Yousof Mousavi; Hossein Azizi; Javad Mirnajafi-Zadeh; Mohammad Javan; Saeed Semnanian
Volume 25, Issue 1 , May and June 2018, , Pages 13-20
Abstract
Background: The locus coeruleus (LC) contains large clusters of noradrenergic neurons which project widely throughout the central nervous system including hypothalamus. The LC is involved in cognitive processes, including attention, learning, memory and drug addiction. Orexin neuropeptides excite the ...
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Background: The locus coeruleus (LC) contains large clusters of noradrenergic neurons which project widely throughout the central nervous system including hypothalamus. The LC is involved in cognitive processes, including attention, learning, memory and drug addiction. Orexin neuropeptides excite the noradrenergic LC neurons; however, its effects on inhibitory synaptic transmission to the LC neurons are unknown. Materials and Methods: Here, we investigated the effect of orexin-A (100 nM) on sIPSCs in LC neurons. We used whole-cell patch clamp recording in rat horizontal slices containing the LC nucleus. Results: Our electrophysiological data indicate that orexin-A application only decreased sIPSCs frequency of LC neurons that was blocked by SB-334867, selective orexin type-1 receptors. Conclusion: In this study, our findings suggest that orexin-A depresses sIPSCs frequency through orexin type-1 receptors. It can be deduced that these changes in inhibitory synaptic transmission may be elicited by prestsynaptic mechanism. These results provide in vitro evidence for a critical role of orexin signaling in LC neurons.
Sohrab Hajizadeh; Mohammad Javan; Mohammadreza Bigdeli; Firozeh Alavian
Volume 19, Issue 3 , September and October 2012, , Pages 287-295
Abstract
Background: Recent studies have shown that normobaric hyperoxia is effective in the treatment of acute ischemia, a phenomenon called preconditioning. However, the exact mechanism of this kind of preconditioning in vivo is not known. In this study, the effect of intermittent normobaric hyperoxia on expression ...
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Background: Recent studies have shown that normobaric hyperoxia is effective in the treatment of acute ischemia, a phenomenon called preconditioning. However, the exact mechanism of this kind of preconditioning in vivo is not known. In this study, the effect of intermittent normobaric hyperoxia on expression of HIF1α in a stroke model was investigated. Materials and Methods: In this experimental study, rats were divided into 4 groups. Hyperoxia groups were exposed to 95% inspired oxygen for 4 h/day and 6 consecutive days. Oxygen concentration in the control groups was 21% (normoxia). After 24 h, rats in stroke groups were subjected to 60 min of right middle cerebral artery occlusion. After 24 h, reperfusion neurological deficit scores were assessed. The brain HIF1α levels were analyzed by Western blot. Statistical analysis was performed using two-way ANOVA, Bonferroni post-test, Fisher exact test, and GraphPad Prism 5 software. Results: The results of this study showed that HIF1α levels increased in stroke groups compared with normoxia groups, while the amount of protein in hyperoxia groups was not significantly different from normoxia groups. Significantly increased HIF1α levels were observed in hyperoxia stroke group. Also, hyperoxia improved neurological deficit scores from 8.83% down to 3.46%. Conclusion: Hydroxylation, instability, and degradation of HIF1α occurred following hyperoxia. In the stroke groups, lack of oxygen delivery to cells prevents hydroxylation and degradation of HIF1α. In hyperoxia stroke group, inflammatory cytokines with increased ROS can induce increased expression of HIF1α.
Saeed Semnanian; Hossein Baharvand; Shiva Khezri; Mohammad Javan
Volume 18, Issue 3 , September and October 2011, , Pages 179-187
Abstract
Background and Purpose: Novel strategies of MS try to stimulate endogenous neural stem cells for demyelination repair. Increased levels of cAMP potentiate the repair mechanisms in CNS by activating PKA or independently. In the present study، we investigated the effect of dbcAMP on neural stem cells ...
