Interferon-alpha, beta and tumor necrosis factor-alpha enhance the frequency of miniature end-plate potentials at rat neuromuscular junction.

The effects of the two cytokines, rat interferon-alpha, beta and human tumor necrosis factor-alpha, were studied at the rat neuromuscular junction by using classical electrophysiological techniques. Both cytokines in a similar way at concentrations of 2,000 and 35,000 U/ml, respectively, increased transiently and with a relatively long delay (15 to 25 min) the frequency of miniature endplate potentials. The observed effects may be related to complex second messenger mechanisms and contribute to modulation and plasticity of neurotransmission.

Blockage of nicotinic acetylcholine receptors by 5-hydroxytryptamine.

The action of 5-hydroxytryptamine (5HT) on nicotinic acetylcholine receptor (nAChR) channels was investigated in mouse myotubes, human cloned TE671/RD cells, and Xenopus laevis oocytes. The decay of the ACh-activated whole-cell currents was reversibly accelerated in the presence of 5HT (10(-5) to 10(-3) M), in a dose-dependent manner. 5HT also reduced the size and accelerated the decay of currents elicited by ACh in Xenopus oocytes injected with mRNA extracted from C2 myotubes or Torpedo electroplaques, or oocytes injected with cloned mouse muscle AChR subunit mRNAs.

Interleukin-2 lengthens extrajunctional acetylcholine receptor channel open time in mammalian muscle cells.

The effect of interleukin-2 (rIL-2) on nicotinic acetylcholine receptors (nAChR) was examined on cultured muscle fibres isolated from the flexor digitorum brevis muscle (FDB) of the rat and on aneural mouse cultured C2 myotubes. Intracellular measurement of the sensitivity to iontophoretically applied ACh demonstrated that the sensitivity of the extrajunctional nAChRs in cultured fibres showed a transient increase after application of rIL-2 (2,000-3,000 units/ml). Cell-attached patch-clamp experiments on the same fibres proved that rIL-2 (2,000 units/ml) induces a significant increase in the mean open time of the extrajunctional nAChR channel.

Effect of calcitonin gene-related peptide on synaptic transmission at the neuromuscular junction of the frog.

The effects of calcitonin gene-related peptide (CGRP) on synaptic mechanisms were studied at the frog neuromuscular junction by using classical electrophysiological techniques. CGRP reduced the quantal content of evoked neurotransmitter release, as well as the sensitivity of postsynaptic nicotinic acetylcholine receptors (AChRs). No effect on the frequency of the miniature end-plate potentials or on the desensitization of the AChRs could be observed.