Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Neurotransmitter release in motor nerve terminals of a mouse model of mild <scp>s</scp>pinal <scp>m</scp>uscular <scp>a</scp>trophy

13 Mar 2013

Abstract excerpt

Spinal muscular atrophy is a genetic disease which severity depends on the amount of SMN protein, the product of the genes SMN1 and SMN2. Symptomatology goes from severe neuromuscular impairment leading to early death in infants to slow progressing motor deficits during adulthood. Much of the knowledge about the pathophysiology of SMA comes from studies using genetically engineered animal models of the disease....

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Neurogenetic and Muscular Disorders Research
Share to RNA modifications and cancer
Share to RNA Research and Splicing

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 23489475
DOI: 10.1111/joa.12038

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Neurotransmitter release in motor nerve terminals of a mouse model of mild <scp>s</scp>pinal <scp>m</scp>uscular <scp>a</scp>trophyPMID 23489475Read ↗

Altered intracellular Ca2+ homeostasis in nerve terminals of severe spinal muscular atrophy mice.Semantic proximity Read ↗

Synaptotagmin-2, and -1, linked to neurotransmission impairment and vulnerability in Spinal Muscular Atrophy.Semantic proximity Read ↗

Motor Neuron Rescue in Spinal Muscular Atrophy Mice Demonstrates That Sensory-Motor Defects Are a Consequence, Not a Cause, of Motor Neuron DysfunctionSemantic proximity Read ↗

SMN deficiency induces an early non-atrophic myopathy with alterations in the contractile and excitatory coupling machinery of skeletal myofibers in the SMNΔ7 mouse model of spinal muscular atrophySemantic proximity Read ↗

Improvement of neuromuscular synaptic phenotypes without enhanced survival and motor function in severe spinal muscular atrophy mice selectively rescued in motor neurons.Semantic proximity Read ↗

Reduced SMN protein impairs maturation of the neuromuscular junctions in mouse models of spinal muscular atrophySemantic proximity Read ↗

The spinal muscular atrophy mouse model, SMAΔ7, displays altered axonal transport without global neurofilament alterations.Semantic proximity Read ↗

SMN expression is required in motor neurons to rescue electrophysiological deficits in the SMNΔ7 mouse model of SMASemantic proximity Read ↗

At the "junction" of spinal muscular atrophy pathogenesis: the role of neuromuscular junction dysfunction in SMA disease progression.Semantic proximity Read ↗

Ciliary neurotrophic factor-induced sprouting preserves motor function in a mouse model of mild spinal muscular atrophySemantic proximity Read ↗

Selective vulnerability of motor neurons and dissociation of pre- and post-synaptic pathology at the neuromuscular junction in mouse models of spinal muscular atrophy.Semantic proximity Read ↗

Restoration of SMN to Emx-1 expressing cortical neurons is not sufficient to provide benefit to a severe mouse model of Spinal Muscular Atrophy.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.