فصلنامه علوم اعصاب شفای خاتم
پیاپی 1 (زمستان 1391)

Epilepsy is the most common neurological disorder. It has been suggested that recurrent seizure attacks may damage brain tissue. Dark neurons are known as unhealthy cells and obserevd in neurosurgical biopsies, experimental ischemia, hypoglycemia and epilepsy. This study was aimed to investigate probable neuronal damage in the amygdala after acute seizures induced by pentylenetetrazol (PTZ) in rat.
Male Wistar rats were divided into control, sham and PTZ groups. EEG recordings were performed before and after the PTZ injection. The number of dark neurons in the amygdala was measured and analysed in all different groups.
There was no significant difference in the number of dark neurons in the amygdala between PTZ, control and sham groups.
The result of present study showed that acute seizure may not damage neurons in the amygdala nuclei.

Nitric oxide (NO), an important modulator of neuronal functions, is involved in synaptic plasticity and long-term potentiation (LTP). Ovarian hormones have important role on the central nervous system functions, especially learning, memory and cognitive ability. The present study was carried out to evaluate the effect of acute (A) and chronic (C) L-Arginine (L-Arg) administration on learning and memory in ovariectomized (OVX) rats.
Forthy-eight female Wistar rats were grouped as: 1) Sham, 2) OVX, 3) Sham-LA-A, 4) OVX-LA-A, 5) Sham-LA-C, 6) OVX-LA-C. The animals of sham-L-Arg-A and OVX -L-Arg-A were acutely treated with 500 mg/kg of L-Arg for 5 days. Sham-L-Arg-C and OVX -L-Arg-C chronically received 500 mg/kg/day of L-Arg during 8 weeks before 5 test days.The animals in sham and OVX groups received 1 ml/kg saline instead of L-Arg. At the end of the experiment, the animals were tested in Morris water maze and the escape latency and traveled path to reach the platform were compared between groups.
Results showed that the escape latency and traveled path in OVX group were significantly higher than in sham group (p This indicates that L-Arg has a role in Morris water maze tasks disturbances in OVX rats.

Neurodegenerative diseases, depending on the cause and condition of disease, destroy neuronal and glial cells at different regions of the brain and the spinal cord. Due to unknown pathogenesis of these diseases, definite treatment is still not available. Furthermore, there is no reliable patient-specific model for experimental and clinical investigations. Despite emerging of new therapeutic methods such as embryonic and adult stem cell therapies in last decades, difficulty of maintaining embryonic stem cells for a long duration, aggressive process of adult stem cells extraction as well as difficulties to differentiation to all variety of cell lines, limited the usage of these techniques for treatment of the patients.
Novel method of induced Pluripotent Stem (iPS) cells production by somatic cells reprogramming may be useful for the treatment of neurodegenerative diseases. The investigators succeed to produce reliable patient-specific iPS cells models for some neurodegenerative diseases such as amyotrophic lateral sclerosis and Parkinson disease.

Spreading depression (SD) is a pathophysiological phenomenon caused by repetitive depolarization of neurons and glial cells. There is a relationship between SD and some disorders, such as migraine with aura. Glycoconjugates play an important role in cell proliferation and differentiation. It has been shown that SD can stimulate the neurogenesis. In the present study, the effect of SD on expressing and distribution of glycoconjugates was evaluated.
Forty rats (30-45 days) were divided into two groups: 1 week and 1 month each group was contained three subgroups: control, sham and SD. Two and four SD was induced by KCL injection in 1 week and 1 month groups, respectively. Histochemical studies were performed by using five different horse radish peroxidase labeled lectins, including PNA, VVA, MPA and LTA in polymorph layer of hippocampal dentate gyrus.
There were no differences in the expression of three lectins (PNA, VVA, and MPA) in all different groups. However, induction of SD significantly enhanced the expression of LTA compared with sham and control groups.
Higher intensity reaction of LTA indicates a possible role of L-focuses monosaccharide in changes of synaptic plasticity induced by SD.

Herpes simplex encephalitis (HSE) is a rare but very serious disorder caused by herpes simplex type 1 virus (HSV-1). Following primary HSV-1 infection, viral latency develops in the trigeminal ganglia (TG). Therefore, prevention from primary HSV -1 infection and subsequent latency establishment is an important feature for vaccine development.
We evaluate efficacy of DNA vaccine encoding Glycoprotein D-1 (gD-1) gene of HSV-1 against lethal ocularly challenge of TCID 5 × 105 plaque-forming units (pfu) per eye of wild HSV-1 versus negative control groups.
The data demonstrated protective effects of DNA vaccine encoding Herpes simplex virus Glycoprotein D gene on latency rate in TG and mortality rate.
These results indicated that immunization with g D-1 DNA vaccine is a promising approach for eliciting a protective immunity against a HSV-1 lethal ocular challenge.

Several genes affect the prognosis of traumatic brain injury. Most studies have been conducted on E apolipoprotein (APOE). APOE may have beneficial effects in coma recovery and reducing the risk of seizures after trauma. However, allele E4 of APOE is associated with accumulation of amyloid, which causes amyloid angiopathy and extensive intracranial hematoma. Prognosis of traumatic brain injury depends on underlying factors, such as APOE, amyloid deposition, cytoskeletal rupture, diss cholinergic function, oxidative stress and the ability of the central nervous system to response to the injury. There is a little research on the effects of genes on the brain injury. DRD2 and COMT genes related to dopamine function in cognitive processes in the frontal lobes are involved.Inflammation also plays an important role in the pathophysiology of traumatic brain injury and is controlled by the gene IL. Apoptosis after traumatic brain injury is also regulated by the P53 gene. Converting enzyme gene through self-regulation mechanism of cerebral blood flow affect the prognosis of cerebral trauma. CACNA1A gene with its effect on calcium channels and its effect on prevention of brain edema affects the prognosis of brain trauma. Neprilysin gene causes a protease that plays an important role in the degradation of amyloid β protein and delayed plaque formation.
It seems that genetic factors may play an important role on the prognosis of brain injury. Further studies will be clarified this role in details.

Although central nervous system (CNS) has long been known as an immune privileged site, in common with all other tissues, it requires effective immune mechanisms to protect against infections. More recent data support that certain areas of healthy CNS are continuously monitored by resident microglia and blood-borne immune cells such as macrophage and T-cell to sustain CNS immune surveillance. Interruption of CNS surveillance by lymphocyte traffic inhibition results in injury and infection by viruses such as JC virus, herpes simplex virus, etc. CNS Immune system has to be regulated in a unique way in order to prevent inflammation and autoimmune reactions against CNS derived antigens, which there is no tolerance for them.
Here, we discuss the anatomical and cellular aspects of immune surveillance in the CNS. Moreover, we review a new model to explain how antigen-specific T-cell responses occur in the CNS.