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Background and Objective: Ischemia-reperfusion invoke cell death in hippocampus. This study was carried out to investigate the effect of transforming growth factor alpha (TGF-alpha) of dentyte jyrus neurons and pyramidal cells of CA1 subfiled of hippocampus following ischemia-reperfusion in rat models. Materials and Methods: This experimental study was done on 40 male Wistar rats weighing 250-300gr. Animals were divided in four groups: control (n=7), sham (n=7), ischemia (n=14) and treatment (n=14). Sham group was just under surgical stress. In ischemia and treatment groups after induction of ischemia-reperfiusion by obstruction of carotid arteries blocked for 30 minutes, reperfusion PBS (phosphate buffer salin) and subsequently TGF-alpha (50 ng) were injected stereotaxicaly in lateral ventricle, respectively. In 12 and 72 days after treatment the brains were fixated by transcardial perfusion and stained by immunohistochemestry and nissle methods. Furthermore, morris water maze was used to evaluate the learning memory. Data were analyzed using SPSS-16 and ANOVA test. Results: Injection of TGF-alpha increased the cell number in hippocampus of treatment group compared to ischemic group. TGF-alpha increased expression of neuron in dentyte jyrus of treatment group in comparison with ischemic group (P<0.05). Also spatial memory improved in treatment group in comparison with ischemia group. Conclusion: TGF-alpha improves ischemia-induced neurodegenration and memory impairment.

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Background and Objective: After axotomy or the compersion the nerve, the death of spinal cord nerves cell body occur. Compersion is one of the factors causing the degeneration of the spinal cord cell body. This degeneration is due to the reversed factors of the damaged area that have reached to cell body. Prosopis farcta is a member of leguminosae family and mimosaceae subfamily. The purpose of this study was to investigate the effect of ethanolic extract of pod prosopis farcta plant, on neuronal density of anterior horn following sciatic nerve compression in rat. Materials and Methods: This experimental study was performed on thirty male wistar rats with the age of about three months years and 300-350 gr weight. The animals were divided into five groups. A) control, B) compression, C) compression + treatment with 25 mg/kg ethanolic extract, D) compression + treatment with 50 mg/kg ethanolic extract and E: compression + treatment with 75 mg/kg ethanolic extract. After anesthetizing the rats, the muscle of thigh was splited and the sciatic nerve was kept under compersion, the muscle and skin were stitched subsequently. In the experimental groups the alchoholic extract of the prosopis farcta was injected to the rats with 25mg/kg, 50mg/kg, 75mg/kg dosage by the intrapritoneal way weekly. After 28 days of compresion, the rat, were put under the perfusion method and some samples were taken of their lumbar spinal cord and after tissue processes, 7 micron slide were provided of the samples serially. Slides were stained by toluidin blue, and some photos were taken and neuronal density of the alpha motoneurons alpha anterior horn of the spinal cord was calculated by the disector method. Data were analyzed using Minitab software, ANOVA and t- tests. Results: The neuronal density in the compression group (628±29.7) was decreased significantly in compare to the control group (1562±35.3) (P<0.05). The neuronal density in group C (1070±91), increased significantly in compare to the compression group (p<0.05). The neuronal density in group D (1117±62.8) and group E (1669±86.5) significantly increased in compare to the compression group (P<0.05). Conclusion: This study showed that alchoholic extract of the prosopis farcta has a neuroprotective effect following sciatic nerve compression in rats.

