Brain research
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The analysis of the functional correlates of "brain oscillations" has become an important branch of neuroscience. Although research on the functional correlates of brain oscillation has progressed to a high level, studies on cognitive disorders are rare and mainly limited to schizophrenia patients. ⋯ Furthermore, the effects of pharmaca and the influence of neurotransmitters in patients with cognitive disorders are also reviewed. Following the review, a short synopsis is given related to the analysis of brain oscillations.
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The brain generates extensive spontaneous network activity patterns, even in the absence of extrinsic afferents. While the cognitive correlates of these complex activities are being unraveled, the rules that govern the generation, synchronization and spread of different patterns of intrinsic network activity in the brain are still enigmatic. Using hippocampal neurons grown in dissociated cultures, we are able to study these rules. ⋯ Thus, the strength of connectivity is inversely correlated with spontaneous activity and synchronicity. In the absence of confirmed 'leader' neurons, synchronous bursting network activity appears to be triggered by at least several local subthreshold synaptic events. We conclude that networks of neurons in culture can produce spontaneous synchronized activity and serve as a viable model system for the analysis of the rules that govern network activity in the brain.
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Pyrithiamine-induced thiamine deficiency (PTD) was used to produce a rodent model of Wernicke-Korsakoff syndrome that results in acute neurological disturbances, thalamic lesions, and learning and memory impairments. There is also cholinergic septohippocampal dysfunction in the PTD model. Systemic (Experiment 1) and intrahippocampal (Experiment 2) injections of the acetylcholinesterase inhibitor physostigmine were administered to determine if increasing acetylcholine levels would eliminate the behavioral impairment produced by PTD. ⋯ In addition, although intrahippocampal infusions of 40 ng of physostigmine increased the available amount of ACh in both pair-fed (PF) and PTD rats, it did so to a greater extent in PF rats. The increase in ACh levels induced by the direct hippocampal application of physostigmine in the PTD model likely increased activation of the extended limbic system, which was dysfunctional, and therefore led to recovery of function on the spontaneous alternation task. In contrast, the lack of behavioral improvement by intrahippocampal physostigmine infusion in the PF rats, despite a greater rise in hippocampal ACh levels, supports the theory that there is an optimal range of cholinergic tone for optimal behavioral and hippocampal function.
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We have previously reported that Ginkgolids which contain Ginkgolids A and B (Ginkgolids (A+B), GKAB) reduce infarct size in a rat model of focal ischemia. NF-kappaB-inducing kinase (NIK)-IkappaBalpha kinase (IKK) pathway plays an important role in activation of nuclear factor kappaB (NF-kappaB). A previous study demonstrated that Ginkgolid B inhibited lipopolysaccharide (LPS)- and platelet activating factor (PAF)-induced NF-kappaB activation in rat pleural polymorphonuclear granulocytes. However, little is known about the inhibitory mechanisms of Ginkgolids on the activation of NF-kappaB. The present study evaluated the effects of GKAB on NIK/IKK/IkappaB/NF-kappaB signaling pathway in a rat model of permanent focal cerebral ischemia. ⋯ These findings suggest that GKAB-mediated neuroprotective effect against ischemia appears to be associated with blocking NF-kappaB activation by suppressing the NIK-IKK pathway.
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The aim of the present study was to explore variation in skin blood flow and temperature following experimental muscle pain. In 14 male human subjects, 2 ml and 4.8 ml of hypertonic (5.8%) saline were injected into the left tibialis anterior (TA) muscle to induce muscle pain. The subjects rated the pain intensity on a 10 cm visual analogue scale (VAS). ⋯ These results suggested that the vasodilation in different skin areas following intramuscular injection of hypertonic saline was dose-dependent. Injection of 4.8 ml hypertonic saline after local intramuscular anesthesia (2% lidocaine) did not evoke any significant changes in skin blood flow or skin temperature in any of the four observation areas. This suggested that both homotopic and heterotopic vascular reactions triggered by hypertonic saline stimulation of thin muscle afferent fibers were a neurogenically associated reaction.