en
jalali
1394
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gregorian
2015
7
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online
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fulltext
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Editorial: Utilization of Hybrid PET/MR in Neuroimaging
No abstract
PET/MR, PET/CT, neuroimaging, neurodegenerative diseases
143
146
http://bcn.iums.ac.ir/browse.php?a_code=A-10-715-1&slc_lang=en&sid=1
2015/02/18
1393/11/29
2015/07/1
1394/4/10
Masoud
Tahmasian
Department of Neurology, University Hospital of Cologne, Cologne, Germany
masoudtahmasian@gmail.com
0031947532846005703
0031947532846005703
Yes
Carsten
Eggers
Department of Neurology, University Hospital of Cologne, Cologne, Germany
arsten.eggers@uk-koeln.de
0031947532846005704
0031947532846005704
No
Valentin
Riedl
Department of Neuroradiology, Klinikum rechts der Isar, Technische Universität München, Munich, Germany
valentin.riedl@mytum.de
0031947532846005705
0031947532846005705
No
Christian
Sorg
Department of Neuroradiology, Klinikum rechts der Isar, Technische Universität München, Munich, Germany
c.sorg@lrz.tu-muenchen.de
0031947532846005706
0031947532846005706
No
Alexander
Drzezga
Department of Nuclear Medicine, University Hospital of Cologne, Cologne, Germany
0031947532846005707
0031947532846005707
No
en
Study the Effect of Endocannabinoid System on Rat Behavior in Elevated Plus-Maze
Introduction: Previous studies have shown that cannabinoidergic system is involved in anxiety. However, there are controversial reports in the experimental studies. The aim of this study is to evaluate the effect of pharmacological stimulation or blocking of CB1 receptors and inhibition of endocannabinoid degradation in anxiety like behavior in elevated plus-maze (EPM) test in rat. The EPM is one of the most widely used animal models of anxiety.
Methods: Male Wistar rats were randomly allocated to ten groups. Different groups of animals intraperitoneally received Win-55212 (0.3, 1 and 5 mg/kg) as CB1 receptor agonist, AM- 251 (0.3, 1 and 5 mg/kg) as CB1 receptor antagonist, URB-597 (0.03, 0.1 and 0.3 mg/kg) as endocannabinoid breakdown inhibitor or saline (as control group) 30 min before submitting into EPM test.
Results: The results showed that compared to the control group, Win-55212 (1 and 5 mg/kg) and URB-597 (0.1 and 0.3 mg/kg) significantly increased both of the time and percentage of entries into open arms. AM-251 (1 and 5 mg/kg) significantly decreased the time and percentage of entries into open arms in the EPM test. These substances have no effects on the total distance covered by animals and number of closed arm entries.
Discussion: It is concluded that activation of cannabinoid receptor exert anxiolytic effect while blocking of cannabinoid receptor resulted in anxiety behavior. The locomotor activity was not significantly changed by cannabinoid system. It is suggested that potentiation of cannabinoid system may be therapeutic strategy for the anxiety behavior.
Anxiety, Cannabinoids, URB 597, Rat
147
153
http://bcn.iums.ac.ir/browse.php?a_code=A-10-290-3&slc_lang=en&sid=1
2015/02/182014/12/9
1393/9/18
2015/07/12015/05/11
1394/2/21
Alireza
Komaki
Hamadan University of Medical Sciences
alirezakomaki@gmail.com
0031947532846009668
0031947532846009668
Yes
Nasrin
Hashemi-Firouzi
Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
nhashemifirozi@yahoo.com
0031947532846009669
0031947532846009669
No
Shiva
Shojaie
Department of Physiology, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran
0031947532846009670
0031947532846009670
No
Zobin
Souri
Department of Physiology, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran
0031947532846009671
0031947532846009671
No
Somayeh
Heidari
Department of Physiology, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran
0031947532846009672
0031947532846009672
No
Siamak
Shahidi
Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
siamakshahidi@gmail.com
0031947532846009673
0031947532846009673
No
en
Glucocorticoids Interact with Cholinergic System in Impairing Memory Reconsolidation of an Inhibitory Avoidance Task in Mice
Introduction: Recent studies suggest that glucocorticoids modulate memory reconsolidation.
