Molecular neurobiology
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Molecular neurobiology · Aug 2016
Meta AnalysisExogenous Melatonin for Delirium Prevention: a Meta-analysis of Randomized Controlled Trials.
Recently, two high-quality clinical randomized controlled trials (RCTs) regarding the preventive effect of exogenous melatonin on delirium drew inconsistent conclusions. We therefore performed a systemic review to explore whether melatonin had a benefit on delirium prevention. MEDLINE, EMBASE, and Cochrane Library were searched from January 1980 to April 2015 for English language studies. ⋯ No differences were found in the incidence of delirium between the two groups in the elderly patients that were presented to surgical wards. In conclusion, melatonin supplementation had a significant preventive effect in decreasing the incidence of delirium in elderly patients that were presented to medical wards. Further studies should provide sufficient evidence about the effect of melatonin on delirium in a large sample size.
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Molecular neurobiology · Aug 2016
ReviewThe Role of Nitric Oxide and Sympathetic Control in Cerebral Autoregulation in the Setting of Subarachnoid Hemorrhage and Traumatic Brain Injury.
Cerebral autoregulation is defined as the mechanism by which constant cerebral blood flow is maintained despite changes of arterial blood pressure, and arterial blood pressure represents the principle aspect of cerebral autoregulation. The impairment of cerebral autoregulation is reported to be involved in several diseases. However, the concept, mechanisms, and pathological dysfunction of cerebral autoregulation are beyond full comprehension. ⋯ Additionally, impaired cerebral autoregulation following subarachnoid hemorrhage and traumatic brain injury has been proven by several descriptive studies, although without corresponding explanations. As the most important mechanisms of cerebral autoregulation, the changes of nitric oxide and sympathetic stimulation play significant roles in these insults. Therefore, the in-depth researches of nitric oxide and sympathetic nerve in cerebral autoregulation may help to develop new therapeutic targets.
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Molecular neurobiology · Aug 2016
BDNF Induces Striatal-Enriched Protein Tyrosine Phosphatase 61 Degradation Through the Proteasome.
Brain-derived neurotrophic factor (BDNF) promotes synaptic strengthening through the regulation of kinase and phosphatase activity. Conversely, striatal-enriched protein tyrosine phosphatase (STEP) opposes synaptic strengthening through inactivation or internalization of signaling molecules. Here, we investigated whether BDNF regulates STEP levels/activity. ⋯ BDNF also promoted UPS-mediated STEP61 degradation in cultured striatal and hippocampal neurons. In contrast, nerve growth factor and neurotrophin-3 had no effect on STEP61 levels. Our results thus indicate that STEP61 degradation is an important event in BDNF-mediated effects.
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Molecular neurobiology · Aug 2016
Hydrogen Sulfide Ameliorates Early Brain Injury Following Subarachnoid Hemorrhage in Rats.
Increasing studies have demonstrated the neuroprotective effect of hydrogen sulfide (H2S) in central nervous system (CNS) diseases. However, the potential application value of H2S in the therapy of subarachnoid hemorrhage (SAH) is still not well known. This study was to investigate the potential effect of H2S on early brain injury (EBI) induced by SAH and explore the underlying mechanisms. ⋯ More importantly, NaHS treatment could significantly attenuate EBI (including brain edema, blood-brain barrier disruption, brain cell apoptosis, inflammatory response, and cerebral vasospasm) after SAH. In vitro, H2S protects neurons and endothelial function by functioning as an antioxidant and antiapoptotic mediator. Our results suggest that NaSH as an exogenous H2S donor could significantly reduce EBI induced by SAH.
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Molecular neurobiology · Aug 2016
Signaling Mechanism of Cannabinoid Receptor-2 Activation-Induced β-Endorphin Release.
Activation of cannabinoid receptor-2 (CB2) results in β-endorphin release from keratinocytes, which then acts on primary afferent neurons to inhibit nociception. However, the underlying mechanism is still unknown. The CB2 receptor is generally thought to couple to Gi/o to inhibit cAMP production, which cannot explain the peripheral stimulatory effects of CB2 receptor activation. ⋯ Using a rat model of inflammatory pain, we showed that the MAPK kinase inhibitor PD98059 abolished the peripheral effect of the CB2 receptor agonist on nociception. We thus present a novel mechanism of CB2 receptor activation-induced β-endorphin release through Gi/o-Gβγ-MAPK-Ca(2+) signaling pathway. Our data also suggest that stimulation of MAPK contributes to the peripheral analgesic effect of CB2 receptor agonists.