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Aconitine,a common and main toxic component of Aconitum,is toxic to the central nervous system.However,the mechanism of aconitine neurotoxicity is not yet clear.In this work,we had the hypothesis that excitatory amino acids can trigger excitotoxicity as a pointcut to explore the mechanism of neurotoxicity induced by aconitine.HT22 cells were simulated by aconitine and the changes of target cell metabolites were real-time online investigated based on a microfluidic chip-mass spectrometry system.Meanwhile,to confirm the metabolic mechanism of aconitine toxicity on HT22 cells,the levels of lactate dehydrogenase,intracellular Ca2+,reactive oxygen species,glutathione and superoxide dismutase,and ratio of Bax/Bcl-2 protein were detected by molecular biotechnology.Integration of the detected results revealed that neurotoxicity induced by aconitine was associated with the process of excitotoxicity caused by glutamic acid and aspartic acid,which was followed by the accumulation of lactic acid and reduction of glucose.The surge of extracellular glutamic acid could further lead to a series of cascade reactions including intracellular Ca2+overload and oxidative stress,and eventually result in cell apoptosis.In general,we illustrated a new mechanism of aconitine neurotoxicity and presented a novel analysis strategy that real-time online monitoring of cell metabolites can provide a new approach to mechanism analysis.
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Objective:To explore the effects of chronic restraint stress (CRS) on the abilities of spatial learning and memory and the levels of excitatory amino acids in the hippocampal dentate gyrus (DG) in the old rats,and to investigate the neurochemical mechanism of CRS in affecting the spatial learning and memory abilities.Methods:Sixteen male SD rats (18 months old) were randomly divided into control group (n =8) and CRS group (n=8),and the rats in CRS group received CRS 2 h every day for 30 d.And then the spatial learning and memory abilities of rats were measured by Morris water maze (MWM) test,and the extracellular levels of excitatory amino acids including asparate (Asp) and glutamate (Glu) in the DG were simultaneously determined by in vivo microdialysis and HPLC.The levels of corticosterone (CORT) and epinephrine (EPI) in serum of the rats wereexamined by ELISA assay.Results:In CRS group,the escape latencies on the 2nd-4th days were significantly increased and the percentage of time spent in target quadrant on the 5th day was markedly decreased in MWM test compared with control group (P＜0.05).Compared with before training,the extracelluar level of Asp in the DG in control group was significantly increased on the 2nd day in MWM test;compared with control group,the extracelluar level of Asp in the DG in CRS group was significantly decreased on the 3rd day in MWM test (P＜0.05).Compared with before training,the Glu levels in the DG in MWM test in both control and CRS groups were markedly increased (P＜0.05),but there was no significant difference between two groups (P＞0.05).Compared with control group,the levels of CORT and EPI in the serum of the rats in CRS group were significantly increased (P＜0.05).Conclusion:CRS impairs the spatial learning and memory abilities in the old rats,which may be related to the decrease of Asp level in the hippicampal DG of the rats.
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Objective: To explore the effects of chronic restraint stress (CRS) on the abilities of spatial learning and memory and the levels of excitatory amino acids in the hippocampal dentate gyrus (DG) in the old rats, and to investigate the neurochemical mechanism of CRS in affecting the spatial learning and memory abilities. Methods: Sixteen male SD rats (18 months old) were randomly divided into control group (n=8) and CRS group (n=8), and the rats in CRS group received CRS 2 h every day for 30 d. And then the spatial learning and memory abilities of rats were measured by Morris water maze (MWM) test, and the extracellular levels of excitatory amino acids including asparate (Asp) and glutamate (Glu) in the DG were simultaneously determined by in vivo microdialysis and HPLC. The levels of corticosterone (CORT) and epinephrine (EPI) in serum of the rats were examined by ELISA assay. Results: In CRS group, the escape latencies on the 2nd-4th days were significantly increased and the percentage of time spent in target quadrant on the 5th day was markedly decreased in MWM test compared with control group (P0. 05). Compared with control group, the levels of CORT and EPI in the serum of the rats in CRS group were significantly increased (P<0. 05). Conclusion: CRS impairs the spatial learning and memory abilities in the old rats, which may be related to the decrease of Asp level in the hippicampal DG of the rats.