Moreover, cholinergic system is involved in memory reconsolidation. Since glucocorticoids
interact with brain cholinergic system in modulating memory processing, we investigated
whether glucocorticoid influences on the reconsolidation of emotionally arousing training
depend on the cholinergic system. Methods: Mice were trained (1mA, 3s footshock) in an inhibitory avoidance task. Forty-eight
hours after training, memory reactivation was occurred (Test 1), and different treatments were
given. Two (Test 2), five (Test 3), and seven days (Test 4) after memory reactivation (Test 1),
animals were retested for fear memory retention. Results: In the first experiment, we observed that administration of corticosterone (CORT, 0.3,
1 and 3 mg/kg) following memory reactivation impaired subsequent expression of memory in a
dose-dependent manner. In the second experiment, we found that CORT-induced impairment of
memory reconsolidation was reversed by the muscarinic receptor antagonist atropine (0.5 and 2
mg/kg). In the third experiment, the nicotinic receptor antagonist mecaylamine (0.5 or 2 mg/kg)
was not able to block the corticosterone response. Discussion: These findings indicate that glucocorticoids impair memory reconsolidation by a
muscarinic cholinergic mechanism.
Memory reconsolidation, Glucocorticoids, Cholinergic agents
155
162
http://bcn.iums.ac.ir/browse.php?a_code=A-10-72-4&slc_lang=en&sid=1
2015/02/182014/12/92014/11/2
1393/8/11
2015/07/12015/05/112015/04/18
1394/1/29
Somayeh
Amiri
Laboratory of Learning and Memory, Department and Research Center of Physiology, School of Medicine, Semnan University of Medical Sciences, 15131-38111, Semnan, Iran.
s.amiri@yahoo.com
0031947532846005714
0031947532846005714
No
Zahra
Jafarian
Laboratory of Learning and Memory, Department and Research Center of Physiology, School of Medicine, Semnan University of Medical Sciences, 15131-38111, Semnan, Iran.
jafarian@yahoo.com
0031947532846005715
0031947532846005715
No
Abbas Ali
Vafaei
Laboratory of Learning and Memory, Department and Research Center of Physiology, School of Medicine, Semnan University of Medical Sciences, 15131-38111, Semnan, Iran.
aavaf43@yahoo.com
0031947532846005716
0031947532846005716
No
Ali
Rashidy-Pour
Semnan University of Medical Sciences
rashidy-pour@semums.ac.or
0031947532846005717
0031947532846005717
Yes
Zahra
Motaghed larijani
zahramotaghedlarijani@yahoo.com
0031947532846005718
0031947532846005718
No
Seyed Afshin
Samaei
0031947532846005719
0031947532846005719
No
en
The Role of Hippocampal 5HT3 Receptors in Harmaline-Induced Memory Deficit
Introduction: The plethora of studies indicated that there is a cross talk relationship between harmaline and serotonergic (5-HT) system on cognitive and non-cognitive behaviors. Thus, the purpose of this study is to assess the effects of hippocampal 5-HT4 receptor on memory acquisition deficit induced by harmaline.
Methods: Harmaline was injected peritoneally, while 5-HT4 receptor agonist (RS67333) and antagonist (RS23597-190) were injected intra-hippocampal. A single-trial step-down passive avoidance, open field and tail flick tasks were used for measurement of memory, locomotor activity and pain responses, respectively.
Results: The data revealed that pre-training injection of higher dose of harmaline (1 mg/kg), RS67333 (0.5 ng/mouse) and RS23597-190 (0.5 ng/mouse) decreased memory acquisition process in the adult mice. Moreover, concurrent pre-training administration of subthreshold dose of RS67333 (0.005 ng/mouse) or RS23597-190 (0.005 ng/mouse) with subthreshold dose of harmaline (0.5 mg/kg, i.p.) intensify impairment of memory acquisition. All above interventions did not change locomotion and tail flick behaviors.
Discussion: The results demonstrated that the synergistic effect between both hippocampal 5-HT4 receptor agonist and antagonist with impairment of memory acquisition induced by harmaline, indicating a modulatory effect for hippocampal 5HT4 receptor on Harmaline induced amnesia.
