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PubMed1985

Anemonia sulcata toxin (ATX II) enhances spontaneous electrical activity and tension in chronically denervated rat diaphragm.

In isolated strips of rat diaphragm denervated 9-21 days prior to experimentation, spontaneous action potentials were recorded extracellularly and twitch and resting tension were measured. The sea anemone toxin ATX II enhances the occurrence of spontaneous action potentials, increases resting tension and depresses twitch tension. These effects are essentially irreversible. In low sodium solution substituted with sucrose the effects of ATX II are attenuated, however, they fully develop upon return to normal sodium solution with a marked transient increase in the incidence of spontaneous action potentials and in resting tension. ATX II remains uneffective after pretreatment with tetrodotoxin. Reelevation of the extracellular sodium concentration after exposure to low sodium solution per se causes a marked increase in occurrence of fibrillation potentials, however the transient increase in resting tension was much smaller than in the presence of ATX II. Substitution of chloride with the impermeable anion methylsulphate enhances spontaneous activity and resting tension without an effect on twitch tension. Addition of ATX II elevates resting tension although the concomitant further increase in incidence of spontaneous action potentials is small. It is concluded that the increase in resting tension reflects a summation of the fibrillatory activity, but fibrillations become more effective when the preparations are exposed to ATX II. This finding points at the possible rôle of sodium ions in excitation contraction coupling of denervated skeletal muscle.

Action Potentials↗
PubMed1989

[Chronic spinal amyotrophy involving the upper limbs in young adults (O'Sullivan and McLeod syndrome). MRI study of the cervical spinal cord].

In 5 cases of sporadic spinal muscular atrophy in young adults the muscular atrophy was localized in the hands and forearms. Age at onset ranged from 7 to 20 years. The duration of the disease was less than 5 years in 3 patients and more than 15 years in 2. Electromyography showed neurogenic anomalies in all wasted muscles, denervation potentials being also present in the proximal muscles of the upper limbs and distal muscles of the lower limbs in 2 patients. Motor nerve conduction velocity and sensory nerve action potentials were normal. Advantages of a topographic classification of the distal form of chronic spinal muscular atrophy are discussed. Spinal cord MRI was performed in 4 patients with a 0.5 Tesla superconducting magnet using surface coils, using a T1-weighted spin-echo technique (ET 26 ms; RT 500 ms) and a T2-weighted spin-echo technique (ET 90, 180 ms; 2,000 ms). With the T1 technique, axial MRI sections 7 to 9 mm thick of spinal cord showed a normal image between C1 and C4, and a flattened image between C5 and T1. This was considered as a possible spinal cord segmental atrophy.

Adolescent↗
PubMed1995

Neuroprotective effect of basic fibroblast growth factor on wobbler mouse motor neuron disease.

Basic fibroblast growth factor (bFGF) possesses neuroprotective effects on a variety of neurons. Here we report that it delays progression of motor neuron disease (MND) in the wobbler mouse. After initial diagnosis of MND at post-natal age 3-4 weeks, wobbler mice receive either recombinant human bFGF (1 mg kg-1, n = 10) or vehicle (n = 10), daily for weeks by subcutaneous injection in a blind fashion. We performed symptomatic and neuropathological assessments in both groups. The treatment was fulfilled at 7-8 weeks of age. In comparison with vehicle, bFGF treatment potentiated grip strength (p < 0.008), attenuated forelimb contracture (p < 0.003), and increased weight of the biceps muscle (p < 0.008). bFGF-treated mice retarded denervation muscle atrophy (p < 0.001) and degeneration of spinal motoneurons (p < 0.001). Our study shows that bFGF treatment is beneficial in a murine MND model. We provide a rationale that bFGF may have therapeutic potential in peripheral motor neuropathy or MND.

Animals↗