Percutaneous Application of Galvanic Current in Rodents Reverses Signs of Myofascial Trigger Points

An increase in the spontaneous release of acetylcholine (ACh) at the motor endplate is directly related to the generation of myofascial trigger points (MTrPs). In this study, percutaneous electric fields were applied to an animal model of MTrPs with high levels of spontaneous ACh release. All experiments were performed on Swiss mice and Sprague Dawley rats. For evaluating the spontaneous neurotransmission, intracellular recordings were performed, and the frequency of miniature endplate potentials was evaluated. Electromyographic recordings were also conducted to evaluate the endplate noise. Finally, the number and strength of local twitch responses (LTR) were evaluated using ultrasound recordings. The protocols used for the electric currents were 0.4 mA for five seconds and four repetitions (protocol 1), 1.5 mA for five seconds and three repetitions (protocol 2), and 3 mA for three seconds and three repetitions (protocol 3). After a subcutaneous injection of neostigmine (NTG), a great increase was observed in the frequency of mEPPs, together with an elevated endplate noise. Protocols 2 and 3 were the most effective. Protocol 3 could completely reverse the action of NTG at both three hours and 24 hours, respectively. The application of percutaneous currents produced both an increase in the number (144%) and in the speed (230% faster) of LTR compared with dry needling. In conclusion, higher doses of electrical current are more effective for decreasing MTrPs findings in an animal model.

The Mechanism of Choline-Mediated Inhibition of Acetylcholine Release in Mouse Motor Synapses

The mechanism of action of tonically applied choline, the agonist of 7 nicotinic acetylcholine receptors (nAChRs), to the spontaneous and evoked release of a neurotransmitter in mouse motor synapses in diaphragm neuromuscular preparations using intracellular microelectrode recordings of miniature endplate potentials (MEPPs) and evoked endplate potentials (EPPs) was studied. Exogenous choline was shown to exhibit a presynaptic inhibitory effect on the amplitude and quantal content of EPPs for the activity of neuromuscular junction evoked by single and rhythmic stimuli. This effect was inhibited either by antagonists of 7-nAChRs, such as methyllycaconitine and -cobratoxin, or by blocking SK-type calcium-activated potassium (K Ca) channels with apamin or blocking intraterminal ryanodine receptors with ryanodine. A hypothesis was put forward that choline in mouse motoneuron nerve terminals can activate presynaptic 7-nAChRs, followed by the release of the stored calcium through ryanodine receptors and activation of SK-type KCa channels, resulting in sustained decay of the quantal content of the evoked neurotransmitter release.

shocked Gene Is Required for the Function of a Premotor Network in the Zebrafish CNS

The analysis of behavioral mutations in zebrafish can be a powerful strategy for identifying genes that regulate the function and development of neural circuits in the vertebrate CNS. A neurophysiological analysis of the shocked ( sho) mutation that affects the initiation of swimming after mechanosensory stimulation was undertaken to identify the function of the sho gene product in the developing motor circuitry. The cutaneous Rohon-Beard (RB) mechanosensory neurons responded normally to stimulation, and muscle fibers were unaffected in sho embryos, suggesting that the output of the CNS is abnormal. Indeed whole cell patch recordings from mutant muscle cells showed normal spontaneous miniature endplate potentials, but abnormal touch-evoked endplate potentials. Furthermore, motor neuron recordings showed that bursts of rhythmic action potentials from synaptically dependent depolarizations are initiated in wild-type motor neurons after sensory stimulation or bath application of N-methyl-d-aspartate. These bursts presumably correspond to bouts of swimming. In sho motor neurons, the touch-evoked depolarizations were not sustained, resulting in an abbreviated burst of action potentials. The defective responses were not due to any obvious defect in sho motor neurons because their basic properties were normal. These results suggest that in sho embryos, there is aberrant motor processing within the CNS and that normal motor processing requires the sho gene product.

Effect of Hypertonicity on Augmentation and Potentiation and on Corresponding Quantal Parameters of Transmitter Release

Effect of hypertonicity on augmentation and potentiation and on corresponding quantal parameters of transmitter release. Augmentation and (posttetanic) potentiation are two of the four components comprising the enhanced release of transmitter following repetitive nerve stimulation. To examine the quantal basis of these components under isotonic and hypertonic conditions, we recorded miniature endplate potentials (MEPPs) from isolated frog ( Rana pipiens) cutaneous pectoris muscles, before and after repetitive nerve stimulation (40 s at 80 Hz). Continuous recordings were made in low Ca2+ high Mg2+ isotonic Ringer solution, in Ringer that was made hypertonic with 100 mM sucrose, and in wash solution. Estimates were obtained of m (no. of quanta released), n (no. of functional release sites), p (mean probability of release), and vars p (spatial variance in p), using a method that employed MEPP counts. Hypertonicity abolished augmentation without affecting potentiation. There were prolonged poststimulation increases in m, n,and p and a marked but transient increase in vars p in the hypertonic solution. All effects were completely reversed with wash. The time constants of decay for potentiation and for vars p were virtually identical. The results are consistent with the notion that augmentation is caused by Ca2+ influx through voltage-gated calcium channels and that potentiation is due to Na+-induced Ca2+ release from mitochondria. The results also demonstrate the utility of this approach for analyzing the dynamics of quantal transmitter release.