Brain research
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Effects of oral hormonal contraceptives (OC) on human brain structure and behavior have only recently become a focus of research. Two explorative reports observed larger regional gray matter (GM) volumes in OC users within the prefrontal cortex, ACC and fusiform gyri, as well as parahippocampal gyri, hippocampus and cerebellum. These studies did however not control for the androgenicity of the progestin compound of OC, did not take into consideration how long OC users had been on their OC, and did not control for age differences between the OC group and the naturally cycling group. ⋯ Total GM volume, as well as absolute GM volumes within the bilateral fusiform gyri, FFA, hippocampus, parahippocampus, PPA, middle frontal gyri and ACC were significantly larger, the longer the duration of OC use, particularly in users of androgenic progestins. Morphological differences between active and inactive pill phase were observed in users of androgenic progestins. These findings suggest differential effects of androgenic and anti-androgenic progestins on human brain structure.
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Ovarian sex hormones modulate neuronal circuits not directly involved in reproductive functions. In the present study, we investigated whether endogenous fluctuations of estradiol and progesterone during the menstrual cycle are associated with early cortical processing stages in a cued spatial attention paradigm. EEG was monitored while young women responded to acoustically cued visual stimuli. ⋯ Progesterone correlated negatively with RTs in luteal women. Therefore, whereas our behavioral data indicate a functional cerebral asymmetry in early follicular women, EEG recording reveal a physiological cerebral hemisphere asymmetry in the alpha frequency band in luteal women. We assume that a progesterone-associated enhancement in synchronization of synaptic activity in the alpha frequency band in luteal women improves early categorization of visual targets in a cued spatial attention paradigm.
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Electroconvulsive therapy (ECT) is an effective treatment for major depression, but can result in memory impairment. Several studies have shown that anesthetic propofol can alleviate the impairment of memory induced by ECT. However, the underlying molecular mechanisms remain unclear. ⋯ Propofol suppressed IL-1β and TNF-α production, up-regulated the expression of GLT-1, decreased the concentration of glutamate in the hippocampus and attenuated the impairment of learning and memory induced by ECS. Propofol alleviate the learning and memory impairment induced by ECS could be partly attributed to its anti-inflammatory effects. This article is part of a Special Issue entitled Brain and Memory.
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Citicoline (CDP-choline; cytidine 5'-diphosphocholine) is an important intermediate in the biosynthesis of cell membrane phospholipids. Citicoline serves as a choline donor in the biosynthetic pathways of acetylcholine and neuronal membrane phospholipids, mainly phosphatidylcholine. The ability of citicoline to reverse neuronal injury has been tested in animal models of cerebral ischemia and clinical trials have been performed in stroke patients. ⋯ To clarify if this adverse effect of citicoline is generalizable across alternative seizure models, we induced seizure by kainate injection (10mg/kg, i.p.) and then injected citicoline as in pilocarpine-induced seizure. We found that citicoline did not modulate kainate seizure-induced neuronal death, BBB disruption or microglial activation. These results suggest that citicoline may not have neuroprotective effects after seizure and that clinical application of citicoline after seizure needs careful consideration.
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JM-1232(-) (JM) is a novel isoindoline derivative with sedative and hypnotic activities that are mediated by binding to the benzodiazepine site of the Gamma-aminobutyric acid type A (GABAA) receptor. Although the neuroprotective effects of other GABAA receptor agonists are well known, there is no published report regarding JM. Thus, we examined the effects of JM on neurons exposed to oxygen-glucose deprivation (OGD) using rat hippocampal slice cultures. ⋯ To analyze more immediate effects of JM, we next measured the fluorescence of Oregon Green 488 BAPTA-1 during the OGD and re-oxygenation periods, and evaluated changes in intracellular Ca(2+) in single CA1 pyramidal neurons. JM reduced the elevation of intracellular Ca(2+) concentration during OGD, and this effect was antagonized by flumazenil. These findings indicate that JM suppressed the elevation of intracellular Ca(2+) concentration during OGD through GABAA receptors, but its neuroprotective effects from necrotic changes also involve other unknown mechanisms.