Neuroscience letters
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Neuroscience letters · May 2015
Monocarboxylate transporter-dependent mechanism confers resistance to oxygen- and glucose-deprivation injury in astrocyte-neuron co-cultures.
Hypoxic and low-glucose stressors contribute to neuronal death in many brain diseases. Astrocytes are anatomically well-positioned to shield neurons from hypoxic injury. During hypoxia/ischemia, lactate released from astrocytes is taken up by neurons and stored for energy. ⋯ OGD significantly increased cell death in neuronal cultures and up-regulated MCT4 expression in astrocyte cultures, but no increased cell death was observed in neuron-astrocyte co-cultures or astrocyte cultures. However, neuronal cell death in co-cultures was increased by exposure to MCT4- or MCT2-specific siRNA, and this effect was attenuated by the addition of lactate into the extracellular medium of neuronal cultures prior to OGD. These findings demonstrate that resistance to OGD injury in astrocyte-neuron co-cultures occurs via an MCT-dependent mechanism.
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Neuroscience letters · Apr 2015
Spinal vasopressin alleviates formalin-induced nociception by enhancing GABAA receptor function in mice.
Arginine vasopressin (AVP) plays a regulatory role in nociception. Intrathecal administration of AVP displays an antinociceptive effect. However, little is understood about the mechanism underlying spinal AVP analgesia. ⋯ The AVP analgesia was also reversed by bicuculline, a GABAA receptor antagonist. Moreover, AVP potentiated GABA-activated currents in dorsal root ganglion neurons from wild-type littermates, but not from V1A-/- mice. Our results may reveal a novel spinal mechanism of AVP analgesia by enhancing the GABAA receptor function in the spinal cord through V1A receptors.
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Neuroscience letters · Apr 2015
Anesthetic agents modulate ECoG potentiation after spreading depression, and insulin-induced hypoglycemia does not modify this effect.
Cortical spreading depression (CSD) is characterized by reversible reduction of spontaneous and evoked electrical activity of the cerebral cortex. Experimental evidence suggests that CSD may modulate neural excitability and synaptic activity, with possible implications for long-term potentiation. Systemic factors like anesthetics and insulin-induced hypoglycemia can influence CSD propagation. ⋯ Comparison of two cortical recording regions in awake rats revealed a similarly significant (p<0.05) potentiation effect in both regions, whereas in the anesthetized groups the potentiation was significant only in the recording region nearer to the stimulating point. Our data suggest that urethane+chloralose and tribromoethanol anesthesia modulate the post-CSD potentiation of spontaneous electrical activity in the adult rat cortex, and insulin-induced hypoglycemia does not modify this effect. Data may help to gain a better understanding of excitability-dependent mechanisms underlying CSD-related neurological diseases.
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Neuroscience letters · Apr 2015
Cerebral autoregulation, beta amyloid, and white matter hyperintensities are interrelated.
Emerging studies link vascular risk factors and cerebrovascular health to the prevalence and rates of progression in Alzheimer's disease (AD). The brain's ability to maintain constant blood flow across a range of cerebral perfusion pressures, or autoregulation, may both promote and result from small vessel cerebrovascular disease and AD-related amyloid pathology. ⋯ For the first time in humans, we demonstrate an interrelationship among AD pathology, small vessel cerebrovascular disease, and cerebral autoregulation. Vascular factors and AD pathology are not independent but rather appear to interact.
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Neuroscience letters · Apr 2015
Interleukin-10 levels in rat models of nerve damage and neuropathic pain.
Interleukin-10 (IL-10) is an anti-inflammatory cytokine that has been shown to play a role in inflammatory and autoimmune disorders as well as in neuropathic pain conditions. The objective of the present study was to assess the levels of IL-10 in rat's dorsal root ganglion (DRG) and the sciatic nerve following four different forms of sciatic nerve injury. The models used to induce the injury included two models of partial nerve injury: partial sciatic ligation (PSL) and chronic constriction injury (CCI), a model of complete sciatic transection (CST) and a model of perineural inflammation with minimal nerve damage (neuritis). ⋯ The results of this study suggest that IL-10's role in the neuropathic pain etiology may be specific to nerve injury type. Complete nerve transection increases while partial nerve injury reduces IL-10 levels in the involved nerve, and DRG. Perineural inflammation with minimal nerve damage has no effect on IL-10 levels.