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Objective To investigate the effect of parecoxib sodium combined with dexmedetomi-dine on postoperative levels of plasma excitatory aminoacid and beta-amyloid protein(β-AP)in jugular bulb venous of elderly patients. Methods A total of 135 patients of either sex, aged 65-79 yr, weighing 47-76 kg, of American Society of Anesthesiologists physical status Ⅱ or Ⅲ, undergoing elective open reduc-tion and internal fixation after tibial fracture and hip replacement, were divided into 3 groups(n=45 each) using a random number table: parecoxib sodium group(group P), dexmedetomidine group(group D)and parecoxib sodium combined with dexmedetomidine group(group PD). In group P, parecoxib sodium 40 mg (diluted to 5 ml in normal saline)was injected intravenously at 15 min before induction of anesthesia. In group D, dexmedetomidine was intravenously infused at a loading dose of 05 μg∕kg over 15 min starting from 15 min before induction of anesthesia, followed by an infusion of 05 μg·kg-1·h-1until the end of surgery. In group PD, parecoxib sodium 40 mg(diluted to 5 ml in normal saline)was intravenously injec-ted at 15 min before induction of anesthesia, and dexmedetomidine was intravenously infused at a loading dose of 05 μg∕kg over 15 min followed by an infusion of 05 μg·kg-1·h-1until the end of surgery at the same time. At 15 min before induction of anesthesia(T0), at the end of surgery(T1)and at 24, 48 and 72 h after surgery(T2-4), jugular bulb venous blood samples were taken for determination of concentrations of glutamate and aspartate in plasma(by reversed phase high-performance liquid chromatography)and β-AP(by enzyme-linked immunosorbent assay). Cognitive function was assessed at 1 day before surgery and 7 days after surgery using a battery of neuropsychologic tests including Wechsler Memory Scale, Digit Span (Forward and Backward), visual recognition and associative learning, Wechsler Adult Intelligence Scale and Trail Making Test Part A. The occurrence of postoperative cognitive dysfunction was recorded at 7 days after surgery. Results Compared with P and D groups, the concentrations of plasma glutamate at T2-3, plasma aspartate at T2and β-AP at T1and incidence of postoperative cognitive dysfunction were significantly decreased in group PD(P< 005). Conclusion The mechanism by which parecoxib sodium combined with dexmedetomidine decreases the occurrence of POCD may be related to inhibiting the levels of excitatory aminoacid and β-AP in brain tissues of elderly patients.
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Time dependent intervention plays a crucial role in preventing neurodegeneration after ischemic insult. The intensity of excitotoxicity is greater in the secondary reperfusion phase (2-4 h) compared to the primary occlusion phase (2 h), which could be attributed to secondary elevation of excitatory amino acids (EAA) in cerebral ischemia. In the present study, we tried to assess the neuroprotective effects of telmisartan and nimodipine (TM-NM) combination on the secondary reperfusion phase. The drug treatments were made immediately after reperfusion and their effects were compared with pre-treatment. The neuroprotective effect was studied using middle cerebral artery occlusion (MCAo) transient ischemic model in rats. On the 7th day after reperfusion, the rats were subjected to behavioral studies. The brain was dissected out on the 9th day to measure neurobiochemical alterations and for histopathological observations. The results have shown that TM-NM (5 mg/kg) attenuated the EAA release in different brain regions with partial restoration of energy levels in secondary reperfusion phase. Similarly, it normalized the behavioral alteration and the effect was comparable to pre-ischemic treatment (2.5 mg/kg). Pre-ischemic treatment of TM-NM (2.5 mg/kg) protected the neurons from ischemic reperfusion injury by energy dependent EAA regulation. It can be concluded from the study that, even though the pre- and post-treatment of TM-NM show similar results, the post-ischemic treatment of TM-NM combination is beneficial due to better EAA control. Since hypertension is the primary risk factor for stroke, clinical incidents of stroke in hypertensive patients receiving angiotensin receptor blockers (ARBs) can be further investigated to understand the present study in the clinical situation.
