The Journal of neuroscience : the official journal of the Society for Neuroscience
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After an incomplete spinal cord injury (SCI) spontaneous motor recovery can occur in mammals, but the underlying neural substrates remain poorly understood. The motor cortex is crucial for skilled motor learning and the voluntary control of movement and is known to reorganize after cortical injury to promote recovery. Motor cortex plasticity has also been shown to parallel the recovery of forelimb function after cervical SCI, but whether cortical plasticity participates in hindlimb recovery after SCI remains unresolved. ⋯ The motor cortex is crucial for the control of voluntary movement and contains topographical movement representations (motor maps) that are highly plastic. We examined the organization of hindlimb motor maps bilaterally after a lateral hemisection of the spinal cord to show that while motor maps are abolished in the deefferented cortex, the spared ipsilesional cortex transiently reorganizes to gain a representation of the affected hindlimb after injury that relates to recovery. This finding demonstrates that plasticity in the ipsilesional motor cortex at early time points after spinal cord hemisection is initially important to support motor recovery.
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In addition to treating depression, antidepressant drugs are also a first-line treatment for neuropathic pain, which is pain secondary to lesion or pathology of the nervous system. Despite the widespread use of these drugs, the mechanism underlying their therapeutic action in this pain context remains partly elusive. The present study combined data collected in male and female mice from a model of neuropathic pain and data from the clinical setting to understand how antidepressant drugs act. ⋯ Indeed, preclinical studies led to contradictions concerning the anatomical and molecular substrates of this action. In the present work, we overcame these apparent contradictions by highlighting the existence of two independent mechanisms. One is rapid and centrally mediated by descending controls from the brain to the spinal cord and the other is delayed, peripheral, and relies on the anti-neuroimmune action of chronic antidepressant treatment.
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Skillful storytelling helps listeners understand the essence of complex concepts and ideas in meaningful and often personal ways. For this reason, storytelling is being embraced by scientists who not only want to connect more authentically with their audiences, but also want to understand how the brain processes this powerful form of communication. Here we present part of a conversation between a group of scientists actively engaged with the practice and/or the science of storytelling. We highlight the brain networks involved in the telling and hearing of stories and show how storytelling is being used well beyond the realm of public communication to add a deeper dimension to communication with our students and colleagues, as well as helping to make our profession more inclusive.
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New myelin sheaths can be restored to demyelinated axons in a spontaneous regenerative process called remyelination. In general, new myelin sheaths are made by oligodendrocytes newly generated from a widespread population of adult CNS progenitors called oligodendrocyte progenitor cells (OPCs). New myelin in CNS remyelination in both experimental models and clinical diseases can also be generated by Schwann cells (SCs), the myelin-forming cells of the PNS. ⋯ Critical to this endeavor is the need to understand the mechanisms of remyelination, including the nature and identity of the cells capable of generating new myelin sheath-forming cells. Here, we report a previously unrecognized subpopulation of nonmyelinating Schwann cells (SCs) in the PNS, identified by the expression of the transcription factor Foxj1, which can give rise to SCs that are capable of remyelinating both PNS and CNS axons. These cells therefore represent a new cellular target for myelin regenerative strategies for the treatment of CNS disorders characterized by persistent demyelination.
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Pain is regulated endogenously through both opioid and non-opioid mechanisms. We hypothesized that two novel pain modulation tasks, one drawing on context/expectations and one using voluntary reappraisal, would show differing levels of opioid dependence. Specifically, we expected that naloxone would block context-related analgesia, whereas mental imagery-based pain reappraisal would be opioid-independent. ⋯ Context/expectation-driven (relative relief-related) analgesia was blocked by naloxone. In contrast, pain reappraisal through mental imagery was intact despite opioid receptor blockade, suggesting opioid independence. These results support mental imagery as a powerful, clinically relevant strategy for regulating pain as it does not rely on a functioning opioidergic system.