Memory reconsolidation, Glucocorticoids, Cholinergic agents
163
170
http://bcn.iums.ac.ir/browse.php?a_code=A-10-273-2&slc_lang=en&sid=1
2015/02/182014/12/92014/11/22014/11/30
1393/9/9
2015/07/12015/05/112015/04/182015/04/25
1394/2/5
Mohammad
Nasehi
Islamic Azad University, Garmsar Branch
Mo58na@yahoo.com
0031947532846009701
0031947532846009701
Yes
en
Involvement of Mu Opioid Receptor Signaling in The Protective Effect of Opioid against 6-Hydroxydopamine-Induced SH-SY5Y Human Neuroblastoma Cells Apoptosis
Introduction: The neuroprotective role of opioid morphine against 6-hydroxydopamineinduced
cell death has been demonstrated. However, the exact mechanism(s) underlying such
neuroprotection, especially the role of subtype receptors, has not yet been fully clarified. Methods: Here, we investigated the effects of different opioid agonists on 6-OHDA-induced
neurotoxicity in human neuroblastoma SH-SY5Y cell line as an in vitro model of Parkinson’s
disease. Cell damage was induced by 150 μM 6-OHDA and the cells viability was examined by
MTT assay. Intracellular calcium, reactive oxygen species and mitochondrial membrane potential
were assessed by fluorescence spectrophotometry method. Immunoblot technique was used to
evaluate cytochrome-c and activated caspase-3 as biochemical markers of apoptosis induction. Results: The data showed that 6-OHDA caused significant cell damage, loss of mitochondrial
membrane potential and increase in intracellular reactive oxygen species and calcium levels
as well as activated caspase-3 and cytochrome-c release. Incubation of SH-SY5Y cells with
μ-opioid agonists, morphine and DAMGO, but not with δ-opioid agonist, DADLE, elicited
protective effect and reduced biochemical markers of cell damage and death. Discussion: The results suggest that μ-opioid receptors signaling participate in the opioid
neuroprotective effects against 6-OHDA-induced neurotoxicity.
Morphine, DAMGO, μ-opioid receptors, 6-hydroxydopamine, Apoptosis, SH-SY5Y cells
171
178
http://bcn.iums.ac.ir/browse.php?a_code=A-10-668-1&slc_lang=en&sid=1
2015/02/182014/12/92014/11/22014/11/302014/11/11
1393/8/20
2015/07/12015/05/112015/04/182015/04/252015/05/21
1394/2/31
Shahrzad
Eftekhar-Vaghefi
Shahid Bahonar University of Kerman. Kerman, Iran
0031947532846005751
0031947532846005751
No
Saeed
Esmaeili Mahani
Shahid Bahonar University of Kerman
semahani@yahoo.com
0031947532846005752
0031947532846005752
Yes
Leila
Elyasi
Neuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences. Kerman, Iran
0031947532846005753
0031947532846005753
No
Mehdi
Abbasnejad
Shahid Bahonar University of Kerman. Kerman, Iran
0031947532846005754
0031947532846005754
No
en
X Chromosome Inactivation in Opioid Addicted Women
Introduction: X chromosome inactivation (XCI) is a process during which one of the two X
chromosomes in female human is silenced leading to equal gene expression with males who
have only one X chromosome. Here we have investigated XCI ratio in females with opioid
addiction to see whether XCI skewness in women could be a risk factor for opioid addiction. Methods: 30 adult females meeting DSM IV criteria for opioid addiction and 30 control females
with no known history of addiction were included in the study. Digested and undigested DNA
samples which were extracted from blood were analyzed after amplification of the polymorphic
androgen receptor (AR) gene located on the X chromosome. XCI skewness was studied in 3
ranges: 50:50–64:36 (random inactivation), 65:35–80:20 (moderately skewed) and >80:20
(highly skewed). Results: XCI from informative females in control group was 63% (N=19) random, 27% (N=8)
moderately skewed and 10% (N=3) highly skewed. Addicted women showed 57%, 23% and
20%, respectively. The distribution and frequency of XCI status in women with opioid addiction
was not significantly different from control group (P=0.55). Discussion: Our data did not approve our hypothesis of increased XCI skewness among women
with opioid addiction or unbalanced (non-random) expression of genes associated with X
chromosome in female opioid addicted subjects.
