Effects of long term perinatal administration of Bupropion on population spike amplitude in neonatal rat hippocampal slices

Introduction: The perinatal effects of antidepressants on CNS due to its common usage are importantissues in neuroscience research. Bupropion is an atypical antidepressant that is used in smoke cessationunder FDA approve widely. The study of synaptic effects of bupropion can reveal its mechanism fornicotine dependence cessation. In this study the long term effects of perinatal bupropion on populationspike (PS) amplitudes were investigated. The PS amplitude is a good parameter for synaptic plasticity.Materials and Methods: Hippocampal slices from 18-25 day old rat’s pups were prepared. The examgroups included control and Bupropion treated groups. Bupropion (40 mg/Kg, i.p) was applied inperinatal period daily as pretreatment. Bupropion also was perfused in ACSF (10, 50, 200 μ mol, 30minutes) and tested for PS amplitude. PS amplitude of Stratum Radiatum was measured before and afterBupropion perfusion. Amplitude of PS before Bupropion perfusion was fitted as 100% for baseline.Results: A concentration of 10 μM did not reduce PS amplitude and Bupropion had no significanteffects on PS amplitude. Bupropion in concentration of 50μM could reduce the amplitude of responses in50% of cases. The 200 μM of Bupropion perfusion reduced population spike amplitude all slices (n=22).In the last state population spike amplitude in 8 out 0f 22 slices completely abolished. Decreasepopulation spike amplitude in non-treated slices with 200 μM perfusion was more than treated slices.Conclusion: Analyzing of data showed that chronic perinatal exposure to Bupropion in concentrations50,200 μM reduced PS amplitude and we found adaptation synaptic in perfusion 200 μM compare withBupropion treated slices with non- treated

The role of glial glutamate transporter in the baseline synaptic response and short-term synaptic plasticity of CA1 area of the hippocampus in male Wistar rat

Background. Glial cells release different gliotransmitters and response to neurotransmitters released from neurons. These cells especially astrocytes, having different transporters, play an important role in synaptic space homeostasis and synaptic plasticity. In this study, the role of hippocampal glial glutamate transporter (EAAT2) in baseline synaptic response and short term synaptic plasticity were investigated. Methods. In this experimental study, ceftriaxone, EAAT2 activator (0.5mmol/0.5μl), was microinjected intrahippcampally for activation of hippocampal glial glutamate transporter in male wistar rats. Baseline synaptic response and short term synaptic plasticity were evaluated by field potential recording. fEPSP was recorded from CA1 following Schaffer collaterals stimulation. After Input/Output curve construction, short term synaptic plasticity was induced by paired pulse stimulations. Results. Activation of EAAT2 by ceftriaxone microinjection in CA1 did not have any effect on baseline synaptic response (P> 0.05, Two Way ANOVA). There was no significant difference in Paired Pulse Index at 20, 80, and 200 ms inter-pulse interval between ceftriaxone treated and control group (P> 0.05, Two Way ANOVA). Conclusion. The results suggest that hippocampal glial glutamate transporter activation does not have effect on baseline synaptic response and short term synaptic plasticity in CA1 area of the hippocampus. Practical implications. Considering the role of glial cells in regulating the excitability of the nervous system as well as synaptic plasticity, correcting these features of the nervous system by manipulating glial cells can help the treatment or prevention of neurological diseases. In this study, the role of glial cells in the homeostasis of the glutamate in the synaptic space of the hippocampus was evaluated, through the stimulation of its uptake, on the basic synaptic activity and short-term synaptic plasticity

The Role of Astrocytic Cx43 in Baseline Synaptic Response and Short Term Synaptic Plasticity in CA1 Area of the Hippocampus