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Aims: Neurotransmitter overflow into the extracellular space and activation of nitric oxide synthase were implicated in neuronal death after cerebral ischemia. A small temperature reduction induced after the insult crucially mitigated the neuronal death. To elucidate the mechanisms, dopamine and glutamate as marker of excitatory amino acid (EAA) overflow and the citrulline/arginine ratio (CAR) as marker of nitric oxide synthase were analysed. Study Design: Animal experiments in rats. Place and Duration of the Study: Laboratory of the Department of Pharmaceutical Chemistry and Drug Analysis, Vrije Universiteit Brussel, Brussels between 2001 and 2003. Methodology: Striatal Glutamate and dopamine and CAR were measured by using microdialysis under normothermic and hypothermic conditions before asphyxial cardiac arrest, during the insult and resuscitation as well as during the weaning process from mechanical ventilation. Results: After the insult, the EAA overflow increased significantly in the normothermic group. In the hypothermic group, however this overflow was not significantly different from the sham group. The CAR increased up to 5-fold compared to the basal value in the normothermic group and only 2.5-fold in the hypothermic group. The brain damage was mitigated in the hypothermic group, while this increased further up 7 days after the insult in the normothermic group. Conclusion: These results suggest that the neuroprotective effect of mild hypothermia resides in attenuation of the striatal EAA overflow and diminution of the CAR and were associated with a reduction of brain damage at 24 hours and 7 days post insult.
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Objective: To observe the impact of electroacupuncture on the pain threshold and the content of excitatory amino acids in the spinal cord of the rats with neuropathic pain to discuss the mechanism of electroacupuncture in treating neuropathic pain. Methods: The rats were randomly divided into a control group (n=10), a sham surgery group (n=10) and a surgery group (n=30) to take spared nerve injury (SNI) surgery of sciatic nerve. The successful SNI model rats in the surgery group were randomly divided into a model group (n=10), an electroacupuncture group (n=10) and a sham electroacupuncture group (n=10). The mechanical pain threshold (MPT) and heat pain threshold (HPT) were measured on the preoperative day, postoperative day 7, postoperative day 9 and the day after the sixth acupuncture treatment. The electroacupuncture was carried out at Huantiao (GB 30) and Weizhong (BL 40) starting from the postoperative day 10 to reflect the impact on the mechanical pain threshold and heat pain threshold. The pre-column deriverization and HPLC fluorescence detection as well as microdialysis method were adopted to test the content of EAAs in spinal cord of rats. Results: The SNI surgery decreased the mechanical pain threshold of rats significantly. The glutamate (Glu) and aspartic acid (Asp) in the microdialysis solution of rats in the model group were higher than in the control group and sham surgery group at the same time point (P<0.05). The contents of Glu and Asp in the microdialysis solution of rats in the electroacupuncture group and sham electroacupuncture group decreased significantly (P<0.05), comparing with model group at the same time point (except the Glu of the sham electroacupuncture group at the second time point). The electroacupuncture reduced the mechanical allodynia markedly. Conclusion: The mechanism of electroacupuncture treating neuropathic pain may relate with the decrease of excitatory amino acids in spinal cord.
