NDEL1 was decreased in the CA3 region but increased in the hippocampal blood vessel network during the spontaneous seizure period after pilocarpine-induced status epilepticus.

Nuclear distribution factor E homolog like 1 (NDEL1) plays an important role in mitosis, neuronal migration, and microtubule organization during brain development by binding to disrupted-in-schizophrenia-1 (DISC1) or lissencephaly (LIS1). Although some evidence has suggested that DISC1 expression is altered in epilepsy, few studies have reported the relationship between NDEL1 and the etiology of epilepsy. In present study, we first investigated the expression of NDEL1 and its binding protein DISC1 after pilocarpine-induced epilepsy in male C57BL/6 mice. Data revealed that the mRNA and protein expression of NDEL1 and DISC1 in the whole hippocampus increased during the spontaneous seizure period after status epilepticus (SE). Interestingly, however, the expression of NDEL1 was decreased in the cornu ammonis 3 (CA3) and dentate gyrus (DG) regions. Moreover, SE also increased the number of blood vessels that fed the CA3 and DG regions of the hippocampus and increased the incidence of abnormalities in capillary network formation where NDEL1 protein was expressed positively. Meanwhile, the expression of phosphorylated ERK (p-ERK) was also increased during the spontaneous seizure period, with a similar expression pattern as NDEL1 and DISC1. Based on these results, we hypothesize that NDEL1 might interact with DISC1 to activate ERK signaling and function as a potential protective factor during the spontaneous seizure period after pilocarpine-induced SE.

Effect of glucose administration on contusion volume after moderate cortical impact injury in rats.

Previous studies had shown that pre- and postinjury glucose administration increased brain injury caused by a mild cortical impact injury only when the traumatic injury was complicated by a secondary ischemic insult. The purpose of this study was to examine the effect of pre- and postinjury glucose administration on a more severe cortical impact injury, where primary ischemia occurs at the site of the impact. Long Evans rats who were fasted overnight and anesthetized with isoflurane were subjected to a 5-m/sec, 2.5-mm impact injury. The animals were randomly assigned one of the following treatments: (1) 2.2 g/kg glucose in 4 ml of saline, 20 min prior to injury; (2) 2.0 g/kg glucose in 4 ml of saline, 20 min after injury; or (3) 4 ml of saline either 20 min before injury or 20 min after the injury. At 2 weeks, the animals were sacrificed and the brains were examined for contusion volume and for neuronal loss in CA1 and CA3 regions of the hippocampus. Contusion volume was increased from a median value of 23 mm3 in the saline-infused animals to 34 mm3 in the preimpact glucose infusion animals (p=0.005). Postimpact glucose infusion had no effect on contusion volume. Neuron density in CA1 and CA3 regions of the hippocampus was similar in all three treatment groups. These studies support the hypothesis that glucose administration adversely affects experimental traumatic brain injury in those circumstances where the trauma is complicated by primary cerebral ischemia, such as around cortical contusions.