3 research outputs found

    Modulation of Spinal GABAergic Inhibition and Mechanical Hypersensitivity following Chronic Compression of Dorsal Root Ganglion in the Rat

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    Chronic compression of dorsal root ganglion (CCD) results in neuropathic pain. We investigated the role of spinal GABA in CCD-induced pain using rats with unilateral CCD. A stereological analysis revealed that the proportion of GABA-immunoreactive neurons to total neurons at L4/5 laminae I-III on the injured side decreased in the early phase of CCD (post-CCD week 1) and then returned to the sham-control level in the late phase (post-CCD week 18). In the early phase, the rats showed an increase in both mechanical sensitivity of the hind paw and spinal WDR neuronal excitability on the injured side, and such increase was suppressed by spinally applied muscimol (GABA-A agonist, 5 nmol) and baclofen (GABA-B agonist, 25 nmol), indicating the reduced spinal GABAergic inhibition involved. In the late phase, the CCD-induced increase in mechanical sensitivity and neuronal excitability returned to pre-CCD levels, and such recovered responses were enhanced by spinally applied bicuculline (GABA-A antagonist, 15 nmol) and CGP52432 (GABA-B antagonist, 15 nmol), indicating the regained spinal GABAergic inhibition involved. In conclusion, the alteration of spinal GABAergic inhibition following CCD and leading to a gradual reduction over time of CCD-induced mechanical hypersensitivity is most likely due to changes in GABA content in spinal GABA neurons.ope

    Cadence and range of motion modulate pedal force in a rat model of motorized cycling after spinal cord injury.

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    Motorized cycling (MC) can be utilized post-spinal cord injury (SCI) in patients who lack the strength and/or stability to participate in traditional physical exercise interventions. MC has been applied with the goal of improving locomotor function or cardiovascular health in both human and animal models of SCI. However, a discrepancy exists between the results of human and animal studies of MC, particularly regarding cardiovascular outcomes. Despite the abundance of studies in both humans and animals, the mechanism behind the improvements in cardiovascular function following MC are poorly understood. We posited that increased venous return during MC is likely due to the skeletal muscle pump, where muscle activity during MC would be triggered by stretch reflexes. As stretch reflexes are dependent on both rate and length of muscle stretch, we hypothesized that cycling cadence and crank length could modulate muscle activity and therefore hindlimb loading during cycling. Initial studies testing the development of the instrumented pedals noted spasticity that was represented in the force traces, and a filtering technique was developed to separate spastic from non-spastic forces. Results using this technique combined with EMG of a knee flexor and extensor suggest that higher cadences (≥30 RPM) increased RMS EMG and non-spastic forces, while lower cadences (≤15 RPM) increased spastic forces. Furthermore, large spastic events were associated with a decrease in BP, while high cadence cycling with limited spasticity appeared to elevate BP and HR above baseline levels. These results suggest that MC in rats may constitute a mild eccentric training regimen; clinical translation may therefore be dependent on the ability to reflexively generate muscle contraction in patients during cycling