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Understanding the central nervous system (CNS) response strategy to trunk perturbations could help in prevention of back injuries and development of rehabilitation and treatment programs. This study aimed to investigate biomechanical response of the trunk musculoskeletal system under sudden forward loads, accounting for pre-perturbation conditions (preloading, initial posture and abdominal antagonistic coactivation) and perturbation magnitudes. Using a trunk kinematics-driven iterative finite element (FE) model, temporal profiles of measured kinematics and external load along with subjects' weights were prescribed to predict thoracolumbar muscle forces/latencies and spinal loads for twelve healthy subjects when tested in six conditions during pre- and post-perturbation periods. Results demonstrated that preloading the trunk significantly (i.e., p<0.05) increased pre-perturbation back muscle forces but significantly decreased post-perturbation peak muscle active forces and muscle latencies. Initial trunk flexion significantly increased muscle active and passive forces before the perturbation and their peak values after the perturbation, which in turn caused much larger spinal loads. Abdominal muscles antagonistic pre-activation did not alter the internal variables investigated in this study. Increase in sudden applied load increased muscle reflex activities and spinal forces; a 50 N increase in sudden load (i.e., when comparing 50 N to 100 N) increased the L5-S1 compression force by 1327 N under 5 N preload and by 1374 N under 50 N preload. Overall, forces on the spine and hence risk of failure substantially increased in sudden forward loading when the magnitude of sudden load increased and when the trunk was initially in a flexed posture. In contrast, a higher initial preload diminished reflex latencies and compression forces., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Retrograde labeling with horseradish peroxidase conjugated to wheat germ agglutinin showed that the pubococcygeus muscles of the female rat are innervated by a population of motoneurons located in a column approximately 2 mm in length in the central region of lamina IX of the sixth lumbar-first sacral spinal cord segments. These neurons have a dendritic distribution that projects to the lateral, medial and ventral regions of the gray matter. Values for soma size, primary dendrite length and arborization area obtained from intact animals that were in diestrous-2, were significantly reduced following ovariectomy. After hormone priming of the ovariectomized animals with estradiol benzoate and progesterone, an additional injection of estradiol benzoate alone or followed by progesterone increased the labeled length of the primary dendrites distributed to the lateral, but not to the medial or ventral regions of the gray matter in the spinal cord. However, dendritic labeling was not significantly increased when only progesterone was additionally injected. It therefore seems that pubococcygeus muscle motoneurons of the female rat are sensitive to the effects of gonadal hormones.

The aim was to determine whether blockade of store-operated Ca(2+) entry, or inhibition of Ca(2+) sensitisation, is the predominant mechanism by which neuronally released nitric oxide mediates relaxation of the mouse anococcygeus. Nitrergic relaxations to field stimulation (10 Hz, 10 s trains) were unaffected by the sarcoplasmic reticulum Ca(2+) ATPase blocking agent thapsigargin (100 nM), known to prevent nitric-oxide-induced inhibition of store-operated Ca(2+) entry. Conversely, the myosin phosphatase inhibitor calyculin-A (1 microM) caused almost complete abolition of nitrergic relaxations. The results provide evidence that inhibition of Ca(2+) sensitisation is the major cellular mechanism underlying nitrergic relaxation of the mouse anococcygeus.

The mechanism of canine penile erection was studied in 6 'chronic' and 15 'acute' male dogs by means of sacral root stimulation combined with pharmacologic studies. The basic mechanism of erection cannot be explained by a pure increase in arterial perfusion of the cavernous spaces due to neural vasomotor regulation. The vasomotor mechanism, whether pure arteriolar vasodilation, or venous drainage impairment, or secondary to as yet undefined behavior of the corporal smooth muscle, can be activated by stimulation of the parasympathetic outflow. Those preganglionic fibers may synapse to noncholinergic and non-beta-adrenergic neurons, which release a yet unidentified vasodilator neurotransmitter mediating the neurovascular effect.