervation developed in contralateral right intact muscles much the same as after axotomy. Surprisingly, axons that were exposed to the drug also sprouted and formed synapses. Furthermore, the sprouting response of axons that were exposed to the drug also was produced in nerve fibers that were separated from their cell bodies. These results suggest two ways in which colchicine may produce sprouting and synapse formation and thereby suggest two mechanisms by which motor neurons may be induced to sprout: (a) transneuronally, by presenting growth stimuli to their cell bodies and central processes in the central nervous system and (b) by presenting growth stimuli to their peripheral extensions.

show abstract

Section: Supernumerary Innervation Produced By Low Doses Of Colchicinesupporting

confidence: 52%

Transneuronal and peripheral mechanisms for the induction of motor neuron sprouting

Rotshenker¹

1982

J. Neurosci.

View full text Add to dashboard Cite

show abstract

“…NMJs are therefore crucial structures in the intercellular signalling processes that control movement and behaviour. Degeneration of motor nerve terminals occurs rapidly after axon injury, axonal transport block or neuromuscular paralysis (Miledi and Slater, 1970;Brown et al, 1980;Hudson et al, 1984) and in early stages of motor neuron diseases, such as amyotrophic lateral sclerosis (ALS) (Fischer et al, 2004;Pun et al, 2006;David et al, 2007). Compensatory responses to such denervation include sprouting from intact neighbouring axons and regeneration of damaged axons (Brown and Ironton, 1978;Barry and Ribchester, 1995;Costanzo et al, 1999;Costanzo et al, 2000;Schaefer et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Identity, developmental restriction and reactivity of extralaminar cells capping mammalian neuromuscular junctions

Court

Gillingwater

Melrose

et al. 2008

Journal of Cell Science

View full text Add to dashboard Cite

Neuromuscular junctions (NMJs) are normally thought to comprise three major cell types: skeletal muscle fibres, motor neuron terminals and perisynaptic terminal Schwann cells. Here we studied a fourth population of junctional cells in mice and rats, revealed using a novel cytoskeletal antibody (2166). These cells lie outside the synaptic basal lamina but form caps over NMJs during postnatal development. NMJ-capping cells also bound rPH, HM-24, CD34 antibodies and cholera toxin B subunit. Bromodeoxyuridine incorporation indicated activation, proliferation and spread of NMJ-capping cells following denervation in adults, in advance of terminal Schwann cell sprouting. The NMJ-capping cell reaction coincided with expression of tenascin-C but was independent of this molecule because capping cells also dispersed after denervation in tenascin-C-null mutant mice. NMJ-capping cells also dispersed after local paralysis with botulinum toxin and in atrophic muscles of transgenic R6/2 mice. We conclude that NMJ-capping cells (proposed name `kranocytes') represent a neglected, canonical cellular constituent of neuromuscular junctions where they could play a permissive role in synaptic regeneration.

show abstract

“…However, the CNTF null mice used in the present study (Masu et al, 1993) share the C57BL/6 background of the line used by Siegel et al, and display similar motor neuron deficits (Masu et al, 1993,DeChiara et al, 1995. The discrepancy is also unlikely to be attributable to variable sprouting competence among muscles examined in the two studies (Brown et al, 1980,Prakash et al, 1999,Pun et al, 2002,De Winter et al, 2006,Burns et al, 2007, because LAL, EDL and LG muscles are all fast-twitch muscles. Its response to paralysis also suggests that LAL is, like LG, a Delayed-synapsing muscle with robust sprouting capability (Pun et al, 2002).…”

Section: Discussionmentioning

confidence: 60%

Ciliary neurotrophic factor is not required for terminal sprouting and compensatory reinnervation of neuromuscular synapses: Re-evaluation of CNTF null mice

Wright

Son

2007

Experimental Neurology

View full text Add to dashboard Cite

Loss of synaptic activity or innervation induces sprouting of intact motor nerve terminals that adds or restores nerve-muscle connectivity. Ciliary neurotrophic factor (CNTF) and terminal Schwann cells (tSCs) have been implicated as molecular and cellular mediators of the compensatory process. We wondered if the previously reported lack of terminal sprouting in CNTF null mice was due to abnormal reactivity of tSCs. To this end, we examined nerve terminal and tSC responses in CNTF null mice using experimental systems that elicited extensive sprouting in wildtype mice. Contrary to the previous report, we found that motor nerve terminals in the null mice sprout extensively in response to major sprouting-stimuli such as exogenously applied CNTF per se, botulinum toxinelicited paralysis, and partial denervation by L4 spinal root transection. In addition, the number, length and growth patterns of terminal sprouts, and the extent of reinnervation by terminal or nodal sprouts, were similar in wildtype and null mice. tSCs in the null mice were also reactive to the sprouting-stimuli, elaborating cellular processes that accompanied terminal sprouts or guided reinnervation of denervated muscle fibers. Lastly, CNTF was absent in quiescent tSCs in intact, wildtype muscles and little if any was detected in reactive tSCs in denervated muscles. Thus, CNTF is not required for induction of nerve terminal sprouting, for reactivation of tSCs, and for compensatory reinnervation after nerve injury. We interpret these results to support the notion that compensatory sprouting in adult muscles is induced primarily by contact-mediated mechanisms, rather than by diffusible factors.

show abstract

Nodal and terminal sprouting from motor nerves in fast and slow muscles of the mouse.

Cited by 141 publications

References 22 publications

Transneuronal and peripheral mechanisms for the induction of motor neuron sprouting

Transneuronal and peripheral mechanisms for the induction of motor neuron sprouting

Identity, developmental restriction and reactivity of extralaminar cells capping mammalian neuromuscular junctions

Ciliary neurotrophic factor is not required for terminal sprouting and compensatory reinnervation of neuromuscular synapses: Re-evaluation of CNTF null mice

Contact Info

Product

Resources

About