British journal of anaesthesia
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Editorial Comment
Quest for new drugs: a way to solve anaesthesia neurotoxicity?
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Caloric restriction (CR) increases both average and maximum lifespan, retards physiological signs of ageing, and delays the onset of several diseases and may mediate neuropathic pain. Neuropathic pain seriously affects the quality of life of patients. In this study, we investigated whether CR exerts anti-nociceptive effects on neuropathic pain, and probed its potential mechanisms. ⋯ These results suggest that the effects of CR on pain behaviours in a rat model of nerve injury are via inhibition of excessive neuro-inflammation induced by the injury. CR may be of benefit in patients with neuropathic pain.
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Exposure of the developing brain to propofol results in cognitive deficits. Recent data suggest that inhibition of neuronal apoptosis does not prevent cognitive defects, suggesting mechanisms other than neuronal apoptosis play a role in anaesthetic neurotoxicity. Proper neuronal growth during development is dependent upon growth cone morphology and axonal transport. Propofol modulates actin dynamics in developing neurones, causes RhoA-dependent depolymerisation of actin, and reduces dendritic spines and synapses. We hypothesised that RhoA inhibition prevents synaptic loss and subsequent cognitive deficits. The present study tested whether RhoA inhibition with the botulinum toxin C3 (TAT-C3) prevents propofol-induced synapse and neurite loss, and preserves cognitive function. ⋯ Inhibition of RhoA prevents propofol-mediated hippocampal neurotoxicity and associated cognitive deficits.