Physiology & Pharmacology
Roya Kaveh; Mohammad Amin Edalatmanesh
Volume 29, Issue 2 , July and August 2022, , Pages 268-280
Abstract
Introduction: Monosodium glutamate (MSG) induced excitotoxicity leads to oxidative stress in different areas of the brain. The aim of this study was to evaluate the neuroprotective effect of coenzyme Q10 (Co-Q10) on amelioration of short-term and long-term memory and oxidative stress parameters in MSG-treated ...
Read More
Introduction: Monosodium glutamate (MSG) induced excitotoxicity leads to oxidative stress in different areas of the brain. The aim of this study was to evaluate the neuroprotective effect of coenzyme Q10 (Co-Q10) on amelioration of short-term and long-term memory and oxidative stress parameters in MSG-treated rats.Material and Methods: In this experimental study, 40 adult male Wistar rats were randomly divided into 4 groups including control, MSG, MSG + Q10-10 and MSG + Q10-20. MSG gavage (4 mg / kg) and coenzyme Q10 injection at doses of 10 and 20 mg / kg (intraperitoneally; i.p.) were performed for 4 weeks. Then, short-term working memory was assessed using the Y maze and long-term avoidance memory was performed with the shuttle box. Hippocampal level of catalase (CAT) and total antioxidant capacity (TAC) were determined by ELISA method and malondialdehyde (MDA) content was determined by thiobarbituric acid method.Results: In MSG group, there was a significant decrease in alteration behavior, increased latency time to the dark room of the shuttle box, decreased CAT, TAC expression and increased MDA compared to the control group (p <0.05). While in the Q10 treated groups, there was an increase in working and avoidance memory, an increase in CAT and TAC expression and a decrease in MDA in the hippocampus compared to the MSG group (p˂0.05).Conclusion: It seems that Co-Q10 ameliorates MSG induced neurotoxicity and cognitive symptoms through preventing oxidative stress in the hippocampus.
Azam Asgari; Saeed Semnanian; Nafiseh Atapour; Amir Shojaee; Vahid Sheybani; Seyyed Javad Mirnajafi Zadeh
Volume 23, Issue 2 , March and April 2016, , Pages 290-303
Abstract
Background and purpose: Low frequency stimulation (LFS) has anticonvulsant effect. However, its mechanism of action has not been completely determined. In the present study the effect of LFS on evoked inhibitory post synaptic GABAergic currents (eIPSC) is investigated in CA1 pyramidal neurons of the ...
Read More
Background and purpose: Low frequency stimulation (LFS) has anticonvulsant effect. However, its mechanism of action has not been completely determined. In the present study the effect of LFS on evoked inhibitory post synaptic GABAergic currents (eIPSC) is investigated in CA1 pyramidal neurons of the hippocampus in kindled rats. Materials and Methods: In this experimental study animals were kindled through electrical stimulation of amygdala. 24 hours following fully kindling achievement in 20 Wistar rats, the effect of LFS on eIPSCs was assessed in hippocampal slices. Results: Obtained results showed that application of LFS at 200 pulses and at the intensity of 1.5 threshold, increased the amplitude and decay time constant of eIPSCs in both control and kindled rats. When 200 pulses of LFS were administered with an intensity equal to threshold, only eIPSC amplitude was increased in both control and kindled groups significantly (P<0.001). Comparing the effectiveness of LFS on control and kindled groups showed that 200 pulses of LFS at the intensity of 1.5 threshold had higher effect in control than kindled group (P<0.001). Conclusion: Results of the present study showed that LFS application increased eIPSCs parameters in a pulse number and intensity dependent manner. This increment can be considered as a possible anticonvulsant mechanism of LFS.