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alpha bungarotoxin antibody

RRID:AB_2313931

Antibody ID

AB_2313931

Target Antigen

Proper Citation

(Molecular Probes Cat# T1175, RRID:AB_2313931)

Clonality

unknown

Comments

Discontinued; This product offered by Molecular Probes (Invitrogen), now part of Thermo Fisher

Vendor

Molecular Probes

Cat Num

T1175 also T1175

Publications that use this research resource

Synaptic Activity and Muscle Contraction Increases PDK1 and PKCβI Phosphorylation in the Presynaptic Membrane of the Neuromuscular Junction.

  • Hurtado E
  • Front Mol Neurosci
  • 2017 Sep 11

Literature context:


Abstract:

Conventional protein kinase C βI (cPKCβI) is a conventional protein kinase C (PKC) isoform directly involved in the regulation of neurotransmitter release in the neuromuscular junction (NMJ). It is located exclusively at the nerve terminal and both synaptic activity and muscle contraction modulate its protein levels and phosphorylation. cPKCβI molecular maturation includes a series of phosphorylation steps, the first of which is mediated by phosphoinositide-dependent kinase 1 (PDK1). Here, we sought to localize PDK1 in the NMJ and investigate the hypothesis that synaptic activity and muscle contraction regulate in parallel PDK1 and cPKCβI phosphorylation in the membrane fraction. To differentiate the presynaptic and postsynaptic activities, we abolished muscle contraction with μ-conotoxin GIIIB (μ-CgTx-GIIIB) in some experiments before stimulation of the phrenic nerve (1 Hz, 30 min). Then, we analyzed total and membrane/cytosol fractions of skeletal muscle by Western blotting. Results showed that PDK1 is located exclusively in the nerve terminal of the NMJ. After nerve stimulation with and without coincident muscle contraction, total PDK1 and phosphorylated PDK1 (pPDK1) protein levels remained unaltered. However, synaptic activity specifically enhanced phosphorylation of PDK1 in the membrane, an important subcellular location for PDK1 function. This increase in pPDK1 coincides with a significant increase in the phosphorylation of its substrate cPKCβI also in the membrane fraction. Moreover, muscle contraction maintains PDK1 and pPDK1 but increases cPKCβI protein levels and its phosphorylation. Thus, even though PDK1 activity is maintained, pcPKCβI levels increase in concordance with total cPKCβI. Together, these results indicate that neuromuscular activity could induce the membrane targeting of pPDK1 in the nerve terminal of the NMJ to promote the phosphorylation of the cPKCβI, which is involved in ACh release.

Genetic specification of left-right asymmetry in the diaphragm muscles and their motor innervation.

  • Charoy C
  • Elife
  • 2017 Jun 22

Literature context:


Abstract:

The diaphragm muscle is essential for breathing in mammals. Its asymmetric elevation during contraction correlates with morphological features suggestive of inherent left-right (L/R) asymmetry. Whether this asymmetry is due to L versus R differences in the muscle or in the phrenic nerve activity is unknown. Here, we have combined the analysis of genetically modified mouse models with transcriptomic analysis to show that both the diaphragm muscle and phrenic nerves have asymmetries, which can be established independently of each other during early embryogenesis in pathway instructed by Nodal, a morphogen that also conveys asymmetry in other organs. We further found that phrenic motoneurons receive an early L/R genetic imprint, with L versus R differences both in Slit/Robo signaling and MMP2 activity and in the contribution of both pathways to establish phrenic nerve asymmetry. Our study therefore demonstrates L-R imprinting of spinal motoneurons and describes how L/R modulation of axon guidance signaling helps to match neural circuit formation to organ asymmetry.

Funding information:
  • NIDCD NIH HHS - R01 DC009410()

Glycoprotein nonmetastatic melanoma protein B ameliorates skeletal muscle lesions in a SOD1G93A mouse model of amyotrophic lateral sclerosis.

