A novel anti-epileptogenesis strategy of temporal lobe epilepsy based on nitric oxide donor.

The molecular mechanism underlying the role of hippocampal hilar interneuron degeneration in temporal lobe epilepsy (TLE) remains unclear. Especially, very few studies have focused on the role of neuronal nitric oxide synthase (nNOS, encoded by Nos1) containing hilar interneurons in TLE. In the present study, Nos1 conditional knockout mice were constructed, and we found that selective deletion of Nos1 in hilar interneurons rather than dentate granular cells (DGCs) triggered epileptogenesis.

Acute single dose of ketamine relieves mechanical allodynia and consequent depression-like behaviors in a rat model.

Both chronic pain and depression are debilitating diseases, which often coexist in clinic. However, current analgesics and antidepressants exhibit limited efficacy for this comorbidity. The present study aimed to investigate the effect of ketamine on the comorbidity of inflammatory pain and consequent depression-like behaviors in a rat model established by intraplantar administration of complete Freunds adjuvant (CFA).

Tert-butylhydroquinone Ameliorates Early Brain Injury After Experimental Subarachnoid Hemorrhage in Mice by Enhancing Nrf2-Independent Autophagy.

Evidence has shown that the activation of the autophagy pathway after experimental subarachnoid hemorrhage (SAH) protects against neuronal damage. Tert-butylhydroquinone (tBHQ), a commonly used nuclear factor erythroid 2-related factor 2 (Nrf2) activator, was found to significantly enhance autophagy activation. The aim of this study was to explore the effect of tBHQ treatment on early stage brain injury at 24 h after SAH.

Management of hydrocephalus secondary to pineal region tumors.

Background: Hydrocephalus is often secondary to pineal region tumors. Hydrocephalus can lead to high intracranial pressure, which in turn results in disturbance of consciousness, cerebral hernia, and even death. Hydrocephalus management is important in the treatment of pineal region tumors.

Zinc as mediator of ubiquitin conjugation following traumatic brain injury.

Previous studies have shown that pathological zinc accumulation and deposition of ubiquitinated protein aggregates are commonly detected in many acute neural injuries, such as trauma, epilepsy and ischemia. However, the underlying mechanisms are poorly understood. Here we assessed the effect of zinc on ubiquitin conjugation and subsequent neurodegeration following traumatic brain injury (TBI).

The expression of PGC-1α in the mice brain after traumatic brain injury.

Background: Peroxisome proliferator activated receptor γ co-activator-1α (PGC-1α) is a transcriptional co-activator that co-ordinately regulates genes required for mitochondrial biogenesis and is a key contributor to the up-regulation of antioxidant activities in response to oxidative stress. The expression pattern of PGC-1α after traumatic brain injury (TBI) has not been studied.

Materials And Methods: Ninety male ICR mice (28-32 g) were randomly assigned to six groups: sham, 3, 6, 12, 24 and 48 hours after TBI.