The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry
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Recovery of locomotion has been considered unattainable following a clinically complete or severe incomplete spinal cord injury even after conventional therapy. However, the locomotion of spinal animals can be improved by training that provides complex temporal patterns of sensory information related to stepping that is interpreted by the spinal cord. This review discusses the evidence that suggests human spinal networks can integrate and interpret complex sensory signals to produce functional efferent output and adapt to repetitive training. Locomotor training, a new rehabilitative approach, is based on principles that promote the movement of limbs and trunk to generate sensory information consistent with locomotion to improve the potential for the recovery of walking after neurologic injury.
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Concentrating a wide range of spinal cord injury (SCI) research laboratories in a single location to accelerate progress and draw attention to the promise of SCI research has made The Miami Project to Cure Paralysis one of the most publicly recognized and often controversial research groups in the neurosciences. A "Center of Excellence" at the University of Miami School of Medicine, the Miami Project also serves as a model for SCI research programs being developed nationally and internationally. Founded in 1985, the Miami Project set out on an unprecedented path-to develop a research center dedicated to improving treatments for SCI by bridging basic and clinical science. ⋯ Highly visible spokespersons, including cofounder ex-Miami Dolphin Nick Buoniconti and his son Marc, brought the issue of SCI paralysis and the promise of research before the public, the media, and sports communities. As progress in the neurosciences has raced ahead, public attention to medical research, and SCI research in particular, has grown exponentially. This review will assess the Miami Project as a model for disease-based research that unites academic, philanthropic, and patient communities in a common cause.
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Morphine and most clinical opioids act through mu opioid receptors. Yet, their pharmacological profiles differ. The presence of incomplete cross-tolerance among these drugs clinically was one of the first indications that these mu opioids differed in their receptor mechanisms of action. ⋯ In one knockout mouse, morphine analgesia is completely lost while the potent mu drugs morphine-6beta-glucuronide and heroin both retain analgesic activity. Finally, cloning studies have identified at least seven different splice variants of the MOR-1 gene, with more likely. These studies illustrate the complexity of mu opioid pharmacology.