  • Nagahara Y
  • J. Neurosci. Res.
  • 2015 Oct 20

Literature context:


Abstract:

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive loss of motor neurons and subsequent muscular atrophy. The quality of life of patients with ALS is significantly improved by ameliorating muscular symptoms. We previously reported that glycoprotein nonmetastatic melanoma protein B (GPNMB; osteoactivin) might serve as a target for ALS therapy. In the present study, superoxide dismutase 1/glycine residue 93 changed to alanine (SOD1(G93A) ) transgenic mice were used as a model of ALS. Expression of the C-terminal fragment of GPNMB was increased in the skeletal muscles of SOD1(G93A) mice and patients with sporadic ALS. SOD1(G93A) /GPNMB transgenic mice were generated to determine whether GPNMB expression ameliorates muscular symptoms. The weight and cross-sectional area of the gastrocnemius muscle, number and cross-sectional area of myofibers, and denervation of neuromuscular junctions were ameliorated in SOD1(G93A) /GPNMB vs. SOD1(G93A) mice. Furthermore, direct injection of a GPNMB expression plasmid into the gastrocnemius muscle of SOD1(G93A) mice increased the numbers of myofibers and prevented myofiber atrophy. These findings suggest that GPNMB directly affects skeletal muscle and prevents muscular pathology in SOD1(G93A) mice and may therefore serve as a target for therapy of ALS.

Funding information:
  • Intramural NIH HHS - (United States)
  • NCRR NIH HHS - S10 RR023540(United States)

A novel and robust conditioning lesion induced by ethidium bromide.

  • Hollis ER
  • Exp. Neurol.
  • 2015 Mar 2

Literature context:


Abstract:

Molecular and cellular mechanisms underlying the peripheral conditioning lesion remain unsolved. We show here that injection of a chemical demyelinating agent, ethidium bromide, into the sciatic nerve induces a similar set of regeneration-associated genes and promotes a 2.7-fold greater extent of sensory axon regeneration in the spinal cord than sciatic nerve crush. We found that more severe peripheral demyelination correlates with more severe functional and electrophysiological deficits, but more robust central regeneration. Ethidium bromide injection does not activate macrophages at the demyelinated sciatic nerve site, as observed after nerve crush, but briefly activates macrophages in the dorsal root ganglion. This study provides a new method for investigating the underlying mechanisms of the conditioning response and suggests that loss of the peripheral myelin may be a major signal to change the intrinsic growth state of adult sensory neurons and promote regeneration.

Funding information:
  • NINDS NIH HHS - 1F31NS084706-01(United States)

Paralysis elicited by spinal cord injury evokes selective disassembly of neuromuscular synapses with and without terminal sprouting in ankle flexors of the adult rat.

  • Burns AS
  • J. Comp. Neurol.
  • 2007 Jan 1

Literature context:


Abstract:

Neuromuscular junctions (NMJs) innervated by motor neurons below spinal cord injury (SCI) have been reported to remain intact despite the interruption of supraspinal pathways and the resultant loss of activity. Here we report notably heterogeneous NMJ responses to SCI that include overt synapse disassembly. Complete transection of the thoracic spinal cord of adult rats evoked massive sprouting of nerve terminals in a subset of NMJs in ankle flexors, extensor digitorum longus, and tibialis anterior. Many of these synapses were extensively disassembled 2 weeks after spinal transection but by 2 months had reestablished synaptic organization despite continuous sprouting of their nerve terminals. In contrast, uniform and persistent loss of acetylcholine receptors (AChRs) was evident in another subset of NMJs in the same flexors, which apparently lacked terminal sprouting and largely maintained terminal arbors. Other synapses in the flexors, and almost all the synapses in the ankle extensors, medial gastrocnemius, and soleus, remained intact, with little pre- or postsynaptic alteration. Additional deafferentation of the transected animals did not alter the incidence or regional distribution of either type of the unstable synapses, whereas cycling exercise diminished their incidence. The muscle- and synapse-specific responses of NMJs therefore reflected differential sensitivity of the NMJs to inactivity rather than to differences in residual activity. These observations demonstrate the existence of multiple subpopulations of NMJs that differ distinctly in pre- and postsynaptic vulnerability to the loss of activity and highlight the anatomical instability of NMJs caudal to SCI, which may influence motor deficit and recovery after SCI.

Funding information:
  • Canadian Institutes of Health Research - 1R01GM084875(Canada)