ABSTRACT
Objective: To observe the effect of subarachnoid nerve block anesthesia on glutamate transporter glutamate-aspartate transporter (GLAST) and GLT-1 expressions in rabbits, and to investigate the effect of peripheral nerve anesthesia on the morphology and function of the spinal cord. Methods: Twenty healthy New Zealand white rabbits were randomly divided into two groups: the experimental group and control group; with 10 rabbits in each group. For spinal nerve anesthesia, 5 g/L of bupivacaine was used in the experimental group, and sterile saline was used in the control group. After 30 min of cardiac perfusion, GLAST and GLT-1 protein expression in spinal neurons were detected by immunohistochemistry and immunofluorescence staining. Results: GLAST and GLT-1 protein-positive cells increased in neurons in the experimental group, compared with the control group (P < 0.05). Conclusions: After subarachnoid nerve block anesthesia, rabbit glutamate transporter GLAST and GLT-1 expression is increased; and spinal cord nerve cell function is inhibited.
ABSTRACT
OBJECTIVE@#To observe the effect of subarachnoid nerve block anesthesia on glutamate transporter glutamate-aspartate transporter (GLAST) and GLT-1 expressions in rabbits, and to investigate the effect of peripheral nerve anesthesia on the morphology and function of the spinal cord.@*METHODS@#Twenty healthy New Zealand white rabbits were randomly divided into two groups: the experimental group and control group; with 10 rabbits in each group. For spinal nerve anesthesia, 5 g/L of bupivacaine was used in the experimental group, and sterile saline was used in the control group. After 30 min of cardiac perfusion, GLAST and GLT-1 protein expression in spinal neurons were detected by immunohistochemistry and immunofluorescence staining.@*RESULTS@#GLAST and GLT-1 protein-positive cells increased in neurons in the experimental group, compared with the control group (P < 0.05).@*CONCLUSIONS@#After subarachnoid nerve block anesthesia, rabbit glutamate transporter GLAST and GLT-1 expression is increased; and spinal cord nerve cell function is inhibited.
ABSTRACT
In the present study, we examined the distribution and amount of two important glutamate transporters, GLT-1 and GLAST in the cerebellum of young and aged rats. Sprague-Dawley rats were used at the age of three months for young control (n=3) and 24 months for aged group (n=4). After transcardial perfusion with 4% paraformaldehyde, brain sections were immunostained for GLT-1, and GLAST. We found that GLT-1- and GLAST-immunoreactive materials were diffusely distributed throughout the gray matter of the cerebellum. Pre-embedding immunoelectron microscopic study demonstrated that the two glutamate transporters in the cerebellum were restricted to glial cells with astrocytic features. The intensity of GLT-1-immunostaining in the cerebellum appeared to be higher in aged rats than in young rats whereas GLAST-immunostaining decreased with aging. Western blot results were also consistent with the immunohistochemical observations. Conclusively, GLT-1 and GLAST expression in the rat cerebellum was changed with aging, i.e, increase of GLT-1 and decrease of GLAST expression with aging, which suggests that the two glutamate transporters might be regulated by different underlying mechanisms with aging.
Subject(s)
Aged , Animals , Humans , Rats , Aging , Blotting, Western , Brain , Cerebellum , Formaldehyde , Glutamic Acid , Neuroglia , Perfusion , Polymers , Rats, Sprague-DawleyABSTRACT
Objective The purpose of this investigation was to observe the effects of the glutamate/aspartate transporter(GLAST) antibody to auditory brainstem response(ABR) and the pathologic morphology of hair cells in the guinea pig's cochlea. Methods 20 guinea pigs were randomly divided into the experimental group and control group. By perfusing the antibody to GLAST into tympanic canal in the cochlea of guinea pigs in experimental group and artificial perilymph into the guinea's cochlea in control group,the results of ABR ,basilar membrane stretched preparation and transmission electron microscope were observed. Results After antibody perfusion,the ABR was not induced from the third day to the ninth day.In control group,the ABR was nearly absent on the third day,but could be evolved,on the sixth day and the ninth day in all guinea pigs with the average threshold of 62.50?5.25 dB SPL and 47.50?6.18 dB SPL,respectively. The ABR thresholds at different time in control group were significantly different(P
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Objective: To observe the expressions of NMDAR2 and GLAST in the hippocampal gyrus and supraoptic nucleus(SON) under sleep deprivation in young rats.Methods: The changes in expressions of NMDAR2 and GLAST in SON and hippocampal gyrus under sleep deprivation in younger rats were observed by immunohistochemistry method. Results:The expressions of NMDAR2 and GLAST in SON and the hippocampal gyrus were significantly increased on the 3rd day of sleep deprivation,even more sigificantly on the 5th day,decreased gradually on 7th day,and became similar to those of control group on the 14th day.Conclusion: Sleep deprivation can affect the expressions of NMDAR2 and GLAST in the hippocampal gyrus and supraoptic nucleus,but the effect diminisshes gradually with prolonged time,which may be associated with self-regulation and self-protection of the central nervous system.
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Objective To study the toxic effects of Rotenone on glutamate transporter and glutamine synthetase in rat brain.Methods The glutamate levels in the striatum of SD rats were detected by high performance liquid chromatography(HPLC),the expression of glutamate tansporter mRNA and proteins were detected by RT-PCR and Western blotting and the activity of glutamine synthetase was determined by using GS detect kit.Results Rotenone was shown to increase the release of glutamate in rat striatum,the expression of glutamate/aspartate transporter(GLAST)mRNA and protein decreased significantly in 0.6 mg/kg and 1.2 mg/kg Rotenone intoxicated groups,but the expression of GLT-1 and the activity of GS enhanced obviously.Conclusion Down-regulation of GLAST may be responsible for increased Glu level in rat brain induced by Rotenone,but the increased expression of GLT-1 and GS activity may represent a protective mechanism of the brain cells by limiting the neurotoxicity of Glu.
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Diabetic hyperglycemia induces transient ischemia in the neural retina. High level of extracellular glutamate resulting from ischemia, in turn, influences on glutamate homeostasis. The present study has been conducted to clarify the alteration of the glutamate homeostasis-associated substances in the retinal Muller cells in response to a diabetic injury by streptozotocin injection. Young adult Sprague -Dawley rats were injected with streptozotocin (60 mg/kg body weight in 0.05 M sodium citrate buffer, pH 5.5) under anesthesia with 4% chloral hydrate. Animals above 300 mg/dl in blood glucose level were cared for 1, 4, 12 and 24 weeks, respectively. At each time-point, the retinas were dissected out and processed for immuno-histochemical and immunoblotting analyses by using guinea pig anti -GLAST and mouse anti-glutamine synthetase (GS) antibodies. In the normal retina, GLAST and GS were immuno-localized in the Muller cells, the outer plexiform layer (OPL), the border between the inner nuclear layer and the inner plexiform layer (IPL), a band in the middle of the IPL, and the border between the IPL and the ganglion cell layer. The expression of both proteins was decreased remarkably in the OPL by 12 weeks of diabetes and increased slightly in the end feet of the Muller cells from 4 weeks onwards. Immunoblotting results of the two proteins in the diabetic retinas were largely consistent with those of immuno-histochemistry. These results suggest that the alteration of glutamate homeostasis in the diabetic state is initiated mainly in the OPL by decreasing the uptake of glutamate via down-regulated GLAST.