Recent observations from our laboratory have led us to hypothesize that d-opioid receptors may play a role in neuronal protection against hypoxic / ischemic or glutamate excitotocity. To test our hypothesis in this work, we used two independent methods, i.e., ‘‘same field quantification’’ of morphologic criteria and a biochemical assay of lactate dehydrogenase (LDH) release (an index of cellula...

BACKGROUND/AIMS Enriched environment (EE) has been reported to exert neuroprotective effect in animal models of ischemic stroke. However, the underlying mechanism remains unclear. The purpose of this study was to investigate the effect of EE treatment on neuronal apoptosis in the periinfarct cortex after cerebral ischemia/reperfusion (I/R) injury. METHODS The cerebral I/R injury was establish...

Peroxisome proliferator-activated receptor-γ (PPAR-γ) has recently emerged as potential therapeutic agents for cerebral ischemia-reperfusion (I/R) injury because of anti-neuronal apoptotic actions. However, whether PPAR-γ activation mediates neuronal autophagy in such conditions remains unclear. Therefore, in this study, we investigated the role of PPAR-γ agonist 15-PGJ(2) on neuronal autophagy...

In the United States over 1.7 million cases of traumatic brain injury are reported yearly, but predictive correlation of cellular injury to impact tissue strain is still lacking, particularly for neuronal injury resulting from compression. Given the prevalence of compressive deformations in most blunt head trauma, this information is critically important for the development of future mitigation...

traumatic brain injury (tbi) initiates a cascade of numerous pathophysiological events that evolve over time. despite the complexity of tbi, research aimed at therapy development has almost exclusively focused on single therapies, all of which have failed in multicenter clinical trials. a variety of brain insults, including traumatic brain injury, encephalitis, stroke, and status epilepticus (s...

seizure activity has been proposed to result in the generation of reactive oxygen species (ros), which then contribute to seizure-induced neuronal damage and eventually cell death. although the mechanisms of seizure-induced ros generation are unclear, mitochondria and cellular calcium overload have been proposed to have a crucial role. we aim to determine the sources of seizure-induced ros and ...

Glucocorticoid and glucocorticoid receptor (GC/GR) interactions alter numerous aspects of neuronal function. These consequences (e.g., anti-inflammatory vs. pro-inflammatory) can vary depending on the duration of GC exposure or central nervous system (CNS) injury model. In this review we discuss how GC/GR interactions impact neuronal recovery after a central or peripheral nerve injury and discu...

Spinal cord injury causes neuronal death, limiting subsequent regeneration and recovery. Thus, there is a need to develop strategies for improving neuronal survival after injury. Relative to our understanding of axon regeneration, comparatively little is known about the mechanisms that promote the survival of damaged neurons. To address this, we took advantage of lamprey giant reticulospinal ne...

We have developed novel device where a localised axonal stretch injury is achieved by the integration of a pressure-flexible valve in the axon compartment of a fluidically isolated neuron culture device. Defined stretch injuries applied using this device resulted in delayed neuronal alterations typical of those observed in vivo. These results confirm the suitability of this system for studying ...

The human brain is interconnected in a plastic manner to form functional net-works. This dynamic and flexible neuronal reorganization process essential for an efficient regeneration the central nervous system, especially when it comes memory, learning, posttraumatic conditions. Here, we tried define basic principles mechanisms underlying neuroplasticity which serve as important template future ...