Brain research
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The P3a is an event-related potential (ERP) component believed to reflect an attention-switch to task-irrelevant stimuli or stimulus information. The present study concerns the automaticity of the processes underlying the auditory P3a. More specifically, we investigated whether the auditory P3a is an attention-independent component, that is, whether it can still be elicited under highly-focused selective attention to a different (visual) channel. ⋯ This finding suggests that the elicitation of the auditory P3a does not require available central capacity, and confirms the automatic nature of the processes underlying this ERP component. Moreover, the difficulty of the visual task did not modulate either the mismatch negativity (MMN) or the P3a but did have an effect on a late (350-400 ms) negativity, an ERP deflection perhaps related to a subsequent evaluation of the auditory change. Together, these results imply that the auditory P3a could reflect a strongly-automatic process, one that does not require and is not modulated by attention.
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Effect of aminoguanidine on post-ischemic brain edema in transient model of focal cerebral ischemia.
Previous experimental studies have shown that aminoguanidine (AG) is beneficial in the late phase of cerebral ischemia. Recently, it has been reported that AG reduces cerebral edema in traumatic brain injury. However, the effects of AG on post-ischemic cerebral edema and blood-brain barrier (BBB) permeability are not clear. ⋯ Additionally, AG at the doses of 75 and 150 mg/kg significantly reduces cortical and striatal infarct volumes (P<0.001), while AG at the dose of 300 mg/kg did not change striatal infarct volumes (P>0.05). Our findings show that AG significantly reduced post-ischemic increase of brain edema with a 3-h therapeutic window in the transient model of focal cerebral ischemia. Moreover, it seems that at least part of the anti-edematous effects of AG is due to decrease of BBB disruption.
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Intramuscular injection of NGF in human subjects has been reported not to elicit pain, whereas 5% NaCl does. On the other hand, NGF injections induce a long-lasting hyperalgesia. In the present study, the possible neuronal basis of these effects was studied at the spinal level. ⋯ Despite the stronger excitatory effect of 5% NaCl, the sensitization of the dorsal horn neurons after hypertonic saline was less than that after NGF (15.3%). Behavioral experiments showed that NGF injections induced stronger mechanical allodynia and hyperalgesia than hypertonic saline i.m. The data demonstrate that low-frequency activation or even subthreshold potentials in dorsal horn neurons evoked by unmyelinated muscle afferents are an effective means of sensitizing these neurons.
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Delayed paraplegia after operation of the thoracic aorta is considered to be related to vulnerability of motor neurons to ischemia. Recently, endoplasmic reticulum (ER) stress has been reported to participate in neuronal cell death. In the present study, we investigate the expression of ER stress-related molecules and discuss the relationship between neuronal vulnerability and ER stress after transient ischemia in the spinal cord. ⋯ These results indicate that the vulnerability of motor neurons in the spinal cord might be partially attributed to an ER stress response to transient ischemia.
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Cortical Spreading Depression (CSD) is a well-studied model of preconditioning that provides a high degree of tolerance to a subsequent ischemic event in the brain. The present study was undertaken in order to determine whether the release of ATP during CSD could contribute to the induction of ischemic tolerance. Direct measurement of ATP levels during CSD indicates that with each CSD wave ATP is released into the extracellular space at levels exceeding 100 microM. ⋯ Although extracellular adenosine or glutamate may make a small contribution, most of the tolerance was found to be induced independently of adenosine or glutamate receptor activation. Multiple signal transduction pathways mediate the response to extracellular ATP with the protein kinase A pathway and activation of phospholipase C contributing the most. The results are consistent with the proposal that CSD releases ATP into the extracellular space and the subsequent activation of P2Y receptors makes a major contribution to the induction of ischemic tolerance in the brain.