X Chromosome inactivation, Opiate addiction, Women
179
184
http://bcn.iums.ac.ir/browse.php?a_code=A-10-255-3&slc_lang=en&sid=1
2015/02/182014/12/92014/11/22014/11/302014/11/112015/02/18
1393/11/29
2015/07/12015/05/112015/04/182015/04/252015/05/212015/05/22
1394/3/1
Nasim
Vousooghi
n-vousooghi@tums.ac.ir
0031947532846005725
0031947532846005725
No
Mitra-Sadat
Sadat Shirazi
n-vousooghi@tums.ac.ir
0031947532846005726
0031947532846005726
No
Ali
Goodarzi
n-vousooghi@tums.ac.ir
0031947532846005727
0031947532846005727
No
Peyman
Hassani Abharian
n-vousooghi@tums.ac.ir
0031947532846005728
0031947532846005728
No
Mohammad-Reza
Zarrindast
Tehran University of Medical Sciences
n-vousooghi@tums.ac.ir
0031947532846005729
0031947532846005729
Yes
en
Vitex Agnus Castus Extract Improves Learning and Memory and Increases the Transcription of Estrogen Receptor α in Hippocampus of Ovariectomized Rats
Introduction: Lower level of estrogen hormone is considered as an important factor for loss of
learning and memory in postmenopausal women. Although estrogen replacement therapy is used
for compensation, but long-term usage of estrogen is associated with a higher risk of hormonedependent
cancers. Phytoestrogens, due to fewer side effects, have been proposed to prevent
menopause-related cognitive decline. Methods: 24 female Wistar rats weighing 180-220 g were used in this study. The animals were
ovariectomized and randomly divided into four groups including, control and two groups which
received 8 and 80 mg/kg Vitex agnus castus (VAC) ethanolic extract orally. The last groups
were treated with 40 μg/kg of estradiol valerat. Step-through passive avoidance (STPA) test was
used for the evaluation of learning and memory. The hippocampal estrogen receptor α (ERα)
expression was measured using Real-Time PCR. Results: The results demonstrated that VAC extract or estradiol had better performance on stepthrough
passive avoidance test than control group (all P<0.05). Moreover, administration of
either estradiol or VAC extract increased the hippocampal mRNA level of ERα and prevented
the decrease in uterine weight of ovariectomized rats. Discussion: Based on our data, VAC extract improves learning and memory in ovariectomized
rats. The positive effect of VAC extract on learning and memory is possibly associated with an
increase in ERα gene expression in the hippocampal formation.
Vitex agnus-castus, Memory, Ovariectomy, Estrogen receptor alpha
185
192
http://bcn.iums.ac.ir/browse.php?a_code=A-10-147-2&slc_lang=en&sid=1
2015/02/182014/12/92014/11/22014/11/302014/11/112015/02/182015/02/23
1393/12/4
2015/07/12015/05/112015/04/182015/04/252015/05/212015/05/222015/05/19
1394/2/29
Mohammad
Allahtavakoli
mohammadatir@yahoo.com
0031947532846005730
0031947532846005730
No
Najmeh
Honari
najme_honari62@yahoo.com
0031947532846005731
0031947532846005731
No
Iran
Pourabolli
pourabolii@yahoo.com
0031947532846005732
0031947532846005732
No
Mohammad
Kazemi Arababadi
kazemi24@yahoo.com
0031947532846005733
0031947532846005733
No
Hossein
Ghafarian
Ghahremani77@yahoo.com
0031947532846005734
0031947532846005734
No
Ali
Roohbakhsh
aroohbakhsh@yahoo.com
0031947532846005735
0031947532846005735
No
Ali
Esmaeili Nadimi
dr_esmaeili_n@yahoo.com
0031947532846005736
0031947532846005736
No
Ali
Shamsizadeh
Rafsanjan University of Medical Sciences
alishamsy@gmail.com
0031947532846005737
0031947532846005737
Yes
en
The Effects of Fifa 2015 Computer Games on Changes in Cognitive, Hormonal and Brain Waves Functions of Young Men Volunteers
Introduction: Computer games have attracted remarkable attentions in general publics with
different cultures and their effects are subject of research by cognitive neuroscientists. In the
present study, possible effects of the game Fifa 2015 on cognitive performance, hormonal levels,
and electroencephalographic (EEG) signals were evaluated in young male volunteers. Methods: Thirty two subjects aged 20 years on average participated mutually in playing
computer game Fifa 2015. Identification information and general knowledge about the game were
collected. Saliva samples from the contestants were obtained before and after the competition.
