Effects Of Paired-pulse Stimulation Research Articles

The Virtual Electrode Recording Tool for EXtracellular Potentials (VERTEX) Version 2.0: Modelling in vitro electrical stimulation of brain tissue

Neuronal circuits can be modelled in detail allowing us to predict the effects of stimulation on individual neurons. Electrical stimulation of neuronal circuits in vitro and in vivo excites a range of neurons within the tissue and measurements of neural activity, e.g the local field potential (LFP), are again an aggregate of a large pool of cells. The previous version of our Virtual Electrode Recording Tool for EXtracellular Potentials (VERTEX) allowed for the simulation of the LFP generated by a patch of brain tissue. Here, we extend VERTEX to simulate the effect of electrical stimulation through a focal electric field. We observe both direct changes in neural activity and changes in synaptic plasticity. Testing our software in a model of a rat neocortical slice, we determine the currents contributing to the LFP, the effects of paired pulse stimulation to induce short term plasticity (STP), and the effect of theta burst stimulation (TBS) to induce long term potentiation (LTP).

The Virtual Electrode Recording Tool for EXtracellular Potentials (VERTEX) Version 2.0: Modelling in vitro electrical stimulation of brain tissue.

Neuronal circuits can be modelled in detail allowing us to predict the effects of stimulation on individual neurons. Electrical stimulation of neuronal circuits in vitro and in vivo excites a range of neurons within the tissue and measurements of neural activity, e.g the local field potential (LFP), are again an aggregate of a large pool of cells. The previous version of our Virtual Electrode Recording Tool for EXtracellular Potentials (VERTEX) allowed for the simulation of the LFP generated by a patch of brain tissue. Here, we extend VERTEX to simulate the effect of electrical stimulation through a focal electric field. We observe both direct changes in neural activity and changes in synaptic plasticity. Testing our software in a model of a rat neocortical slice, we determine the currents contributing to the LFP, the effects of paired pulse stimulation to induce short term plasticity (STP), and the effect of theta burst stimulation (TBS) to induce long term potentiation (LTP).

Increased intracortical inhibition in middle-aged humans; a study using paired-pulse transcranial magnetic stimulation

Using single and paired-pulse transcranial magnetic stimulation we compared the cortical excitability in two different age groups of healthy subjects (mean±SD age: 28.5±5.2 vs. 56.1±4.9 years). Motor evoked potentials were recorded from right extensor and flexor carpi radialis muscles. The effect of paired-pulse stimulation was assessed by the ratio conditioned/unconditioned response area with interstimulus intervals of 3 and 13 ms to test for intracortical inhibition and facilitation, respectively. To test the influence of sensory input the experiments were conducted without and with vibration of the extensor carpi radialis muscle. The intracortical inhibition was significantly greater in older subjects; however, during muscle vibration this difference between the two groups vanished. The different effect of vibration favors compensatory mechanisms to be responsible for a different paired-pulse excitability in middle-aged subjects.

Repletion of sarcoplasmic reticulum Ca after ryanodine in rat ventricular myocytes.

The ryanodine (R)-induced loss of sarcoplasmic reticulum (SR) Ca2+ and the abilities of the SR to accumulate Ca2+ and participate in contractile activation after R were studied in rat ventricular myocytes. Indo 1 fluorescence (IF) indexed cytosolic Ca2+, and caffeine assayed SR Ca2+. Before R, there was a negative staircase, and the SR accumulated Ca2+ at rest. During stimulation (0.5 Hz), R decreased IF and contraction, converting the negative staircase to positive. When R was pulsed onto resting cells, IF increased and cells shortened, subsequently behaving as if stimulated in R. After R, there was no caffeine-releasable Ca2+ at rest, and little accumulated during 0.5-Hz stimulation. At high rates, caffeine-releasable Ca2+ and diastolic IF increased. In isoproterenol and R, IF transients and contractions recovered at 0.5 Hz with a marked positive staircase and little diastolic IF increase. Within 10 beats, SR Ca2+ accumulated to pre-R levels. R eliminated the positive inotropic effect of paired-pulse stimulation, but isoproterenol temporarily restored it. Twitch contractions in thapsigargin, an SR Ca2+ pump blocker, and isoproterenol were slow compared with control or R + isoproterenol. R leaks SR Ca2+ into the cytosol. SR Ca2+ can be repleted in R by high-rate stimulation or by low-rate stimulation with a beta-adrenergic agonist. SR Ca2+ release in R can be temporarily restored if Ca2+ influx and SR Ca2+ pumping are increased enough to overcome the SR Ca2+ leak.

The relationship between action potential duration and force of contraction in rat myocardium.

Intracellular action potentials and peak force (F) of isometric contractions were recorded from ventricular trabeculae of adult rats at 26 degrees C. The duration of the action potentials was measured at 50% of the amplitude (APD50) and at 10% of the amplitude (APD10). The effect of a variety of experimental interventions on the three variables was studied. APD50 reflects the duration of the plateau phase which is typically about 30 ms in rat myocardium. APD10 reflects the sum of the duration of the plateau phase and of the slow final repolarization phase (phase 3') and is about 80 ms. During paired-pulse stimulation, strong contractions coincided with shortened APD50 and prolonged APD10, i.e. a negative APD50-F and a positive APD10-F relationship was obtained. Addition of Sr2+ to the medium caused an increase of F and prolongation of APD50 and APD10. Nifedipine caused a decrease of F and a shortening of APD50 and APD10. Substitution of extracellular NaCl by LiCl caused an increase of F but a shortening of APD50 and APD10. An increase of [Ca2+]o caused an increase of F whereas APD50 was almost constant and APD10 increased. A simple model is proposed which explains the results, assuming that: the effect of paired-pulse stimulation is related to time dependent intracellular Ca2+ transport; Sr2+ and nifedipine act mainly on isi; NaCl substitution inhibits Na+/Ca2+ exchange; and [Ca2+]o affects both isi and Na+/Ca2+ exchange.

The contractile state of cat and dog heart in relation to the interval between beats.

We induced atrioventricular dissociation and initiated ventricular pacing in intact dogs and isolated cat hearts. Left ventricular pressure, its time derivative (dP/t), and action potentials were recorded. When a test pulse was introduced at varying intervals after a period of steady pacing, an optimum contractile response was obtained at an average interval of 720 msec. A similar optimum interval was obtained after pacing at various frequencies and after paired pulse stimulation but was shortened to 560 msec after infusion of epinephrine. The magnitude of the optimum contractile response increased with an increase in the frequency of prior pacing which was accompanied by an increase in the time the cell membrane was depolarized. The optimum contractile response following paired pulse stimulation was greater than that following regular pacing, with the same number of stimuli per minute and the same time of membrane depolarization. The results are explicable in terms of intracellular calcium ion recirculation with separate compartments for release to and uptake from the contractile proteins. A negative feedback control of Ca2+ inflow to the cell by intracellular Ca2+ content is postulated to explain the effect of paired pulse stimulation and shortening of action potential duration following an increase in regular pacing frequency.

Effect of ventricular pacing (paired and single) on coronary hemodynamics and myocardial contractility.

The effect of paired pulse stimulation (PPS) and single pulse stimulation (SPS) at different rates on coronary hemodynamics was studied in 16 open chest right heart bypass dogs. Intrinsic rate was con

Hemodynamic effects of paired-pulse stimulation in normal and brisket-disease calves.

Hemodynamic effects of paired-pulse stimulation in normal and brisket-disease calves.