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Objective To investigate the relationship between the changes in intracranial excitatory amino acid(EAA) levels and the incidence of postoperative cognitive dysfunction (POCD) in eldedy patients after general anesthesia. Methods Forty ASA Ⅰ-Ⅲ patients of both sexes aged 65-79 yr weighing 48-76 kg undergoing elective non-cardiac surgery under general anesthesia were studied.Anesthesia was induced with midazolam,fentanyl,etomidate and succinylcholine and maintained with continuous iv infusion of propofol,remifentanil,isoflurane inhalation and intermittent iv boluses of vecuronium.The right internal jugular vein was cannulated with a catheter which was advanced cephalad until jugular bulb.The jugular bulb venous blood samples were taken before (T0,baseline),at the end of (T1) and at 24,48 and 72h(T2-4) after operation for measurement of plasma concentrations of glutamate (Glu),aspartate (Asp) and glycine (Gly) by RP-HPLC.The cognitive function was evaluated by mini-mental state examination (MMSE) at T0 and T4.Results Eleven of the 40 patients developed POCD (28%).The plasma Gh,Asp and Gly concentrations were significantly increased after operation as compared with the baseline values in POCD patients and were significantly higher than in non-POCD patients.The plasma concentrations of Glu and Asp were negatively correlated with MMSE score(Glu:r=-0.86.P<0.01;Asp:r=-0.99,P<0.01).Conclusion Elderly patients may develop POCD after operation performed under general anesthesia through increase in intracranial EAA levels.
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Objective Role of melanocortin receptor 4 (MCAR) in excitatory amino acid release from rat astrocytes in spinal cord. Methods Astrocytes were isolated from the spinal cord of newborn pathogen-free Wistar rats ( 1-3 days after birth) and cultured in serum-free Neurobasal/B27 liquid culture medium. After 4 passages the primary cultured astrocytes were randomly divided into 3 groups (6 wells each): group Ⅰ control (group C); group Ⅱ the astrocytes were exposed to TNF-α 10 μg/L (group T) and group Ⅲ the astrocytes were exposed to TNF-α 10 μg/L and HS014 (selective MC4R antagonist) 1 μmol/L (group TH). The astrocytes were incubated at 37 ℃ for 3 h. The supernatant was collected for determination of glutamic acid (Glu) and aspartic acid (Asp)concentrations by HPLC-MS/MS. Results TNF-α significantly increased Glu and Asp release from astrocytes in group T as compared with group C. The Glu and Asp concentrations were significantly lower in group TH than in group T. Conclusion MG4R is involved in the excitatory amino acid release from astrocytes in the spinal cord.
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resulting in the increased excitatory amino acids, and the mechanism of excitatory amino acid-induced stroke.
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Objective To investigate the changes of excitatory amino acids (EAAs) of cerebrospinalfluid (CSF) in patients with delayed encephalopathy after acute carbon monoxide poisoning(DEACMP).Method The EAAs levels of CSF including glutamate (Glu) and aspartate (Asp) in 24 patients with DEACMP and 20 controls with migraine were measured by high performance liquid chromatography( HPLC ).Results Glu and Asp levels in patients with DEACMP were significantly higher than those of the controls [(3.76 ± 1.52) μmol/L vs ( 1.55 ± 1.03 ) μmol/L, (0.73 ± 0.44) μmol/L vs (0.38 ± 0.33 ) μmol/L, P all <0.01]. Glu and Asp levels in moderate and severe DEACMP patients were higher than those in mild DEACMP patients. Conclusion It suggests that EAAs participated in the pathogenesis of DEACMP. The Glu and Asp levels in CSF may be regarded as indicator of DEACMP.
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Objective To observe the effects of lanthanum on learning and memory,and explore the corresponding mechanism on the basis of the levels of excitatory amino acids and calcium homeostasis of cerebral cortex in rats.Methods Forty female Wistar rats were randomly divided into control,low-,moderate-and high-dose lanthanum groups(ten rats in each group).The offspring of lanthanum exposure groups were administrated with lanthanum from weaning for one month.The capability of learning and memory was measured by neuroethology testing.The levels of excitatory amino acids,intracellular calcium ion and Nissl body expression of cerebral cortex were also detected.Results The capabilities of learning and memory in lanthanum exposure groups were significantly lower compared with the control,with a dose-dependent manner.The levels of glutamate and intracellular calcium ion of cerebral cortex in low-and moderate-dose group were significantly higher than those in controls,and the levels of glutamate,aspartate and intracellular calcium ion of cerebral cortex in high-dose group were increased significantly as compared with the control group,low dose group and moderate dose lanthanum group.Besides,Nissl body expression of cerebral cortex in low-dose group was lower than that in control group,and the levels of Nissl body expression of cerebral cortex in middle dose lanthanum group and high dose groups decreased further.Conclusion The increased levels of excitatory amino acids,calcium homeostasis unbalance and cellular injuries in cerebral cortex may be involved in lower capacity of learning and memory in the rats exposed to lanthanum.
