The Journal of comparative neurology
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Comparative Study
Autonomic and motor neuron death is progressive and parallel in a lumbosacral ventral root avulsion model of cauda equina injury.
Injuries to the cauda equina of the spinal cord result in autonomic and motor neuron dysfunction. We developed a rodent lumbosacral ventral root avulsion injury model of cauda equina injury to investigate the lesion effect in the spinal cord. We studied the retrograde effects of a unilateral L5-S2 ventral root avulsion on efferent preganglionic parasympathetic neurons (PPNs) and pelvic motoneurons in the L6 and S1 segments at 1, 2, 4, and 6 weeks postoperatively in the adult male rat. ⋯ Nuclear condensation and cleaved caspase-3 were detected in axotomized PPNs and motoneurons, suggesting apoptosis as a contributing mechanism of the neural death. We conclude that lumbosacral ventral root avulsions progressively deplete autonomic and motor neurons. The findings suggest that early neuroprotection will be an important consideration in future attempts of treating acute cauda equina injuries.
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Hyperpolarization-activated cation currents (I(h)) have been identified in neurons in the central nervous system, including the retina. There is growing evidence that these currents, mediated by the hyperpolarization-activated cyclic nucleotide-gated cation channel (HCN), may play important roles in visual processing in the retina. This study was conducted to identify and characterize HCN1-immunoreactive (IR) bipolar cells by immunocytochemistry, quantitative analysis, and electron microscopy. ⋯ In the IPL, they were presynaptic to amacrine cell processes. The most frequent postsynaptic dyads formed of HCN1-IR bipolar cell axon terminals are pairs composed of both amacrine cell processes. These results suggest that these HCN1-IR cone bipolar cells might be the same as the DAPI-Ba1 bipolar population, and might therefore be involved in a direction-selective mechanism, providing inputs to the OFF-starburst amacrine cells and/or the OFF-plexus of the ON-OFF ganglion cells.