Brain research
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Spinal cord stimulation (SCS) is an alternative approach for treatment of neuropathic pain when conservative management is ineffective. Previously we showed both 4 Hz and 60 Hz SCS reduces hyperalgesia in an animal model of neuropathic pain. However, the mechanisms underlying the pain reduction by SCS and how different frequencies of SCS produce the analgesic effect are unclear. ⋯ The number of c-fos positive cells was significantly increased bilaterally 2 h after either 4 Hz or 60 Hz SCS in the spinal cord dorsal horn in the cervical enlargement and under the electrode, but not in the lumbar enlargement in animals with nerve injury. In uninjured animals 4 Hz SCS increased c-fos expression at the electrode site and lumbar enlargement when compared to animals implanted with the electrode who did not receive SCS. 100 Hz SCS had no effect on c-fos expression. Thus, at the time points examined in this model, low frequency SCS likely activates supraspinal and spinal mechanisms to produce analgesia, while higher frequencies activate spinal mechanisms.
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Sleep loss/disruption has been shown to suppress adult hippocampal neurogenesis. Whether the administration of hypnotic drugs, by promoting sleep, especially in older subjects, who typically exhibit poor sleep, has a beneficial effect on neurogenesis parameters is unknown. We examined the effects of zolpidem, a widely prescribed nonbenzodiazepine hypnotic, on cell proliferation and survival in the dentate gyrus of young ( approximately 2 1/2 months) and old ( approximately 13 months) male Sprague-Dawley rats. ⋯ Similarly, there was little change in cell survival following chronic zolpidem administration in young versus old animals. A slight reduction of cell survival in the granular cell layer (GCL)/SGZ was observed in young animals and a slight augmentation in aged animals. To the extent that zolpidem improves sleep, these data suggest little or no benefit of hypnotic drug treatment on neurogenesis parameters in young or old rats.
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Reperfusion injury induced by cardiac arrest and resuscitation leads to secondary challenges to the brainstem. A 12-minute cardiac arrest results in about a 50% survival rate in resuscitated rats over a 4-day recovery period. ⋯ Our results indicate that after cardiac arrest and resuscitation the baseline spontaneous ventilation was elevated significantly in all rats due to both increased frequency and tidal volume; HVR in the non-survivor group was essentially absent while the brainstem responsiveness to hypoxia is fully maintained in the survivor group. Thus, the HVR was shown in this study to be a reliable indicator of survival vs. non-survival during early days of recovery following cardiac arrest and resuscitation.