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Background and Purpose: Novel strategies of MS try to stimulate endogenous neural stem cells for demyelination repair. Increased levels of cAMP potentiate the repair mechanisms in CNS by activating PKA or independently. In the present study، we investigated the effect of dbcAMP on neural stem cells migration in experimental autoimmune encephalomyelitis (EAE) model of MS. Methods and Materials: Mice were immunized with 300 µg MOG peptide emulsified in complete Freund''s adjuvant (CFA) and pertussis toxin (PT). Control mice received CFA and PT. Groups of EAE- mice received i.p. injections of dbcAMP 10mg/kg from day 9-14 or 9-21. Animals were observed daily for neurological deficit. Nestin expression was used as a marker to detect neural stem cells. The number of Nestin+ cells in SVZ and olfactory bulb (OB) was evaluated using immunohistochemical staining. GraphPad Prism Version 5 was used for analyzing the data. For the clinical signs of EAE، the differences between the same days were compared by unpaired t-test. For the number of Nestin+ cells، the statistical differences between the groups were determined by one-way ANOVA and Tukey post-test. Results: EAE induction caused clinical signs and paralysis of tail and hind limbs. dbcAMP significantly reduced the incidence and severity of EAE in mice immunized with MOG. Maximum of scores reached 0.66±0.13 for dbcAMP treated mice (2.5±0.2 for EAE mice) on 21 dpi (day post inductin). EAE induction did not change number of nestin+ cells in SVZ but it increased it in OB. With developing of scores on 21dpi، the number of cells decreased (5.66±1.20). dbcAMP injection from 9-21 dpi increased these cells in SVZ. With developing of EAE scores on 21 dpi، the number of these cells in OB increased (19.5±2.04) and has significant differences with the control group. The treatment of EAE induced mice with dbcAMP from 9-21 dpi was assosiated with a significant elevation of Nestin+ cells in OB (40±2.73) (P
Mohammad Javan; Seyyed Javad Mirnajafizadeh; Maryam Zeraati; Simin Namvar
Volume 17, Issue 3 , September and October 2010, , Pages 158-169
Abstract
Background and Purpose: Despite widespread research on epilepsy, the mechanism of its insidnece is still unknown. Since the activity of ATPase plays a vital role in changing ATP into AMP, and this substance can later turn into adenosine which is the most important endogenous anticonvulsant agent in brain, ...
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Background and Purpose: Despite widespread research on epilepsy, the mechanism of its insidnece is still unknown. Since the activity of ATPase plays a vital role in changing ATP into AMP, and this substance can later turn into adenosine which is the most important endogenous anticonvulsant agent in brain, the effect of inhibition of ATPase on perforant path kindling was investigated in the present study. Methods and Materials: In this experimental study, animals were kindled by electrical stimulations of the perforant path (12 times a day with a frequency of 50 Hz and pulse duration of 1 millisecond). Upon kindling, behavioral and electrophysiologic measures of convulsions and filed potentials were recorded. For investigating the role of ATPase in animal groups, FPL 67156 was injected as the inhibitor of the ATPase after kindling stimulations ended each day. Kindled animals were 6, and there were 4 rats in other groups. Repeated measures ANOVA and Bonferoni test were used to compare the statistical quantities of fEPSP and PS of epilepsy creation in different groups of the study. Comparing the difference of paired pulses between groups was conducted by Bonferoni test. The five-stage convulsion of the groups was compared through Kruskall Wallis and Mann Whitney U tests. Statistical analyses were conducted in Prism 5. Results: The results indicated that ATPase inhibition (by injecting FPL 67156) causes no change in various behavioral stages of convulsion and daily afterdischarge duration following kindling (P>0.05); however, it affects synapsis formation, so that PS increases in comparison with the kindled group (P
Mohammad Javan; Seyyed Javad Mirnajafizadeh; Mehdi Godarznavd; Taghi Tarihi
Volume 16, Issue 2 , July and August 2009, , Pages 62-71
Abstract
Background and purpose: Antioxidants and vitamin D3 are currently used for the treatment of neurodegenerative diseases although their mechanism of action is not well understood. The present study was conducted to investigate the effect of combined administration of vitamins D3 and E on demyelination ...
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Background and purpose: Antioxidants and vitamin D3 are currently used for the treatment of neurodegenerative diseases although their mechanism of action is not well understood. The present study was conducted to investigate the effect of combined administration of vitamins D3 and E on demyelination cell death and remyelination of rat hippocampus following the local ethidium bromide (EB) injection. Methods and Materials: This experimental study was conducted on 32 Spague rats. After EB-induced demyelination animals received intraperitoneal vitamin E (100 mg/kg) and D3 (5µg/kg) together for 7 days. The extent and intensity of demyelination were studied by luxol fats blue staining the activated caspase-3 genes and MBP. The study data were analyzed in SPSS using one-way ANOVA and Tukey post test. Results: The findings revealed that the combined administration of vitamins E and D3 for 7 days caused a significant reduction in the expression of activated caspase-3 (10±0) (p