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Background and Objective: Brain ischemia is one of the most important factor of morbidity and mortality and leaving many people with mental and physical disabilities. Until now there are no appropriate medications to prevent and cure ischemic injury. This study was done to evaluate the protective effect of Adenosine A1 receptor and ascorbic acid on hippocampal neuronal density and memory disorder in ischemia reperfusion induced Rats. Materials and Methods: This experimental study was performed on the hippocampus pyramidal neurons on 56 male BALB/c mice. Animals randmly allocated into 8 groups (N=7) including: 1) intact, 2) ischemic control group, 3) ischemic, plus agonist and adenosine of A1 receptor, 4) ascorbic acid (100 mg/daily), 5) ischemic plus agonist adenosine receptor (1 mg/1 kg) one week after ischemia, 6) ischemia, ascorbic acid befor and after ischemia and A1 receptor (1 mg/1 kg) agonist after ischemia, 7) A1 receptor, antagonist (2.25 / 1 kg), one weed after ischemia, 8) Ascorbic acid (100 mg/1kg) before and after ischemia plus A1 receptor antagonist (2.25 / 1 kg) after ischemia. Ischemia induced by clamping of common carotid artery and the drugs was injected subsequently into peritoneum after reduction of inflammation of ischemic zone. The Y-maze memory test performed after completing the treatment period, afterward brains fixed and prepared for microscopic nissl staining method. The counting of pyramidal cells were performed at 53500 square micrometer of CA1. Data were analyzed using SPSS-15 and ANOVA test. Results: The Y-maze test showed extensive deficit in short-term memory in ischemic group (PA=200) but in treatment groups this deficit significantly reduced (PA=243, 248 and 265). The normal neuronal cell in ischemic group was significantly lowered (n=87) than treatment groups (n=111, 105 and 125) including ascorbic acid group (125), adenosine receptor agonist (105) and ascorbic acid plus agonist adenosine receptor (111). The number of normal neuronal cell in ischemic groups significantly is reduced compared to treatment group (P<0.05). Conclusion: This study showed that concurrent treatment of ascorbic acid and Adenosine A1 receptor agonist can significantly reduce the complications caused by brain ischemia in CA1 area of hippocampus.

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Background and Objective: Antiepileptic drugs can partiality control or achieve the convulsion. There are controversial issues about the use and effect of ethanol to control epileptic convulsion seizers. This study was done to determine the effect of ethanol on microvascular alterations in the brain cortex of epileptic mice treated by valporic acid (VPA). Materials and Methods: In this experimental study, 36 BALB/c mice were allocated randomly into six groups including: 1-PTZ (Pentylenetetrazol), 2- Ethanol, 3- VPA+ PTZ, 4- ethanol + PTZ, 5-ethanol+ VPA+ PTZ and control groups. The animal brains were excluded and stained by Hematoxilin and eosin. Thirty-six optical microscopic field from each group were selected and microvascular count were determined. Immunohistochemical method was used for detection of injuries in the vascular brain tissue. Results: Mean number of brain microvascular cortex significantly increaed in PTZ+ethanol and PTZ+ethanol+VPA groups in compare to controls (P<0.05). Infiltration and thrombophlebitis were observed in vessels and cortical brain tissues in mice which received ethanol and PTZ. Proliferations in endothelial vascular cells were seen in PTZ and VPA+ethanol groups. Immunohistochemical method showed the endothelial cells of PTZ+ethanol groups were more stained in compare to the other experimental groups. Conclusion: Ethanol + PTZ cause cellular infiltration and damage to the cortical brain vessels although VPA reduces histological altheretions.

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Background and Objective: Oxidative damage associated with the presence of Lead in the brain has been proposed as one possible molecular mechanism involved in Lead toxicity. Aerobic exercise is known to protect the brain through a cascade of molecular and cellular processes. The purpose of this study was to investigate the effect of 8 week aerobic training on the brain-derived neurotrophic factor (BDNF) and malondialdehyde (MDA) levels in rat's cerebellum exposed to Lead acetate. Materials and Methods: In this experimental study, 40 Male Wistar rats were randomly allocated into four groups: sedentary base, sham (30 mg/kg of ethyloleate), Lead and exercise+Lead (20 mg/kg Lead acetate, intraperitoneally). The exercise program consisted of progressive running training on the treadmill for 15 to 22 m/min, 25 to 64 min/day, and 5 days/week for 8 weeks. BDNF and MDA levels were measured by ELISA and TBARS methods, respectively. Results: Chronic Lead acetate administration enhanced significantly (P<0.05) cerebellar MDA levels in rats compare to base and sham groups but had no effect on BDNF levels. Cerebellar MDA significantly was reduced and BDNF non significantly was increased in Lead acetate+ training group. Conclusion: Regular aerobic exercise with moderate intense may exert role neuroprotective against Lead-induced cerebellar injury by down-regulating oxidative stress and promotes brain health through increases in BDNF.

