Search

Firing pattern of skeletomotor neurones innervating triceps surae muscles in response to pseudorandom muscle stretching and white noise modulated transmembrane current stimulation was investigated in decerebrate cats. Pseudo-random muscle stretching (upper cut-off frequency 60 Hz, amplitude ? (standard deviation) ranging from 18.5 μm to 40 μm) was applied to triceps surae muscles. Membrane potential changes and action potentials of skeletomotor neurones were recorded intracellularly. White noise modulated current was applied through the same (recording) microelectrode. Sequences of ten identical 5 s periods of either muscle stretching or transmembrane current stimulation were applied. Skeletomotor neurones belonging to slow motor units (rheobase less than 8.5 nA) generated action potentials in response to both pseudo-random muscle stretching and transmembrane current stimulation, while firing threshold of those belonging to fast motor units could not be reached by the muscle stretches applied. Peri-spike averaging of muscle length and injected current records showed that the action potentials appeared at the peak of either depolarizing current wave or muscle stretching both preceded by a change in opposite direction (the spikes coinciding with the peak in muscle length PSA being actually elicited by muscle spindle action potentials triggered at the moment of the peak stretching velocity). Time coupling of action potentials occurred during both muscle stretching and transmembrane stimulation, being more tight in the latter case as well as when larger amplitudes of the stimuli were applied. It is supposed that discharges from muscle spindle primary endings phase-locked to small pseudo-random muscle length changes may, due to the time coupling of skeletomotor action potentials, provoke a synchronous firing of skeletomotor neurones, mostly of those belonging to slow motor units. Possible effects of such a firing pattern on the resulting muscle reflex contraction and the stretch reflex stability as well as a possibility of it being provoked by fusimotor discharges are discussed.

Stimulation-induced plasticity represents an experimental model of motor cortex reorganization. It can be produced in awaked humans by combining the non-invasive electrical stimulation of somatosensory afferents via mixed peripheral nerves with the transcranial magnetic stimulation (TMS) of the motor cortex. Animal experiments indicate that an application of two converging inputs from various sources in a tightly coupled manner, following the so called Hebbian rule of learning, leads to an increase in motor cortical excitability. The aim of our study was to compare the effects of two plasticity-inducing protocols by quantifying the motor cortex changes using TMS. Plasticity was induced by combining peripheral nerve stimulation with TMS (paired associative stimulation - PAS) and by peripheral motor point stimulation of two adjacent hand muscles (dual associative stimulation - DAS). The protocols were randomly applied in 12 right-handed healthy volunteers. The amplitudes of TMS-induced motor-evoked potentials (MEPs) in the right abductor pollicis brevis muscle were recorded before, immediately after PAS or DAS stimulation, and 10, 20 and 30 min later. Both protocols led to significant and lasting changes in MEP amplitudes, however, a significantly larger increase in MEPs was observed after PAS than DAS. The results indicate that afferent input can differently affect cortical motor circuits and produce variable motor output. Thus, the efficacy of LTP-like mechanisms, presumably involved in Hebbian-like plasticity in humans, varies with the types/origin of the converging inputs. Our findings may be relevant when designing therapeutic interventions for improving motor function after neurological injury or disease.

Diabetes mellitus is associated with a variety of cardiovascular complications including impaired cardiac muscle function. The effects of insulin treatment on heart rate, body temperature and physical activity in the alloxan (ALX)-induced diabetic rat were investigated using in vivo biotelemetry techniques. The electrocardiogram, physical activity and body temperature were recorded in vivo with a biotelemetry system for 10 days before ALX treatment, for 20 days following administration of ALX (120 mg/kg) and thereafter, for 15 days whilst rats received daily insulin. Heart rate declined rapidly after administration of ALX. Pre-ALX heart rate was 321±9 beats per minute, falling to 285±12 beats per minute 15-20 days after ALX and recovering to 331±10 beats per minute 5-10 days after commencement of insulin. Heart rate variability declined and PQ, QRS and QT intervals were prolonged after administration of ALX. Physical activity and body temperature declined after administration of ALX. Pre-ALX body temperature was 37.6±0.1 °C, falling to 37.3±0.1 °C 15-20 days after ALX and recovering to 37.8±0.1 °C 5-10 days after commencement insulin. ALX-induced diabetes is associated with disturbances in heart rhythm, physical activity and body temperature that are variously affected during insulin treatment.