Neuroscience
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Acute pain alters motor unit discharge properties in muscles that are painful or influence loading of painful structures. Less is known about the changes in discharge when pain is induced in distant tissues that are unable or have limited capacity to modify the load of the contracting muscle. We aimed to determine whether acute experimental pain alters quadriceps motor unit discharge when pain is induced in; (i) a muscle that is unlikely to be mechanically influenced by modified quadriceps activity (tibialis anterior: TA), or (ii) the antagonist muscle (biceps femoris: BF). ⋯ Despite maintained force, discharge rate of quadriceps motor units was lower during Pain than Control conditions for TA and BF trials (both P < 0.001). Redistribution of motor unit activity was observed; some units were recruited in control or pain but not both. As modified quadriceps motor unit discharge has limited/no potential to modify load in the painful tissue to protect the painful part, the findings might support an alternative hypothesis that activity is redistributed to larger motor units.
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Varicella zoster virus (VZV) is responsible for chronic pain. VZV injection has similarities to herpes zoster (HZ) "shingles" pain in humans. In this study orofacial pain was induced by injecting male rats with the human VZV. ⋯ Attenuating Nrxn3 expression also increases VZV associated orofacial pain. Activating GABAergic neurons within the central amygdala with opsins increase GABA release in the parabrachial and reduced the pain response after Nrxn3 shRNA treatment. These results are consistent with the idea that Nrxn3 within the central amygdala controls VZV associated pain by regulating GABA release in the lateral parabrachial that then controls the activity of ascending pain neurons.
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Subtypes of microglia/macrophage regulate the inflammation in the opposite direction during ischemic stroke. JAK2/STAT3 signaling pathway participates in the development of stroke-related inflammation via ischemic stimulation. However, the relationship between JAK2/STAT3 pathway and microglia/macrophage phenotype transformation is unclear. ⋯ Collectively, these results reveal that JAK2/STAT3 signaling pathway regulates the microglia/macrophage polarization (skewing toward the M2 polarization) during the CIRI, thus alleviating brain damage. Therefore, approaches targeting JAK2/STAT3 activation are promising therapies for ischemic stroke.
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The neurotrophin receptor p75 (p75NTR) is a circadian rhythm regulator and mediates cognitive deficits induced by sleep deprivation (SD). The soluble extracellular domain of p75NTR (p75ECD) has been shown to exert a neuroprotective function in Alzheimer's disease (AD) and depression animal models. Nevertheless, the role of p75ECD in SD-induced cognitive dysfunction is unclear. ⋯ The results revealed that peripheral supplementation of high-dose p75ECD-Fc (10 mg/kg) recovered the balance between Aβ and p75ECD in the hippocampus and rescued the cognitive deficits in SD mice. We also found that p75ECD-Fc ameliorated other pathologies induced by SD, including neuronal apoptosis, synaptic plasticity impairment and neuroinflammation. The current study suggests that p75ECD-Fc is a potential candidate for SD and peripheral supplementation of p75ECD-Fc may be a prospective preventive measure for cognitive decline in SD.