Background and purpose: Astrocytic connexins (Cxs) play roles in ion diffusion to the extracellular milieu and in release of ATP and gliotransmitters including glutamate. Connexin 43 (Cx43) is one of the most abundant Cxs in brain tissue, especially in the hippocampus, so, we investigated its role on CA1 baseline synaptic response and short term synaptic plasticity. Materials and methods: In this experimental study, bilateral intrahippocampal microinjection of TAT-Gap19, Cx43 blocker (1nmol/1μl) was performed for inhibition of hippocampal astrocytic connexin 43. Baseline synaptic response and short term synaptic plasticity were evaluated by field potential recording. Results:  According to two-way ANOVA, inhibition of hippocampal Cx43 did not have any effect on baseline synaptic response (P>0.05). TAT-Gap19 decreased paired pulse index (PPI) at 20 and 80 ms inter pulse intervals (IPI, Unpaired t-test, P0.05). Conclusion: The results suggest that the function of hippocampal astrocytic Cx43 does not affect baseline synaptic response but affects short term synaptic plasticity in CA1 area of the hippocampus

Ameliorating Effects of Dorema ammoniacum on PTZ-Induced Seizures and Epileptiform Brain Activity in Rats

The objective of the current study was to investigate the anti-epileptogenic and anticonvulsant effects of Dorema ammoniacum gum, which is used in Iranian traditional medicine for the treatment of seizures. Animals received pentylenetetrazol (IP, 30 mg/kg/48 h) for inducing seizures. Five different seizure stages were evaluated for 20 min and parameters including maximum seizure stage, the latency to the onset of stage 4, stage 4 duration, and seizure duration were measured. D. ammoniacum (50 and 100 mg/kg) or its vehicle was administered 30 min before or after pentylenetetrazol injection in different groups. In addition, the effective dose of D. ammoniacum (100 mg/kg) on different seizure stages was compared with the common antiseizure drug phenobarbital. In another set of experiments, we investigated the effective dose of D. ammoniacum on fully kindled animals in which an interictal electroencephalogram was recorded by superficial electrodes placed on the skull. The results showed that D. ammoniacum administration, before and after pentylenetetrazol injections, significantly decreased seizure stage, seizure duration, stage 4 duration, and 1/stage 4 latency. The anti-epileptogenic effect of D. ammoniacum was about 50 to 60 of phenobarbital. In addition, D. ammoniacum significantly decreased seizure stage, seizure duration, stage 4 duration, and 1/stage 4 latency when administered to fully kindled animals but had no effect on the power of EEG sub-bands. These results indicate that D. ammoniacum has anti-epileptogenic and anticonvulsant effects in a chemical kindling model of seizures. © 2020 Georg Thieme Verlag. All rights reserved

Protective effects of salicylate on PKA inhibitor (H-89)-induced spatial memory deficit via lessening autophagy and apoptosis in rats

In this study, the effects of salicylate on spatial learning and memory, through its effects on autophagy and apoptosis, were evaluated in the presence of the PKA inhibitor H-89. Adult male Wistar rats were divided into experimental groups as follows: salicylate (30, 50, 100 μg/0.5 μl/side, intra-hippocampal; 400 mg/kg, intra-peritoneal), donepezil (1 mg/kg as a positive control for behavioral effects of salicylate), H-89 (1 μl/side of 5 or 20 μM), H-89 plus salicylate and H-89 plus donepezil. The Morris water maze test was used for evaluation of spatial learning and memory. The levels of different apoptotic and autophagic biomarkers were evaluated using the western blot technique. Salicylate (100 μg/0.5 μl/side) significantly reduced the escape latency on training days, increased the percentage of time spent in the target quadrant during the probe trial and reversed the inhibitory effects of H-89 during the process of spatial learning and memory. The behavioral efficacy of salicylate was comparable to that of donepezil. In addition, salicylate significantly decreased the levels of apoptotic proteins, Bax and caspase 3, and increased the Bcl2 levels in all groups. Furthermore, the levels of LC3II and Atg7 were decreased by salicylate. Our study revealed that both systemic and direct intra-hippocampal administration of salicylate can facilitate the spatial learning and memory. Additionally, intra-hippocampal administration of salicylate can reduce apoptotic and autophagic proteins. The antioxidant activity of salicylate might lead to increased pCREB via stimulation of signaling pathways, resulting in reduction of H-89-induced apoptosis and autophagy. © 2016 Elsevier Inc