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Background and Objective: Reduction in cerebral blood flow following cereblal ischemia cause the production of oxygen free radicals and finally leads to brain tissue destruction. Pyramidal cells of the CA1 region of hippocampus are highly sensitive to hypoxic condition. This study was done to determine the effect of human chorionic gonadotropin (hCG) and vitamine E on cellular density of CA1 hippocampal area, learning ability and memory, following ischemia - reperfusion injury in mice. Materials and Methods: This experimental study was done on 40 male mice in 5 groups as follow: sham control, ischemia, hCG treated, vitamine E treated and hCG + vitamine E treated groups. Single dose of vitamin E was injected intraperitonaly during the establishment of reperfusion and hCG was injected from 48h after ischemia for 5 days. Folowing the treatment period, mice brains were fixated by transcardial perfusion and stained by nissle method. The shuttle box was used to evaluate the learning memory. Results: Co-administartion of vitamine E and hCG, significantly increased the cell numbers in hippocampus compared to the ischemic group (P<0.001). Also learning and memory improved in treatment group in comparison with ischemia group (P<0.05). Conclusion: Co-administration of vitamin E and hCG improved ischemia-induced neurodegenration and memory impairment.

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Background and Objective: Compression or sciatic axotomy induces neuronal death in spinal cord alpha motor neuron. This study was carried out to determine the effect of Nigella sativa seed alcoholic extract on spinal motor neuron density in anterior horn after sciatic nerve compression in rat. Materials and Methods: In this experimental study 24 wistar rats were divided into four groups A: control, B: compression, C: compression+treatment with 75 mg/kg alcoholic extract, D: compression+treatment with 50 mg/kg alcoholic extract. In control group muscle was exposed without any injury to sciatic nerve. In compression and treatment group, the right leg sciatic nerve compressed for 60 sec. After four weeks of post operation, L2-L4 and S1, S2 and S3 segments of spinal cord were sampled, processed, serially sectioned and stained with toluidine blue. The number of alpha motor neurons was counted using dissector method. Results: Neuronal density in compression group (650±32) significantly decreased in comparison with control group (1803±24). Neuronal density in C treated group (1581±47) and D treated group (1543±49) significantly increased compare to compression group (P<0.001). Conclusion: Alcoholic extract of Nigella sativa seed increased the density of alpha motor neurons in spinal cord after sciatic nerve compression in rats.

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Background and Objective: Monosodium glutamate (MSG) is used as a food additive. Several studies have reported the adverse effects of Monosodium glutamate on the testis and brain. This study was performed to determine the effect of Monosodium glutamate in rat cerebellum. Methods: In this experimental study, 24 adult wistar rats randomly allocated into three groups including experiment A, experiment B and control (C). The animals in experiment A and B were received 3g and 6g of MSG thoroughly mixed with their feeds for 14 days, respectively. Animals in control group were received MSG free diet. Food and water for rats to be free in all of experimental time. The rats were sacrificed on fifteen day. The cerebellum dissected and fixed with formalin 10% buffer and stained with hematoxylin and eosin. Results: Disorders and detachment were observed in Purkinje and granular cell layers. Neural cell distribution in granular layer redeuced in the experimental groups. Cellular degenerative changes in the granular layer of the experimental B were more severe than experimental group A. The mean number of neuron of the granular layer in the experimental A, B and control groups were 2750, 2140 and 3150, respectively. Conclusion: The consumption of monosodium glutamate dose dependly causes histopathological changes and reduces the number of the cerebellumllar neurons in adult rat.

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Background and Objective: Parkinson disease (PD) is the second most common neurologic disorder that results following degeneration of dopaminergic neurons in the pars compacta of substintia nigra (SNc). The 1-methyl-1,2,3,6-tetrahydropiridine (MPTP) is a chemical neurotoxin that widely used in animal models of PD. This study was carried out to evaluate the numerical density of dark neurons (DNs) in the SNc in mice subjected to intraperitoneal and intranasal injection of different doses of MPTP. Methods: In this experimental study, 90 male adult BALB/c mice were randomly allocated into four experimental groups including: group 1 (MPTP was injected via i.p. at the dose of 20mg/kg per 2 hours for 4 times), group 2 (MPTP was injected via i.p. at the dose of 30mg/kg for 5 consecutive days), group 3 (MPTP was injected via i.n. at a single dose of 1mg/kg), group 4 (MPTP was injected via i.n. at a single dose of 1mg/kg), four sham and one normal groups. 20 days after the final injection, the animal's brain were removed and stained by toluidine blue. Numerical density of DNs was counted. Results: Intranasal injection of MPTP significantly increased density of dark neurons in the pars compacta of substintia nigra in compare to intraperitoneally injection of MPTP (P<0.05). Conclusion: Intranasal injection of MPTP is more effective manner to induce degeneration of neurons in substintia nigra in animal model of Parkinson's disease.