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Objective To explore the protective effect of astragalus injection(黄芪注射液)on cerebral cells after craniocerebral injury.Methods Sixty male Sprague-Dawley(SD)rats were randomly divided into five groups(each n=12).In the control group,only anesthesia and cranial bone surgery was performed, which did not impact on dura mater.In the model group,a freefall method was used to cause the left parietal lobe of brain limited contusion and saline was given.In the low,medium and high-dose astragalus injection (5,10,20 ml/kg)treatment groups,astragalus injection was injected intraperitoneally after injury at 30 minutes and 12 hours after injury respectively.After 24 hours of injury in each group,the rats were executed.The brain tissue from contusion was taken out and content changes of Ca~(2+),Mg~(2+),glutamate (Glu)and plasma endothelin(ET)were measured.Results In the model group,the Ca~(2+),Glu and ET contents in the rat brain tissues were significantly higher,but Mg~(2+)content was markedly lower than that of the control group(all P0.05).Conclusion Astragalus has a protective effect on nerve cells after craniocerebral injury.
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Objective To observe the changes of intracerebral amino acid transmitters in the periventricular leukomalacia (PVL) of newborn rats with microdialysis and so as to explore the role of excitotoxicity in PVL.Methods Replicated the model for PVL at the age of postnatal day 5 (P5) by intracerebral injection of 3-nitropropionic acid (3-NPA).Before injection of 3-NPA,and 15 min,30 min,45 min,60 min,75 min,90 min after injection of 3-NPA,collected the sample of extracellular fluid (ECF) at the corpus callosum above the left ventricle through microdialysis,respectively.After microdialysis,the experimental rats were allowed to survive to P6-P14,and then they were killed and the brains were prepared for HE stain.The amino accids of dialysate were quantified through high performance liquid chromatography(HPLC),and then the excitotoxic index (EI) was calculated.Results Fifteen min to 45 min after injection of 3-NPA,the concentrations of glumate (Glu) and aspartic acid (Asp) of ECF elevated significantly,and then returned to the normal levels.Fifteen min to 75 min and 15 min to 30 min after injection of 3-NPA,the concentrations of glycine (Gly) and GABA significantly elevated,respectively,and returned to normal levels at 90 min and 45 min after injection of 3-NPA,respectively.But the EI,which indicated the balance of excitatory amino acids(EAAs) and inhibitory amno aciols(IAAs),significantly elevated 15 min to 75 min after injection of 3-NPA,then retured to normal level after 90 min.Sub-cortical and periventricular white matter rarefaction and significant lateral ventricle enlargement were observed in HE staining.Conclusions Changes of intracerebral amino acid transmitters in the PVL of newborn rats show regularity:EAAs,IAAs of ECF and EI elavate in the early stage,and then return to the normal level quickly.It indicates that excitotoxicity play a great role in PVL,especially at the early stage.Therefore,the preventions of PVL must be executed at the early stage.
