Neuroscience
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Electrical muscle stimulation has been demonstrated to facilitate nerve regeneration and functional recovery, but the underlying mechanism remains only partially understood. In this study, we investigated the positive effect of electrical muscle stimulation following nerve injury and its molecular mechanisms of autophagy regulation. The sciatic nerves of Sprague-Dawley rats were transected and immediately repaired. ⋯ The number of autophagosomes and the expression of autophagy marker LC3-Ⅱ in distal nerve stump were increased while the level of autophagy substrate protein P62 was decreased following electrical muscle stimulation. Blockage of the autophagy flux by chloroquine (CQ) diminished the positive effect of electrical muscle stimulation on nerve injury. These results illustrated that electrical muscle stimulation accelerates axon regeneration and functional recovery through promoting autophagy flux in distal nerve segments following nerve injury and immediate repair (IR) by a so far unknown mechanism.
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Paclitaxel (PTX) is one of the most commonly used chemotherapeutic agents for various cancer diseases. Despite its advantages, PTX also causes behavioral deficits related to nervous-system dysfunction, such as neuropathic pain, depression, anxiety, and cognitive impairments. The prefrontal cortex (PFC) is one of the areas that is susceptible to adverse effects of chemotherapeutic agents. ⋯ RNA sequencing and in-depth gene expression analysis of the PFC in paired vehicle and PTX-treated mice showed that PTX induced 1755 differentially expressed genes in the PFCs of male and female mice. Quantitative real-time RT-PCR verified that some gene expressions in the medial PFC (mPFC) were related to neurotransmission. In conclusion, this study identified a sex-biased effect of PTX on PFC function and gene expression, which provides a foundation for future studies to explore the precise mechanisms of PTX-induced behavioral deficits.
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Compared with the biological paradigms of classical conditioning, non-adaptive computational models are not capable of realistically simulating the biological behavioural functions of the hippocampal regions, because of their implausible requirement for a large number of learning trials, which can be on the order of hundreds. Additionally, these models did not attain a unified, final stable state even after hundreds of learning trials. Conversely, the output response has a different threshold for similar tasks in various models with prolonged transient response of unspecified status via the training or even testing phases. ⋯ The results of the Green model showed a significant improvement confirmed by empirical studies of different tasks. In addition, the results indicated that the model outperforms the previously published models. All the obtained results successfully and quickly attained a stable, desired final state (with a unified concluding state of either "1" or "0") with a significantly shorter transient duration.
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Neurons from several brain regions resonate in the theta frequency range (4-12 Hz), displaying a higher voltage response to oscillatory currents at a preferred 'resonant' frequency (fR). Subthreshold resonance could influence spiking and contribute to the selective entrainment of neurons during the network oscillatory activity that accompanies several cognitive processes. Neurons from different regions display resonance in specific theta subranges, suggesting a functional specialization. ⋯ In all the neurons studied, fR inversely correlated with the effective input resistance (Rin), a measurable variable that depends on passive and active membrane features. We showed that resonance can be adjusted by manipulations mimicking naturally occurring processes, as the incorporation of a virtual constant conductance or cell depolarization, in a way that preserves the fR-Rin relationship. The modulation of frequency selectivity influences firing by shifting spike frequency and timing, which could influence neuronal communication in an active network.
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After ischemic stroke, the degenerated myelin caused by ischemic injury cannot be rapidly cleared away by microglia and interferes with the recovery process. Complement receptor 3 (CR3, CD11b/CD18), belonging to β2 integrin family primarily expressed in phagocytes, is involved in the microglial phagocytosis of myelin debris. We previously found that pseudoginsenoside-F11 (PF11), an ocotillol-type saponin, exerts neuroprotective effects against ischemic stroke and neuroinflammation. ⋯ Meanwhile, PF11 strengthened the OGD-activated RhoA/ROCK signaling associated with the internalization during myelin debris phagocytosis through CR3. Consistently, the anti-CD11b mAb could markedly attenuated the nrueoprotective effects of PF11 (12 mg/kg, i.v.) on infarction and brain edema, neurological functions and loss of neurons of pMCAO rats. These findings suggest that PF11 accelerates the phagocytosis of myelin debris by microglia mainly through CR3, which may likely contribute to its neuroprotection against ischemic stroke.