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Background and Objective: After chronic stress, brain volume and weight reduces and in turn, adrenal weight and volume increases. This study was performed to determine the effect of chronic stress and memantine administration within amygdala on the alterations of brain’s volume and weight ratio to volume and weight of the adrenal gland on male mice.

Methods: In this experimental study, bi- or unilateral amygdala cannulation was preformed stereotaxically. A week after recovery, animals were received different doses of memantine (1, 0.5, and 0.1 µg/mouse), five min before stress induction. Electric foot shock induced to animals for seven consecutive days. At the end of the seventh day, animals were sacrificed and their brain and adrenal glands were fixed in formalin 4%. The volume and weight was determined by mercury immersion and accurate balance respectively.

Results: Stress non- significantly reduced brain’s volume ratio to volume of the adrenal gland and brain’s weight ratio to weight of the adrenal gland. Memantine administration within amygdala inhibited stress effect. Memantine administration in low and medium doses within right and left amygdala significantly increased brain’s volume and weight ratio to volume and weight of the adrenal gland (P<0.05).

Conclusion: Memantine dose and side dependently inhibits the effect of induced stress in male mice. Also, unilateral memantine administration within the left and right amygdala was more effective.

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Background and Objective: Hippocampus is the main region in cortex of the brain that involved in epilepsy. This study was done to determine the effect of intraventricular injection of vitamin C on histological structure of dentate gyrus of hipocampus in adult male epileptic rats.

Methods: In this experimental study, 40 adult male rats were randomly allocated into 5 groups (n=8). Animals in three groups were received vitamin C at dose (12.5, 25 and 50 mg/kg/bw) during 28 days, intraventricularly after were kindled by (pentylentetrazol; 40 mg/kg). Animals in forth group were received normal saline after were kindled by (pentylentetrazol; 40 mg/kg). Animals in the fifth group were received normal saline. After 28 days, rats were anesthetized by ketamin, then structure of hypocamp dissected. Histological passage was done in samples and coronal section was carried out. The sections of samples were stained by Hematoxyline-eosin. Forty fields systematicly were counted the normal neurons in dentate gyrus. Morphological change was determined by immunohistochemical method.

Results: The mean  number of normal neurons in dentate gyrus in epileptic rats which  received 25 g/kg vitamin C was more than animals in groups which were received doses of 12.5, 25 and 50 mg/kg vitamin C (P<0.05). This mean number of normal neurons in dentate gyrus of hypocamp in epileptic rats which received normal saline was lower than control and other experimental groups (P<0.05). Extensive morphological change in neurons of dentate gyrus in epileptic rats which received normal saline were observed (P<0.05). The lowest  morphological change were observed in neurons of dentate gyrus in epileptic rats which received at dose 25 mg/kg vitamin C in compared to the other groups (P<0.05).

Conclusion: Intraventricular injection of vitamin C in epileptic rat's dose dependly had neuroprotective effect on dentate gyrus neurons.

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Background and Objective: Transaction or laceration and compression of peripheral nerves in accidents and different circumstances resulting Wallerian degeneration which go back to perikaryon through retrograde reaction. This study was done to determine the effect of alchohlic extract of Achillea wilhelmsii on density of motor neurons of spinal cord after sciatic nerve compression in male Wistar rats.

Methods: In this experimental study, 30 male wistar rats were randomly allocated into 5 groups: group A: control, group B: compression, group C: compression and treatment with 50 mg/kg/bw of ethanolic extract, group D: compression and treatment with 75 mg/kg/bw of ethanolic extract and group E: compression and treatment with 100 mg/kg/bw of ethanolic extract of Achillea wilhelmsii. After anesthetizing rats, skin and sub cutaneous muscles of right thigh were cut to sciatic nerve appears. Then, compression of sciatic nerve was done by a surgical forceps for 60 seconds, followed by suturing muscle and skin. Extract injection was done intraperitoneally for three weeks after compression. Group A and B were received normal saline. 28 days after compression, samples were prepared from lumbar spinal cord under perfusion method and histological sections were provided serially. After staining, density of motor neurons was calculated by dissector method.

