Theophylline treatment improves mitochondrial function after upper cervical spinal cord hemisection.

The importance of mitochondria in spinal cord injury has mainly been attributed to their participation in apoptosis at the site of injury. But another aspect of mitochondrial function is the generation of more than 90% of cellular energy in the form of ATP, mediated by the oxidative phosphorylation (OxPhos) process. Cytochrome c oxidase (CcO) is a central OxPhos component and changes in its activity reflect changes in energy demand.

Amelioration of hypoperfusion after traumatic brain injury by in vivo endothelin-1 knockout.

Endothelin 1 (ET-1) is one of the most powerful vasoconstrictors in the brain. Its expression is upregulated after traumatic brain injury (TBI) and is a major factor in the ensuing hypoperfusion. Attenuation of ET-1 effects has been mainly achieved by blockade of its receptors.

Differential expression of adenosine A1 and A2A receptors after upper cervical (C2) spinal cord hemisection in adult rats.

Background: In an animal model of spinal cord injury, a latent respiratory motor pathway can be pharmacologically activated via adenosine receptors to restore respiratory function after cervical (C2) spinal cord hemisection that paralyzes the hemidiaphragm ipsilateral to injury. Although spinal phrenic motoneurons immunopositive for adenosine receptors have been demonstrated (C3-C5), it is unclear if adenosine receptor protein levels are altered after C2 hemisection and theophylline administration.

Objective: To assess the effects of C2 spinal cord hemisection and theophylline administration on the expression of adenosine receptor proteins.

Spatial alterations in endothelin receptor expression are temporally associated with the altered microcirculation after brain trauma.

Objectives: To study the cellular distribution of endothelin receptors A and B (ETrA and ETrB) in the post-traumatic sensorimotor cortex and hippocampus.

Materials And Methods: We inflicted closed head trauma to male Sprague-Dawley rats and visualized ETrA and ETrB immunoreactivity with 3,3'-diaminobenzidine.

Results: ETrA immunolabeling was the most prominent in pyramidal neurons 24 and 48 hours post-trauma, while it reached its peak in the microvasculature at hour 4.

Alterations in cerebral cortex microvessels and the microcirculation in a rat model of traumatic brain injury: a correlative EM and laser Doppler flowmetry study.

Objectives: We sought to establish the temporal association of fluctuations in cortical cerebral blood flow (CBF) with ultrastructural alterations of microvessels in rat sensorimotor cortex (smCx) following administration of a rodent acceleration impact model of traumatic brain injury (TBI).

Methods: Laser Doppler flowmetry (LDF) and electron microscopy (EM) were used in parallel experiments that lasted for up to 48 hours after induction of TBI.

Results: Compared to sham-operated control, there was a 37% reduction of cortical CBF between 12 and 24 hours, this reduction remaining unchanged for up to 48 hours post-TBI.

Subcellular redistribution of calponin underlies sustained vascular contractility following traumatic brain injury.

Objectives: The purpose of this study was to observe temporal changes in calponin (Cp), a contractile protein, in response to traumatic brain injury (TBI).

Methods: Double immunocytochemistry in conjunction with morphometric methods was used to study Cp temporal migration in smooth muscle cells (SM) of reacting microvessels following TBI, as induced using a weight-drop, acceleration impact method.

Results: Quantification of migrated Cp in the SM wall after TBI was carried out on three-dimensional orthographic reconstructions of serial, digitally acquired images and optical densitometry.

In vivo measurement of tissue damage, oxygen saturation changes and blood flow changes after experimental traumatic brain injury in rats using susceptibility weighted imaging.

Traumatic brain injury (TBI) is a prevalent disease, and many TBI patients experience disturbed cerebral blood flow (CBF) after injury. Moreover, TBI is difficult to quantify with conventional imaging modalities. In this paper, we utilized susceptibility weighted imaging (SWI) as a means to monitor functional blood oxygenation changes and to quantify CBF changes in animals after trauma.

Calponin and caldesmon cellular domains in reacting microvessels following traumatic brain injury.

Calponin (Cp) and caldesmon (Cd) are actin-binding proteins involved in the regulation of smooth muscle (SM) tone during blood vessel contraction. While in vitro studies have reported modifications of these proteins during vessel contractility, their role in vivo remains unclear. Traumatic brain injury (TBI) causes disruption of cerebral microvascular tone, leading to sustained contractility in reacting microvessels and cerebral hypoperfusion.

Cellular compartmentalization of phosphorylated eIF2alpha and neuronal NOS in human temporal lobe epilepsy with hippocampal sclerosis.

Hippocampal sclerosis (HS) is the most common neuropathologic finding in patients with medically refractory temporal lobe epilepsy (TLE). The mechanisms resulting in neuronal injury and cell loss in HS are incompletely understood, but inhibition of protein synthesis may play a pivotal role in these processes. This study examined the relationships between two molecules known to be involved in reduced protein synthesis in animals subjected to traumatic brain injury.