Resection of arteriovenous malformation in the middle cerebellar peduncle by a posterior transpetrosal approach: illustration of a case and correlative microsurgical anatomy.

Background: Lesions located in the posterolateral brain stem, particularly the middle cerebellar peduncle, have presented surgeons with a challenge associated with significant morbidity.

Methods: We present a case of a 20-year-old woman who had a hematoma in the right middle cerebellar peduncle with a ventricular rupture. Angiography revealed an arteriovenous malformation (AVM) located in the same portion, extending from the lateral surface near the entry zone of the trigeminal nerve to the paraventricular area of the fourth ventricle, which was completely resected through a posterior transpetrosal approach.

[Autopsy findings of meningitis associated with multiple brain infarctions in two adult patients].

Cerebrovascular complications of meningitis have been extensively documented in the literature. It is little known, however, that paroxysmal, devastating, and potentially fatal complications can occur when the early signs of infection are subtle and missed. We describe the clinical course and neuropathological findings of the occurrence of brain infarctions during two atypical clinical courses of meningitis.

Continuous exposure to nitric oxide enhances diazepam binding inhibitor mRNA expression in mouse cerebral cortical neurons.

Effects of sustained exposure to nitric oxide (NO) formed by long-term activation of N-methyl-D-aspartate (NMDA) receptors and liberated from a long-lasting NO generator, DETA NONOate, on diazepam binding inhibitor (DBI) and its mRNA expressions were examined using mouse cerebral cortical neurons. Long-term exposure to NMDA increased DBI mRNA expression, and NO synthase inhibitors dose-dependently inhibited this increase. DETA NONOate dose-dependently increased DBI mRNA expression when exposing the neurons to this agent for 3 days and a maximal enhancement of the expression was found at 100 microM of the NO generator.

L-type high voltage-gated calcium channels cause an increase in diazepam binding inhibitor mRNA expression after sustained exposure to ethanol in mouse cerebral cortical neurons.

Mechanisms for increase in diazepam binding inhibitor (DBI) mRNA expression after sustained exposure to ethanol (EtOH) were investigated. Increases in 30 mM KCl-induced [45Ca(2+)] influx and DBI mRNA expression after EtOH (50 mM) exposure for 3 days were completely abolished by nifedipine, but not by omega-agatoxin VIA and omega-conotoxin GIVA. These results indicate that EtOH-induced increase in DBI mRNA expression is mediated via increased Ca(2+) entry through up-regulated L-type high voltage-gated calcium channels.

Psychological stress, but not physical stress, causes increase in diazepam binding inhibitor (DBI) mRNA expression in mouse brains.

Effects of conditioned emotional stimuli (CES), which induce psychological stress, on the expression of cerebral diazepam binding inhibitor (DBI) mRNA in mouse were examined using a communication box. Cerebral DBI mRNA expression significantly increased in a time-dependent manner after the application of CES. The maximal enhancement of DBI mRNA expression was observed 2 days after the application of CES, and this increase faded out over 7 days after the treatment.

Functional significance of nitric oxide in ionomycin-evoked [3H]GABA release from mouse cerebral cortical neurons.

We investigated a role of nitric oxide (NO) on ionomycin-evoked [3H]GABA release using mouse cerebral cortical neurons. lonomycin dose-dependently released [3H]GABA up to 1 microM. The extent of the release by 0.

Up-regulation of L-type voltage-dependent calcium channels after long term exposure to nicotine in cerebral cortical neurons.

Effects of long term (72-h) exposure to low concentration (0.1 mum) of nicotine on various types of voltage-dependent Ca(2+) channels (VDCCs) and neuronal nicotinic acetylcholine receptors (nnAChRs) were examined using primary cultures of mouse cerebral cortical neurons. High potassium (30 mm KCl)-stimulated (45)Ca(2+) influx into the neurons increased with increasing the duration of nicotine exposure and its concentrations.