Results: Neuronal density in the compression group (707±38.56) significantly reduced in compare to control group (1740±49.81), (P<0.05). Neuronal density in group C (1208±57.58), group D (1370±33.91), and group E (1437±64.46) significantly increased in compare to compression group (P<0.05), respectively.

Conclusion: Ethanolic extract of Achillea wilhelmsii increased neuronal density of rat's spinal cord after compression of sciatic nerve.

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Background and Objective: Ducrosia anethifolia (Dc.) is a medicinal odor plant contains CNS effective compounds which has been used in Iranian traditional medicine. This study was done to determine the effect of Ducrosia anethifolia (Dc.) Boiss essential oil on spatial learning and memory in adult male rats.

Methods: In this experimental study, 35 wistar adult male rats were randomly allocated into the five groups (n=7) including: control, sham (injected vehicle) and Ducrosia anethifolia (Dc.) Boiss essential oil groups 0.125, 0.25 and 0.5ml/kg/bw, intraperitonally during four days. Morris water maze test was used to assess learning and memory.

Results: Ducrosia anethifolia (Dc.) Boiss essential oil (0.5 ml/kg/bw) was significantly increased escape latency in the second and third (P<0.05) as well as forth (P<0.05) days of acquisition test in compare to control group. In addition latency to find the hidden platform was significantly decreased with 0.25 essential oil in all days except first day (P<0.05) and in essential oil- treated rats at 0.125 ml/kg/bw in the second and third days (P<0.05) in compare to the control group.  Time spent and distance travelled in target zone were significantly increased in Ducrosia anethifolia (Dc.) Boiss essential oil -treated rats (0.5ml/kg/bw) in compare to control group (P<0.05).

Conclusion: Intraperental administration of the Ducrosia anethifolia (Dc.) Boiss essential oil at doses of 0.5 and 0.25 ml/kg/bw during four days can improves spatial learning and memory in adult male rats.

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Background and Objective: The degeneration of motor neuron in anterior horn of spinal cord can be caused by compression. Hyssopus officinalis of Laminacea family demonstrate antioxidant and anti-inflammation effects. This study was done to evaluate the effect of alcoholic extract of Hyssopus officinalis leaves, on motor neuron in spinal cord after sciatic nerve compression in male rats.

Methods: In this experimental research, 60 male wistar rats were randomly allocated into six groups including; control, compression, and compression + treatment (25, 50, 75, 100 mg/kg/bw). In order to induce compression, sciatic nerve of right leg was exposed to compression for 60 second using locker pincers. Extract injected intraperitoneally in the first and second week after compression. 28 days after compression under profusion method, the lumber spinal cord was sampled. The density of motor neurons (9-20 micron) was measured using dissector and stereological method.

Results: Density of neurons in compression group (611±34) significantly reduced compared to the control group (1658±30) (P<0.05). Moreover, neuronal density was significantly increased in
25 (1179±22), 50 (1260±20), 75 (1350±15) and 100 (1120±10) mg/kg/bw doses in treatment groups in compared to the compression group (P<0.05).

Conclusion: Alcoholic extract of Hyssopus officinalis leaves exhibite neuroprotective effect on neurons in anterior horn of the spinal cord after injury. This effect probably is related to the antioxidant and anti inflammation properties in alcoholic extract of Hyssopus officinalis, dose dependly.

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Background and Objective: Neurotrophic factors increase neuron survival and growth. In addition their expression is altered in response to nerve injury. This study was done to evaluate the neuroprotective effect of n-butanol, ethylacetate, aqueous and hydro-alcoholic fractions of Anthemis nobilis extracts through nerve growth factor (NGF) gene expression after sciatic nerve injury in rats.

Methods: In this experimental study, 36 male Wistar rats were randomly allocated into 6 groups including control group, compression, compression + hydro-alcoholic extract, compression + n-butanol, compression + ethyl acetate fraction and compression + aqueous fraction with dose of 75 mg/kg/bw, respectively. Hydro-alcoholic, aqueous, n-butanol and ethyl acetate extract of Anthemis nobilis from aerial parts was prepared by soxhlet method. In control group, after anesthetizing the animals, the muscle was cut at the site of sciatic nerve without damaging and in compression and treatment group, the right sciatic nerve was compressed for 60 sec. The extract first time was injected intraperitoneally after nerve compression and the second was performed 7 days later. After 28 days, samples were prepared from the lumbar portion of spinal cord and cDNA was synthesized and total RNA was extracted. The changes in NGF gene expression evaluated using Δct and Real Time PCR methods.

