Neuroscience
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Central neuropathic pain (CNP) in the spinal cord, such as chronic pain after spinal cord injury (SCI), is an incurable ailment. However, little is known about the spinal cord mechanisms underlying CNP. Recently, reactive oxygen species (ROS) have been recognized to play an important role in CNP of the spinal cord. ⋯ Furthermore, in the presence of a transient receptor potential ankyrin 1 (TRPA1) channel antagonist (HC-030031) or a transient receptor potential vanilloid 1 (TRPV1) channel antagonist (capsazepine or AMG9810), the t-BOOH-induced increase in the frequency of sEPSCs was inhibited. These results indicate that ROS enhance the spontaneous release of glutamate from presynaptic terminals onto SG neurons through TRPA1 and TRPV1 channel activation. Excessive activation of these ion channels by ROS may induce central sensitization in the spinal cord and result in chronic pain such as that following SCI.
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Adult neurogenesis occurs throughout life; however the majority of new neurons do not survive. Enhancing the survival of these new neurons will increase the likelihood that these neurons could return function following injury. Inhibition of Rho kinase is known to increase neurite outgrowth and regeneration. ⋯ These mice also demonstrated enhanced spatial memory as tested by the Y maze with no significant changes in anxiety or novel object recognition. Rho kinase inhibition enhanced the survival of new born neurons in the dentate gyrus with a specific dosage effect. These results suggest that inhibition of Rho kinase following injury could be beneficial for increasing the survival of new neurons that may aid recovery.
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The article reviews evidence for sensitive periods in the sensory systems and considers their neuronal mechanisms from the viewpoint of the system's neuroscience. It reviews the essential cortical developmental steps and shows its dependence on experience. It differentiates feature representation and object representation and their neuronal mechanisms. ⋯ Additional to developmental molecular effects on synaptic plasticity, a combination of several integrative effects of deprivation on brain functions, including feature representation (affecting the starting point for learning), categorization function, top-down interactions and cross-modal reorganization close the sensitive periods and may contribute to their critical nature. Further, non-auditory effects of auditory deprivation are discussed. To reopen critical periods, removal of molecular breaks in synaptic plasticity and focused training therapy on the integrative effects are required.
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Randomized Controlled Trial
Illumination influences working memory: an EEG study.
Illumination conditions appear to influence working efficacy in everyday life. In the present study, we obtained electroencephalogram (EEG) correlates of working-memory load, and investigated how these waveforms are modulated by illumination conditions. We hypothesized that illumination conditions may affect cognitive performance. ⋯ The fact that the illumination condition affects brain activity but not behavioral performance suggests that the lighting conditions used in the present study did not influence the performance stage of behavioral processing. Nevertheless, our findings provide objective evidence that illumination conditions modulate brain activity. Further studies are necessary to refine the optimal lighting parameters for facilitating working memory.
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Accumulating evidence indicates that activation of spinal cord astrocytes contributes importantly to nerve injury and inflammation-induced persistent pain and chronic opioid-induced antinociceptive tolerance. Phosphorylation of extracellular signal-regulated kinase (pERK) and induction of interleukin-1 beta (IL-1β) in spinal astrocytes have been implicated in astrocytes-mediated pain. Tissue plasminogen activator (tPA) is a serine protease that has been extensively used to treat stroke. ⋯ Intrathecal injection of tPA results in up-regulation of GFAP and pERK in spinal astrocytes but not up-regulation of ionized calcium binding adapter molecule 1 in spinal microglia. Finally, intrathecal tPA elicits persistent mechanical allodynia, which is inhibited by the astroglial toxin alpha-amino adipate and the MEK (ERK kinase) inhibitor U0126. Collectively, these data suggest an important role of tPA in regulating astrocytic signaling, pain hypersensitivity, and morphine tolerance.