فصلنامه علوم اعصاب شفای خاتم
سال دوم شماره 3 (پیاپی 7، تابستان 1393)

It is suggested that repetitive seizure attacks lead to the hippocampal neuronal damage and memory impairments. Some therapeutic effects, including analgesic, neuroprotective, antioxidant and anticonvulsant properties, of Nigella sativa (NS) have been reported. In the present study, the effects of hydro-alcoholic extract of NS were investigated on spatial memory damage in penthylenetetrazole (PTZ)-induced seizures in rats.
Male Wistar rats were divided into five groups: group 1 (control group) received saline. The animals in group 2 (PTZ group) were treated by saline and were injected by PTZ (50mg/kg, ip). Groups 3 (PTZ 100), 4 (PTZ 200) and 5 (PTZ 400) were treated by 100, 200, and 400 mg/kg of NS extract (ip), respectively, 30 min prior to each PTZ injection for 5 consecutive days. Finally, the animals were examined by Morris water maze test.
The animals of PTZ 100, PTZ 200, and PTZ 400 had significant lower seizure scores compared to PTZ group. The latency to the onset of seizures were also significantly higher in these groups than that of PTZ group. In Morris water maze test, the time spent and traveled distance in target quadrant by the animals of PTZ group was lower than that of control group. Pretreatment by all doses of the extract increased the time spent and traveled distance in target quadrant compared to PTZ group.
The present data suggest that the hydro-alcoholic extract of NS possesses beneficial effects on spatial memory impairments in PTZ seizures model.

Acrylamide (ACR) is a substance chemical used in industrial and laboratory procedures. Acrylamide according to the method of cooking foods are increasingly usedand its adverse effects on multiple organ systems have been described sporadically in the literature. The aim of this study was to investigate the effects of prenatal (maternal) ACR consumption on the physical development and thechanges of cerebellar volume in the rat embryo.
Female pregnant Wistarrats were orally administered 10 mg/kg ACR and/or 200 mg/kg vitamin C (vit C) solution. Pregnant rats were sacrificed on the 15thday of gestation and mother’s weight was measured. After that, their fetuses were taken out and were evaluated for fetus number and weight, crown-rump length (CRL) and cerebellar development. A total of 100 sections were cut through the entire cerebellum. From these sections, approximately 10 equidistant sections were systematic uniformly random sampled with an initial random start and stained with hematoxylin-eosin for volume estimation. The cerebellar volume was estimated by micro-projection and cavaliers’method.
The results showed that ACR caused a significant reduction in mother’s weight and volume of cerebellum as well as in the number of fetus.Histological and stereological examinations revealed that the cerebellar volume was decreased in ACR and ACR븫 C groupsvs control animals.
ACR exhibits a harmful effect on the development of the brain, which may be prevented by administration of vit C.

Trimethyltin (TMT) acts as a potent neurotoxic compound, especially in the hippocampus and therefore, it induces cognitive and memory impairments in both human and animals. The beneficial effects of sodium valproate (VPA) on cognitive functions of the brain havebeen suggested.In the present study, the effect of VPA on learning and memory deficits induced by trimethyltin was investigated in rats using Morris water maze test.
Twenty three male Wistar rats were divided into control, TMT and TMT哰 groups. TMT was injected as a single dose (12 mg/kg) in the TMT as well as TMT哰 groups. Animals of the TMT哰 group were treated by 10 mg/kg of the VPA daily for 2 weeks. Then, Morris water maze test was performed for all groups.
The escape latency and traveled path to reach the platform in the TMT group were significantly higher than control group.Treatment with VPA 10 mg/kg prevented prolongation of escape latency and traveled path induced by TMT application. There were no significant differences between TMT哰 and control groups.
The results of the present study showed that valproic acid prevented TMT-induced memory deficits. Further investigations are needed to elucidate the mechanism of neuroprotective action of VPA in TMT model.