Results: NGF gene expression significantly reduced in the compression group in compare to control (P<0.05). The expression of NGF significantly increased in treated groups including hydro-alcoholic extract, n-butanol, ethyl acetate and aqueous fractions in compare to compression group (P<0.05). The expression of NGF was more in hydro-alcoholic extract treated group in comparision with other factions treated groups.

Conclusion: Neuroprotective effect of of the aerial parts of Anthemis nobilis may be due to increase of NGF gene expression.

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Background and Objective: Dysfunction and loss of basal forebrain cholinergic neurons and their cortical projections are the earliest pathological events in the pathogenesis of alzheimer disease (AD). This study was done to evaluate the effect of donepezil hydrochloride on reference and working memory caused by mutual electrical lesion of the nucleus basalis magnocellularis (NBM) in animal model of AD.
Methods: In this experimental study, 56 adult male Wistar rats were allocated into 8 group (n=7) including: control (intact), NBM lesion group, which received electrically- induced lesion (0.5 m A, 3s) in NBM, Sham group (the electrode was impaled in to the NBM with no lesion), donepezil groups (lesion + 0.1, 1, 5, 10 mg/kg/bw of donepezil hydrochloride) and vehicle group (NBM lesion+ saline). Acquisition and retention testing were done by using an eight-radial arm maze, in which, the patterns of arm entries in each group was recorded for calculating correct choice, working memory errors, reference memory error and latency.
Results: The spatial learning of animals in the lesion of NBM group significantly reduced in compared to controls (P<0.05). Moreover, no effect on spatial learning was seen in the sham group compared with the lesion group. The post-lesion treatment with donepezil hydrochloride in dose-dependent manner improved the parameters of spatial memory errors in the acquisition and retention tasks in comparision with the lesion group (P<0.05).
Conclusion: Treatment with donepezil hydrochloride, dose-dependently improves cognitive impairment induced by the destruction of the nucleus basalis magnocellularis.

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Background and Objective: Memantine (MEM) an uncompetitive N-methyl-D-aspartate receptor antagonist is used for treatment of patients with Alzheimer disease. This study aimed to examine the effect of Memantine on the spatial learning and memory in electrical lesion’s model of nucleus basalis magnocellularis (NBM) in animal model of Alzheimer's disease.
Methods: In this experimental study, 56 adult male Wistar rats were allocated into eight groups: control group; lesion group, which received bilateral electrically lesion (0.5 mA, 3s) in NBM; sham group (the electrode was entered into the NBM with no lesion); Memantine groups (lesion+1 mg/kg/bw of MEM; lesion+3 mg/kg/bw of  MEM; lesion+5 mg/kg/bw of  MEM; lesion+7 mg/kg/bw of MEM) and Vehicle group (lesion+0.2 mL saline). After one week, animals were trained to perform the Y-maze task for five days. Twenty five days after training, a retention test was performed to determine long-term memory.
Results: The bilateral lesion of NBM impaired the spatial learning compared to the control and sham groups (P<0.05). No effect on spatial learning was seen in saline group compared with the lesion group. The treatment with Memantine in  lesion+MEM 3 mg/kg/bw, lesion+MEM 5mg/kg/bw and lesion+MEM 7mg/kg/bw groups significantly improved spatial learning (P<0.05). Moreover, no significant difference of memory was observed between the results in the 5th day of training and the retention test of the 30th day.
Conclusion: Treatment with memantine improves spatial learning defects in electrical leisions model of NBM of Alzheimer's disease in dose dependent manner in animal model.

