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Showing 4 results for Synaptosome

Ameneh Shahroukhi, Asghar Qassemi, Fereshteh Pourabdolhossein, Ali Khoshbaten, Alireza Asgari,
Volume 10, Issue 3 (11-2006)
Abstract

Introduction: Compounds which are used to treat organophosphate (OP) poisoning are not able to fully alleviate long lasting effects. They are mainly used to antagonize cholinergic effects of Ops. However, non-cholinergic effects, such as interference with different neurotransmitter systems, especially GABA release and uptake, are recently attracting more attentions. We have tried to investigate any potential interaction between paraoxon and GABA uptake. Methods: We used cerebellar synaptosomes. Cerebellum of 250-280 g Wistar rats were rapidly dissected out, homogenized, centrifuged, and incubated with 0.01 μ M [3H]GABA in the presence of different doses of paraoxon for 10 minutes at 37 oC. At the end of the incubation period, synaptosomes were layered in chambers of superfusion system. In order to assay the amounts of [3H]GABA taken up, radioactivity was measured using a β-counter. Results: Our findings reveal that mean GABA uptake was 111.42, 95.37, 71.6, 73.53 and 75 percent of the control values in the presence of different concentrations of paraoxon (0.01, 0.1, 1, 10 and 100μ M) respectively. GABA uptake was significantly reduced at doses 1, 10 and 100μ M (p<0.05). Conclusion: It seems that paraoxon at higher doses may interfere with GABA uptake by cerebellar synaptosomes.
Mozhdeh Mansouri, Homayoun Khazali,
Volume 12, Issue 2 (8-2008)
Abstract

Introduction: Previous studies have shown that ghrelin inhibits the activity of Hypothalamus –Pituitary – Thyroid (H–P-T) axis. It is also proved that ghrelin increases appetite via Agouti Related Protein and neuropeptide Y pathway, decreases T3 & T4 secretion and inhibits serotonin release from hypothalamic synaptosomes. Serotonin may interact with ghrelin in control of thyroid hormones secretion. Thus, the goal of this study was to determine the influence of the interaction between ghrelin and serotonin agonist on thyroid hormones concentration. This is a suugestive mechanism to determine the effect of serotonin agonist in decreasing the effect of ghrelin. Methods: Twenty four male Wistar rats weighing 230-250 g were randomly divided into 3 groups. The groups respectively received 5 nmol ghrelin ,20 nmol serotonin agonist (R)-8-OH-DPAT or 5 nmol ghrelin with 20 nmol (R)-8-OH-DPAT in the volume of 5μl during 3 days via lateral cerebral ventricle. The blood samples were collected from one day before to one day after injections and brain slices were taken to ensure the place of the canulae is right. The plasma were analysed by Radio Immuno Assay technique to determine T3 and T4 concentrations. Results: The results of this experience showed that the (.i.c.v) injection of ghrelin and (R)-8-OH-DPAT respectively decreased and increased the mean plasma concentrations of thyroid hormones significantly (p<0.05), while the interaction of these two substances showed that (R)-8-OH-DPAT can decease the inhibitory effect of ghrelin on thyroid hormones concentration, but this effect is not statistically significant. (p<0.05) Conclusion: This study showed that ghrelin decreased mean plasma concentration of T3 & T4 significantly and serotonin agonist while injected with ghrelin , because of the stronger effect of ghrelin, could not significantly inhibit this effect of ghrelin. (p<0.05)
Moslem Mohammadi, Asghar Ghasemi, Esmaeel Ghani, Ali Khoshbaten, Alireza Asgari,
Volume 13, Issue 2 (8-2009)
Abstract

Introduction: Paraoxon (the neurotoxic metabolite of organophosphorus (OP) insecticide, parathion) exerts acute toxicity by inhibition of acetylcholinesterase (AChE), leading to the accumulation of acetylcholine in cholinergic synapses and hence overstimulation of the cholinergic system. Since, reports on changes in the level of γ- amino butyric acid (GABA) during OP-induced convulsion have been controversial, in present study we used cortical and hippocampal synaptosomes from rats after paraoxon poisoning to detect changes in GABA uptake. Methods: Male Wistar rats (200-270 g) were used in this study. Animals were given a single intraperitoneal injection of corn oil (vehicle group) or one of doses of paraoxon (0.1, 0.3, or 0.7 mg/kg) and [3H]GABA uptake by cerebral cortex and hippocampal synaptosomes was measured at 30 min, 4 h, and 18 h after the exposure (n= 7 rats/group). Type of transporter involved in the uptake was also determined using β-alnine, and L-diaminobutyric acid (L-DABA), a glial and a neuronal GABA uptake inhibitor, respectively. Results: GABA uptake was significantly (p<0.001) reduced by both cerebral cortex (18-32%) and hippocampal (16-21%) synaptosomes compared with their respective control groups at all three time points after administering 0.7 of paraoxon (convulsive dose). β-alnine had no inhibitory effect on the uptake, whereas L-DABA abolished most of the transporter mediated GABA uptake. Conclusion: Since GABA uptake did not change in other two paraoxon treated groups, it may be indicating that decrement of GABA uptake is convulsion-related. The decrease in GABA uptake, presumably due to a change in the function of GABA transporters, may represent a compensatory response modulating neuronal overexcitation. Most of synaptosomal GABA uptake was blocked by L-DABA, indicating that the uptake was primarily by a neuronal GABA transporter (GAT), GAT-1.
Sahand Asharfpour, Fereshteh Pourabdolhossein, Forough Ebrahim Tabar, Manouchehr Ashrafpour, Mojdeh Navidhamidi, Sima Shahabi, Maryam Ghasemi-Kasman, Alireza Asgari,
Volume 22, Issue 2 (6-2018)
Abstract

Introduction: Synaptosomes are sealed particles that contain mitochondria, cytoskeleton and vesicles which are necessary to synaptic events like neurotransmitter release and uptake in the nervous system. However, the effect of high and low temperatures on synaptosome membrane integrity and function during a time course after its extraction is less known. The purpose of this study was to assess synaptosome viability and function at 37, 4°C and room temperature (RT) during 6 hours after its extraction. Methods: Hippocampi of 40 male Wistar rats were used for synaptosome preparation. To ensure synaptosome membrane integrity and function, lactate dehydrogenase activity (LDH) and GABA uptake were assessed during 6 successive hours after their extraction at 37, 4°C and RT. Results: Our results showed that at 37°C, synaptosome membrane integrity was reduced 3 hours but at 4°C and RT, it occurred 5 hours following their extraction. The results of synaptosome function analysis coincide with LDH enzyme assay data, meaning that GABA uptake faced a 50% reduction from the initial value at 37°C after 3 hours and at RT after 5 hours. We also found that GABA uptake was reduced at 4°C in the first hour after extraction because the low temperature inhibits GABA transporters. Conclusion: Synaptosomes preserved their viability and function at RT, 37 and 4°C at least for 3 hours after extraction and reduced over time. For long term application of synaptosomes, it is better to keep them at 4°C.



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