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Showing 4 results for Hosseinmardi

Leila Hosseinmardi, Abdolhossein Shiravi, Gholam Hossein Meftahi, Mohammad Reza Afarinesh,
Volume 0, Issue 0 (7-2019)

Introduction: The basolateral amygdala (BLA) is implicated in stress-related disorders such as anxiety-like behavior. Substantial data exist demonstrating a close relationship between anxiety and adrenergic receptor function in patients with anxiety disorders, however, little is known about the effects of the β1 adrenergic receptor in the BLA on anxiety. These experiments examined the effects of the β1 adrenergic receptor in the BLA on anxiety-like behavior.
Methods: Male Wistar rats were exposed to foot-shock stress four consecutive days that were uncontrollable. The β1-adrenoreceptor agonist (Dobutamine; 0.5 µl/side) or antagonist (Atenolol; 0.25 µl/side) bilaterally infused into the BLA five minutes before foot-shock stress. Anxiety-like behaviors were assessed 24 h after four consecutive day’s uncontrollable stress using Elevated Plus-Maze (EPM) and Open Field Test (OFT).
: Findings of EMP revealed that foot-shock stress leads to effect with reduction the time spent and the number of entries into the open arms, and increased head-dipping. Intra-BLA infusions of Atenolol before stress affected animal behavior differently, such that it significantly (P<0.05) increased the time spent and the number of entries into the open arms and decreased head-dipping. Also, OFT results showed the intra-BLA infusion of Atenolol increased the time periods spent in the center, number of center entries and reduced the number of rearing as compared with the stress group.
Conclusion: These results suggest that the anxiety-like behavior observed after the foot-shock stress is mediated, in part, by exaggerated β1 adrenergic receptor acting at the BLA.

Jafar Doost Mohammad Pour, Narges Hosseinmardi, Mahyar Janahmadi, Yaghoub Fathollahi, Fereshteh Motamedi, Mehdi Hooshmandi,
Volume 17, Issue 3 (Fall 2013)

Introduction: The prostaglandin E2 (PGE2), a cyclooxygenase (COX) product, play critical roles in the synaptic plasticity. Therefore, long term use of COX inhibitors may impair the synaptic plasticity. Considering the wide clinical administration of aspirin and its unknown effects on information processing in the brain, the effect of aspirin and sodium salicylate on the short term synaptic plasticity was investigated. Methods: Field excitatory post synaptic potential (fEPSP) from stratum radiatum of CA1 neurons were recorded following Schaffer collateral stimulation in rats receiving aspirin in drinking water (2 mg/ml) for 6 weeks or sodium salicylate (six injection of 300 mg/kg, IP, twice daily) for 3 days. In order to examine the short-term synaptic plasticity, paired pulse stimulations with inter pulse intervals (IPI) of 20, 80, and 200 ms were applied and paired pulse index (PPI) was calculated. Results: The data showed that both sodium salicylate and aspirin decreased basal synaptic responses, although this change was significant in the sodium salicylate group, but not in aspirin treated rats (ANOVA P<0.001). Sodium salicylate significantly increased PPI at 20 ms IPI (%90.7±1.6, n=5Vs. control: %76.1±1.5, n=5). Also significant increase in PPI was observed in aspirin treated rats (%125.9±6.6, n=5) at 20 ms IPI compared to control ones (%76.3±2.4, n=5, P<0.05, unpaired t-test). Conclusion: In summary, our study suggests that aspirin and sodium salicylate may affect synaptic transmission and short term synaptic plasticity in the rat hippocampus.
Sharareh Daryani, Alireza Farzaei, Narges Hosseinmardi, Farideh Bahrami, Mahyar Janahmadi,
Volume 20, Issue 2 (June 2016)

Introduction: Although aging is the most important risk factor for Alzheimer's disease (AD), there is evidence indicating that neuroinflammation may contribute to the development and progression of the disease. Several studies indicated that minocycline may exert neuroprotective effects in rodent models of neurodegenerative diseases. Nevertheless, there are also other studies implying that minocycline has no positive beneficial effects. Thus, the aim of the present study was to assess the preventive effect of minocycline against Aβ-induced changes in intrinsic electrophysiological properties in a rat model of AD. Methods: The present study extended this line of research by examining whether inhibition of microglial activation may alter the intrinsic electrophysiological properties of CA1 pyramidal neurons in a rat model of Aβ neurotoxicity, using whole cell patch clamp. Results: Findings showed that bilateral injection of the Aβ (1-42) into the prefrontal cortex caused membrane hyperpolarization, action potential (AP) narrowing and after hyperpolarization (AHP) amplitude enhancement. It was also resulted in a faster decay time of AP, higher rheobase current, lower firing frequency and smaller post stimulus AHP amplitude. Administration of minocycline (45mg/kg, i.p) not only failed to prevent Aβ-induced alterations in the intrinsic electrophysiological properties, but also enhanced the effects of Aβ on neuronal firing behavior. Conclusion: It can be concluded that minocycline, as a microglial inhibitor, may enhance the disruption of electrophysiological properties of CA1 pyramidal neurons induced by Aβ neurotoxin, including AP parameters and intrinsic neuronal excitability.

Mohsen Fathi, Narges Hosseinmardi, Kambiz Rohampour, Mahyar Janahmadi, Ali Sonboli, Jalal Zaringhalam,
Volume 20, Issue 3 (September 2016)

Introduction: The management of pain and inflammation related problem is a real challenge that people face daily. Although several drugs are available for these conditions, medicinal plants are believed to be an important source of new chemical substances with potential therapeutic effects. The objective of current study was to investigate the anti-nociceptive effect of Tanacetum Fisherae which has been traditionally used for treatment of pain. Methods: In this experimental study, formalin test was performed with drug (Tanacetum Fisherae) or DMSO pretreatment 30 min prior to formalin injection in 40 male Wistar rats. Fifty microliters of 2.5% formalin was injected into the plantar surface of the right hind paw. Immediately after injection, licking and flinching number and paw-shaking responses were observed at 5-min intervals for 1 h. Animals were divided into five experimental groups. There were 8 animals in each group. Each group received vehicle (7% DMSO) or Tanacetum Fisherae essential oil (25, 50 or 100 μg) or morphine (5 mg/kg). Two-way and one-way ANOVA were used for data analysis. Differences were considered significant at the level of P<0.05 (with 95% confidence interval). Results: Results showed that Tanacetum Fisherae essential oil dose dependently reduced licking and flinching number and also pain score in the late (15-35 min) and recovery phase (35-60 min) of formalin test (p<0.05, p<0.01, and p<0.001). It had no anti-nociceptive effect (p>0.05) in early (0-5 min) phase and interphase (5-15 min). Conclusion: Results demonstrate the effectiveness of Tanacetum Fisherae to mitigate the inflammatory pain.

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