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Background and Objective: Adult neurogenesis occurs in most mammalian species in two main areas of brain: 1- subventricular zone 2- the dentate gyrus of the hippocampus. Many factors such as 17-B estradiol affect neurogenesis in the hippocampus. The aim of this study was to investigate the effect of exogenous 17-B estradiol on neurogenesis and astrocyte functions in the ovariectomized mice.
Methods: In this experimental study; NMRI mice were allocated into five experimental groups including Sham, Control, Treatment with single dose of 17-B estradiol two weeks after ovariectomy (OVX) and were sacrificed 24 hours later, Treatment with single dose of 17-B estradiol two weeks after Ovx and were sacrificed 48 hours later and   Treatment with single dose of Seasame Oil 2 weeks after OVX and were sacrificed after 24 hours. Animals were transcardially perfused with paraformaldehyde. Brains were removed and its sections for cresyl fast violet staining and GFAP immunohistochemistry were prepared. Cells were counted and investigated.
Results: Neuronal density and Proliferation of hippocampal progenitor cells in the CA1 region of 17-B estradiol treated mice significantly increased up to 24 hours (P<0.05). Density of glia and particularly astrocytes in different regions of the hippocampus significantly reduced after treatment with 17-B estradiol (P<0.05).
Conclusion: Density of hippocampal CA1 neurons are influenced by 17-B estradiol. Also, density and morphology of glia cells, especially astrocytes in different regions of the hippocampus are affected by 17-B estradiol.

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Multiple sclerosis (MS) is a chronic and multiphasic autoimmune disease which affecting the nervous system. Recently, neurotrophic factor secreting cells have been proposed as one of the best sources for cell therapy in MS disease. Therefore, this review study was done with aimed to introduce neurotrophic factor secreting cells and the role of neurotrophic factors in the treatment of MS. The present study, based on the Systematic Review and using multiple sclerosis, neurotrophin and cell therapy keywords, 98 articles were searched from various databases including Pubmed, SID, Springer, SinceDirect Magiran, Web of Sciences and the Google Scholar. After removing irrelevant and repetitive articles, 50 articles were selected. The results of these studies showed that cell-based therapies in MS have been designed with the aim of replacing destroyed cells or with the goal of neuronal support using neural growth factors. Neurotrophic factors secreting cells with the ability to migrate to neurological lesions and secretion of neurotrophic factors can play a major role in supporting neural tissue and preventing its destruction. These factors, through tyrosine kinase receptors, have a variety of effects on the development and proper functioning of neurons. On conclusion, neurotrophic factor secreting cells due to the secretion of a wide range of neural growth factors which required for neural development might be one of the ideal cell sources for cell-based therapy in MS disease.

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Background and Objective: Multiple Sclerosis (MS) is a neurologic necrotic and chronic illness that causes by demyelination in CNS. One of the common clinical symptoms in MS is cognitive disorders. The most common cognitive defects in patients with MS are reduction of memory and information processing rate hippocampus functions in brain are memory and learning. This study was done to determine the function mechanism of memory discover by study on hippocampus. Nowadays tendency of herbal therapy is increased because of drug's side effects. This study's purpose that is from experimental typ effect of compaind extract of Portulaca olerace, Urtica dioica and Boswellia serrata on memory and number of neurons in CA1 area of hippocampus in induced multiple sclerosis rats.
Methods: In this experimental study 30 male adult rats were randomly allocated into control group, sham group (salin injection), (MS + salin) group, (MS + mixture extract, dose of 200 mg/kg), (MS + mixture extract, dose of 400 mg/kg). MS model was induced by intra hippocampal injection a single dose of ethidium bromide (0.01% ethidium bromide sulotion in 0.9% salin) and in 3 microlitre volume with 1 microlitre in minute rate intraperitoneally. Compaind extract of Portulaca olerace, Urtica dioica and Boswellia serrata were injected as the treatment for 21 days. The shuttle box test was used for evaluation of memory. Dissector method was used for neural density in CA1 of hippocampus. Histopathology method was used for evaluation of the alteration of cells.
Results: Neural density in MS induced group was singnificantly reduced in comparison with control and sham groups (P<0.05). Neural density was singnificantly increased in treatment groups in comparison with MS induced group (P<0.05). Histological results showed that induction of MS caused the disrution of neuron cells in compare to controls, but intraperitonal injection of compaind extract cause neurogenesis in tertment groups. Memory in MS induced group was singnificantly reduced in comparison with control and sham groups (P<0.05), but memory was singnificantly increased in treatment groups in comparison with MS induced group (P<0.05).
Conclusion: Compaind extract of Portulaca olerace, Urtica dioica and Boswellia serrata with dosages of 200 and 400 mg/kg/bw due to neurogenesis and amilioration can effective in memory recovery and neural necrosis in MS disease.