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R Bournaud

Publications and source records attributed to R Bournaud.

27 records · Page 2Linked to original sources
PubMed1987

Potassium channel blockers and impulse propagation in murine motor endplate disease.

An electrophysiologic study has been performed on motor nerves of mice affected with hereditary "motor endplate disease" (MED). Bath application of potassium channel blockers, such as tetraethylammonium and 3,4-diaminopyridine, which are almost without effect on the monophasic compound action potential of normal nerves, considerably enhanced the action potential duration in nerves from mutant mice. Furthermore, external current recordings from motor endings revealed an absence of the K-dependent waveform component in MED mice, which indicates a similar K current intensity in the terminal part of the endings and in the heminode. These observations suggest that in the mutant, unlike in normal mice, K channels play a role in action potential electrogenesis. Possible relationships with paranodal dysmyelination are discussed.

4-Aminopyridine↗
PubMed1987

An electrophysiological study of skeletal muscle fibres in the 'muscular dysgenesis' mutation of the mouse.

Experiments were performed on muscles of 18-19 day mice fetuses affected with muscular dysgenesis (mdg). Action potentials generated by electrical stimulation or potassium depolarization failed to trigger muscle contraction in mdg muscle fibres. By contrast, muscle contraction could be obtained by caffeine (15 mM) and, to a lesser degree, by nerve stimulation. We conclude that a defect in excitation-contraction (E-C) coupling is the cause of muscle paralysis. An early after potential (EAP) was present in the decay phase of the action potential and a potential 'creep' occurred in response to hyperpolarizing current pulses which can be taken as evidence for the presence of T-tubules in mdg muscle fibres. Data obtained from square pulse analysis and EAP measurements indicate larger input impedance and membrane time constant in mdg as compared to controls, which contrasts with similar surface membrane time constant (as estimated from the foot of the action potential) in both types of muscle. The excitability of the T-tubule system was tested by recording action potentials at early stages of TTX (5 X 10(-7) M) perfusion or washout in mdg and control muscles. In both cases, the action potentials decreased in amplitude and rate of rise and displayed two peaks, the second of which was suppressed by detubulation using the formamide treatment. This indicates action potential generation in the T-tubule membrane of mdg muscles. In all the impaled muscle fibers, nerve stimulation evoked epps which were accompanied by a weak local contraction in relation with Ca2+ influx through postsynaptic channels.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1982

Electrophysiological and morphological studies of a motor nerve in 'motor endplate disease' of the mouse.

Motor nerves of mice affected with hereditary 'motor endplate disease' were examined by means of electrophysiological and morphological techniques. Conduction velocity was slower, the refractory period was prolonged and the temperature sensitivity higher in mutants as compared to controls of the same age. Most of the axons examined in the electron microscope showed signs of paranodal demyelination. The relationship between the morphological and the electrophysiological findings is discussed. We conclude that alterations in the motor axons can account for the failures in neuromuscular transmission described previously in the med mutation.

Animals↗
PubMed1981

Advantages of the triangularis sterni muscle of the mouse for investigations of synaptic phenomena.

The triangularis sterni muscle (TS) of the mouse is a thin trapezoidal sheet of fibres in which individual neuromuscular junctions are easily observed with Nomarski optics. Thus, microelectrodes are readily positioned to accurately record various synaptic phenomena. For example, miniature end-plate currents were easily recorded with a focally positioned extracellular electrode and the end-plate sensitivity to acetylcholine averaged 2062 mV/nC. In addition, the intercostal nerves segmentally innervate the TS. Electrophysiologic and histologic analysis showed that each nerve innervates a sharply defined territory of the muscle surface. These preliminary observations suggest that the TS may be ideal for studies of synaptic function and the processes underlying synapse stabilization in the mammal.

Acetylcholine↗
PubMed1977

[Variation of the time constant (tau) of the decay of end-plate current during focalized transmitter release].

The variations of the time constant tau of the end-plate current (epc) have been studied at the clamped neuromuscular junction of the frog while transmitter release was focalised by local iontophoretic application of Ca++. In the absence of any anticholinesterasic drug, tau varies according to the variations of the intensity of epc (Iepc) due to pre or postsynaptic experimental procedure. It is suggested that focalisation of transmitter release induces local acetylcholinesterase inhibition by an excess of substrate; then the transmitter life time in the synaptic cleft is momentarily increased, allowing repeated binding of Ach to postsynaptic receptors.

Acetylcholinesterase↗
PubMedDate not supplied

cAMP-dependent modulation of L-type calcium currents in mouse diaphragmatic cells.

The regulation of calcium channels by cAMP-dependent phosphorylation was investigated in the diaphragm muscle. Experiments were performed on dissociated costal diaphragmatic cells from 16- to 17-day-old fetal mice. The ionic current through calcium channels was measured using the whole cell clamp technique with barium as the charge carrier. A depolarizing pulse delivered from a holding potential of -80 mV elicited a low-threshold dihydropyridine (DHP)-insensitive T-type current and a high-threshold DHP-sensitive L-type current. Agents that either increase intracellular cAMP levels (forskolin, 10(-4) M, and dibutyryladenosine 3'-5' cyclic monophosphate, 10(-4) M) or inhibit cAMP degradation (theophylline, 10(-4) M) produced relative increases in L-type current amplitude of 24.4 +/- 13.8%, 13.4 +/- 4.6%, and 15.9 +/- 2.8% (p < 0.05), respectively. Current intensity increased after application of the beta-adrenergic agonist isoproterenol (10(-5) M, 16.5 +/- 3.6%, P < 0.005). None of these agents affected the T-type current. These results suggest that L-type calcium channel activities of the diaphragm muscle are regulated by cAMP-dependent phosphorylation.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMedDate not supplied

Restoration of dysgenic muscle contraction and calcium channel function by co-culture with normal spinal cord neurons.

Muscular dysgenesis (mdg) is a spontaneous recessive lethal mutation in the mouse. The disease is characterized by a total lack of excitation-contraction coupling in embryonic skeletal muscle. This developmental abnormality is associated with a drastic deficiency in the expression of voltage-sensitive Ca2+ channels in skeletal muscle without alteration of the properties of voltage-sensitive Na+ channels or of voltage-sensitive Ca2+ channels in cardiac and neuronal cells. Membrane couplings between sarcoplasmic reticulum and the transverse tubules, known as triads, were also found to be drastically altered in embryonic muscle of the homozygous mutant (mdg/mdg). Triads in the mdg/mdg muscle were less numerous, disorganized and lacked spaced densities. This paper shows that co-culture of mdg/mdg myotubes with normal spinal cord neurons re-establishes Ca2+ channel activity, contraction and normal triad organization. The decrease thus cannot be due to a mutation of the Ca2+ channel as previously suggested. Normal nerve cells may supply an essential factor to mutant muscle cells.

Animals↗