Epilepsy has been known as a chronic brain disorder, influences large number of population around the world. Seizures should be treated as soon as possible to avoid the development of chronic epilepsy. Furthermore, there are some complications following surgical resection of epileptic focus and drug treatment. Transcranial magnetic stimulation has been suggested to generate current flow in the brain and could be an alternative to drug treatment or surgery. We study the protective effects of repetitive transcranial magnetic stimulation (rTMS) on seizure attacks and cellular damage in the amygdala in rats.
In the present study four groups of rats including intact, pentylenetetrazole, rTMSꗩ垧竗궭골 and rTMS were used to investigate rTMS effects on cellular activity and seizure attacks in a model of epilepsy. The rTMS was applied for a month and then seizures was induced by intraperitoneally injection of pentylenetetrazole and seizure scores were determined. Finally, rats were killed and neuronal injury was evaluated in the amygdala.
Seizure scores as well as histological assessment revealed a significant reduction on seizure attacks and the mean number of necrotic cells in the amygdala following rTMS application.
This study advocated a protective effect of rTMS on cellular structure in epilepsy. However, safety of rTMS in clinical practice need further investigations.

Spreading depression (SD) is a transient and self-propagating wave of neuronal and glial depolarization, followed by temporary loss of all brain activities. SD has been implicated in migraine and other headaches and can be evoked in experimental animals by electrical or chemical stimulation. It has been shown that repetitive SD produced memory deficits in juvenile rats. The effect of migraine prophylactic drugs on SD has been reported. In the present study, the effect of sumatriptan, a migraine prophylactic drug, on SD-induced memory impairments in juvenile rats was investigated.
Wistar rats (60-80 gr) were divided into SD, Sham, 0.1 sumatriptan- and 0.5 sumatriptan-treated groups and SD was induced weekly for four weeks by KCl (2 M) application. Sumatriptan (0.1 and 0.5 mg/kg) was also administrated weekly for 4 weeks in treatment groups. Memory retention of passive avoidance learning in rats was evaluated by shuttle box test in different time points.
SD significantly increased the initial latency to enter the dark compartment. SD also impaired the retention of the learned tasks. Administration of low dose sumatriptan caused improvement in memory retention 30 minutes after learning, while the high doses could improve the memory 30 minutes, 24 hours and 1 week after learning.
This study shows the positive role of sumatriptan in learning and memory impairment induced by repetitive SD.

The aim of this study was to investigate the efficacy of metacognitive therapy (MCT) on improvement of symptoms of major depression, cognitive attentional syndrome, and maladaptive copings in two patients with major depression.
Case Description: In a single case experiment with multiple baseline design 2 women suffering from major depressive disorder (MDD) were treated with eighth weekly sessions of MCT and antidepressant medications. Instruments used in this research were included Beck depression inventory, major depressive disorder scale (MDD-S), metacognitive beliefs, metacognitions questionnaires, ruminative response style (RRS), and cognitive attentional syndrome (CAS) scale.
Data indicated that metacognitive treatment resulted in reduction of subject's scores in metacognitive scale and RRS scale in post-test and 2 months follow up. The CAS and MDD-S scores showed remarkable reduction.
Metacognitive therapy as a new emerging approach appears to be an effective treatment approach for patients suffering from MDD. The effect of MCT can be due to decrease in rumination and/or positive and negative metacognitive beliefs.

Spreading depression is a transient and self-propagating wave of neuronal and glial depolarization, followed by a temporary loss of brain activities. Spreading depression is known by a huge redistribution of ions between extra- and intracellular spaces and spreads at the velocity of 2-3 mm/min in all directions. Investigations indicate the role of spreading depression in several neurological disorders, including migraine with aura, epilepsy, traumatic brain injuries, transient global amnesia, stroke, and spinal cord diseases.
Despite decades of research and hundreds of reports on the mechanism of spreading depression propagation, the exact mechanism of propagation still need to be elucidated. The present study reviews a group of these observations, in order to give some new insights into the complex mechanism of the propagation of spreading depression.

Brain development requires a complex interplay of genetic and environmental factors. Disruption of these elements can affect neuronal structure, function, or connectivity and can alter developmental trajectory. Neurotransmitters and neuromodulators, such as dopamine, participate in a wide range of behavioral and cognitive functions in the adult brain. Dopamine-mediated signaling plays a fundamental neurodevelopmental role in forebrain differentiation and circuit formation. In addition, D1 and D2 dopaminergic receptors activation influences neuronal proliferation, migration and differentiation.
As dopamine receptors affect the developing brain and play an essential role in adult brain, better understanding of the role of these receptors in different regions of the developing brain can be helpful for treatment of brain developmental disorders.