Perceptive and cognitive performance including the general cognitive health, response delay,
attention maintenance, and mental fatigue were measured using PASAT test. EEG were recorded
during the play using EEG device and analyzed later using QEEG. Simultaneously, the players’
behavior were recorded using a video camera. Saliva cortisol levels were assessed by ELISA kit.
Data were analyzed by SPSS program. Results: The impact of playing computer games on cortisol concentration of saliva before and
after the game showed that the amount of saliva plasma after playing the game has dropped
significantly. Also the impact of playing computer games on mental health, before and after the
game indicated that the number of correct answers has not changed significantly. This indicates
that sustained attention has increased in participants after the game in comparison with before
that. Also it is shown that mental fatigue measured by PASAT test, did not changed significantly
after the game in comparison to before that. The impact of game on changes in brain waves
showed that the subjects in high activity state during playing the game had higher power of the
EEG signals in most of the channels in lower frequency bands in compared to normal state. Discussion: The present study showed that computer games can positively affect the stress
system and the perceptual-cognitive system. Even though this impact was not significant in most
cases, the changes in cognitive and hormonal test and also in brain waves were visible. Hence,
due to the importance of this matter, it is necessary to create control systems in selecting the types
of games for playing.
Cognitive, EEG, Saliva, Cortisol, Video Games
193
201
http://bcn.iums.ac.ir/browse.php?a_code=A-10-724-1&slc_lang=en&sid=1
2015/02/182014/12/92014/11/22014/11/302014/11/112015/02/182015/02/232014/09/17
1393/6/26
2015/07/12015/05/112015/04/182015/04/252015/05/212015/05/222015/05/192015/05/11
1394/2/21
Hamed
Aliyari
Department of Electrical, Biomedical and Mechatronics Engineering, Qazvin Branch, Islamic Azad University, Qazvin, Iran
Hamedaliyary@ut.ac.ir
0031947532846005738
0031947532846005738
No
Masoomeh
Kazemi
Neuroscience Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran.
mkazemih@yahoo.com
0031947532846005739
0031947532846005739
No
Elaheh
Tekieh
Neuroscience Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran.
elahehtekieh@yahoo.com
0031947532846005740
0031947532846005740
No
Maryam
Salehi
Neuroscience Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran.
maryam.salehi60@gmail.com
0031947532846005741
0031947532846005741
No
Hedayat
Sahraei
Baqiyatallah University of Medical Sciences
hsahraei1343@gmail.com
0031947532846005742
0031947532846005742
Yes
Mohammad Reza
Daliri
Department of Electrical Engineering, University of Science and Technology ,Tehran, Iran
daliri@iust.ac.ir
0031947532846005743
0031947532846005743
No
Hassan
Agaei
Neuroscience Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran.
sayyedagha313@gmail.com
0031947532846005744
0031947532846005744
No
Behroz
Minaei
School of Computer Engineering, University of Science and Technology ,Tehran, Iran
b-minaei@iust.ac.ir
0031947532846005745
0031947532846005745
No
Reza
Lashgari
Department of Electrical Engineering, University of Science and Technology ,Tehran, Iran
e_tekieh@yahoo.com
0031947532846005746
0031947532846005746
No
Nahid
Srahian
Neuroscience Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran.
sarahiannahid@yahoo.com
0031947532846005747
0031947532846005747
No
Mohammad mehdi
Hadipour
Neuroscience Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran.
mm.hadipour@gmail.com
0031947532846005748
0031947532846005748
No
Mostafa
Salehi
Industrial Engineering Department, K.N.Toosi university and technology
hamedaliyary@gmail.om
0031947532846005749
0031947532846005749
No
Asghar
Ranjbar Aghdam
From Daj Scientific co-Research dept
hamedaliyary@yahoo.com
0031947532846005750
0031947532846005750
No