Brain research
-
Vasogenic brain edema is one of the major determinants for mortality following subarachnoid hemorrhage (SAH). Although the formation of vasogenic brain edema occurs on the microvascular level by opening of endothelial tight junctions and disruption of the basal lamina, microvascular changes following experimental SAH are poorly characterized. The aim of the present study was therefore to investigate the time course of blood-brain barrier (BBB) dysfunction and basal lamina damage following SAH as a basis for the better understanding of the pathophysiology of SAH. ⋯ Microvascular damage as documented by collagen IV degradation and albumin extravasation is a long lasting and ongoing process following SAH. Due to its delayed manner microvascular damage may be prone for therapeutic interventions. However, further investigations are needed to determine the molecular mechanisms responsible for basal lamina degradation and hence damage of the microvasculature following SAH.
-
Cerebral blood flow (CBF), a surrogate of neural activity in the identification of brain regions involved in specific functions, has been used in this report to trace the compensatory enhancement of activity in non-traumatized areas of the brain following a focal lesion. We have previously shown activation of CBF in the cortex contralateral to a focal contusion, 24 h after the event. The present report extends the characterization of this trans-hemispheric cortical blood flow activation by studying its time course and regional distribution from 4 days to 4 weeks post-trauma. ⋯ This phenomenon was present in all cortical regions symmetrical to the impact zone, but also in auditory, visual, entorhinal and insular cortex. These results suggest that the participation of the contralateral cortex in the recovery from unilateral brain trauma is not limited to the regions homologous to those that received the impact. The time course of CBF changes was found to be consistent with the recovery of motor function in this model.
-
Subthreshold membrane potential oscillations (SMPO) in the injured dorsal root ganglion (DRG) neurons are involved in the generation of spontaneous activity, which can directly evoke neuropathic pain. Nerve injury usually triggers the synthesis of large quantities of membrane protein in nerve injured DRG neurons. Membrane proteins are glycosylated by addition of sugars, especially negatively charged sialic acid residues, which may depolarize the resting membrane potential (Vm), open voltage-gated channels in injured neurons, and cause spontaneous activity. ⋯ Topical application of neuraminidase to selectively remove sialic acid residues on the extracellular membrane normalized the depolarized Vm and inhibited both spontaneous and evoked SMPO. However, application of Ca(2+), Mg(2+), Mn(2+) or neuraminidase had no effect on excitability and Vm in normal neurons. The results demonstrated that the increase in negatively charged sialic acid residues on the extracellular membrane of neuronal somata is a critical factor in the generation of SMPO and hyperexcitability in injured sensory neurons.
-
This paper studied the effects of crocin, a pharmacologically active component of Crocus sativus L., on ischemia/reperfusion (I/R) injury in mice cerebral microvessels. Transient global cerebral ischemia (20 min), followed by 24 h of reperfusion, significantly promoted the generation of nitric oxide (NO) and malondialdehyde (MDA) in cortical microvascular homogenates, as well as markedly reduced the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-px) and promoted the activity of nitric oxide synthase (NOs). Reperfusion for 24 h led to serous edema with substantial microvilli loss, vacuolation, membrane damage and mitochondrial injuries in cortical microvascular endothelial cells (CMEC). ⋯ Pretreatment with crocin markedly inhibited oxidizing reactions and modulated the ultrastructure of CMEC in mice with 20 min of bilateral common carotid artery occlusion (BCCAO) followed by 24 h of reperfusion in vivo. Furthermore, crocin inhibited GRK2 translocation from the cytosol to the membrane and reduced ERK1/2 phosphorylation and MMP-9 expression in cortical microvessels. We propose that crocin protects the brain against excessive oxidative stress and constitutes a potential therapeutic candidate in transient global cerebral ischemia.
-
A number of electroencephalographic (EEG) studies report on motor event-related desynchronization and synchronization (ERD/ERS) in the beta band, i.e. a decrease and increase of spectral amplitudes of central beta rhythms in the range from 13 to 35 Hz. Following an ERD that occurs shortly before and during the movement, bursts of beta oscillations (beta ERS) appear within a 1-s interval after movement offset. Such a post-movement beta ERS has been reported after voluntary hand movements, passive movements, movement imagination, and also after movements induced by functional electrical stimulation. ⋯ This is in contrast to a diffuse and broad distributed ERD/ERS pattern during attempted foot movements in patients. Only one patient showed a similar ERD/ERS pattern. Furthermore, no significant ERD/ERS patterns during passive foot movement in the group of the paraplegics could be found.