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Objective To figure out changes of serum excitatory amino acids (EAAs) levels in patients with amnestic mild cognitive impairment (aMCI) and Alzheimer's disease (AD).Methods The levels of serum EAAs was assessed in 34 cognitively normal control subjects,30 patients with aMCI,and 32 patients with AD using high performance liquid chromatography (HPLC).Results ①Higher serum concentrations of glutamate((39.6?22.1) ?mol/L),alanine((282.5?71.3) ?mol/L) were found in the aMCI patients (P=0.044,P=0.007),and higher serum concentrations of glutamate ((42.2?21.8) ?mol/L),glycine ((464.2?142.6) ?moL/L) were found in the AD patients than in the control subjects (P=0.010,P=0.010).②No statistically significant difference of EAAs level between the aMCI and AD groups was found.③A close and positive correlation between the serum concentrations of glutamate, aspartate and the mini-mental status examination scores were found in AD patients:the 2 amino acid levels were higher in patients with mild dementia((42.1?21.3),(55.0?29.0) ?mol/L) than those with moderate or severe dementia ((25.4?9.2) ?mol/L,P=0.023;(34.6?11.1) ?mol/L,P=0.036). Conclusion EAAs,correlating with the severity of the condition,play a significant role in AD,while aMCI patients also have disturbance of metabolism of EAAs,indicating that it has similar pathogenesis to AD.
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·AIM: To investigate whether Erigeron Breviscapus (vant) Hand-Mazz (EBHM) EBHM has neuroprotective effect against N-methyl-D-aspartate (NMDA)-induced neuron death in retinal ganglion cell layer (RGCL).· METHODS: 60 healthy SD rats were randomly divided into four groups. 6 animals were normal control group (group A). The others were divided as group B (EBHM group), group C (normal saline+NMDA group) and group D (EBHM + NMDA group). Each group had 18 rats.10nmol NMDA was intravitreally injected to induce partial damage of the neurons in RGCL in the right eyes of Groups C and D. Same volume PBS was intravitreally injected into the left eyes as self-control. Groups B and D were pre-treated intraperitoneally with 6g/L EBHM solution at a dose of 150mg/kg body weight/day seven days before and after NMDA treatment. Group C were administrated intraperitoneally with 9g/L normal saline at the same time of EBHM injection. Rats were sacrificed at 4,7,14d after NMDA treatment. Flat whole retinas were stained with 5g/L cresyl violet and neuron counting in RGCL from both eyes were observed. Each subgroup had 6 rats.· RESULTS: There was no significant difference of neuron counting in RGCL between the right eye and the left eye in group A (P=0.200). There was no significant difference between normal control group and EBHM group either in the right eyes or in the left eyes at 4, 7 and 14 d respectively after intravitreal injection of 10nmol NMDA in group C and group D. (P=0.636, P=0.193). Neuron counting of RGCL in group C and D was significantly decreased in the NMDA-treated eyes at 4, 7 and 14d after intravitreal injection (P＜0.001). There was no significant difference between self-control eyes group and normai control group(P＞0.05). However, neuron counting was significantly higher in the EBHM+NMDA group than normal saline +NMDA group at 14days after intravitreal injection (P=0.044), but was lowered than normal control group (P＜0.05).· CONCLUSION: EBHM has no effect on neuron counting of RGCL when administered alone in normal rats.The results indicates that EBHM plays a partial protective role in NMDA-induced neuron loss in RGCL in the rats.
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Objective: To discuss the neurobiochemical mechanism of Lidan Bushen Granules in treating saturnine children. Methods: Saturnine rats model was established by intragastric, and was treated with Lidan Bushen Granules for 5 weeks. The acetylcholine and excitatory amino acids of hippocampus in saturnine rats were measured. Results: Compared with the normal group, the ACH and EAA contents of hippocampus in model group rats were dramatically lower (P
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Objective To study changes of aspartate(ASP) and glutamaic acid(GLU) in cerebral cortex of neonatal Sprague-Dawely(SD) rats after hypoxia-ischemia and nitric oxide synthase(NOS) immunoactive expression in cerebral neurons were examined to explore mailuoning′s protective effect on hypoxia-ischemia brain damage(HIBD).Methods The HIBD model was established as follows.The right common carotids of the neonatal SD rats 7 days were temporaily ligatured for 1 hour.Then the neonatal SD rats were exposed to 8% oxygen and 92% nitrogen gas mixture for 2 hours. The ASP and GLU were determined in right cerebral cortex using chromatograph,compared with sham-operated group and mailuoning administrated. Ultrastructure changes of neurons in the right cerebral cortex of neonatal SD rats were observed after sham-operated,hypoxia-ischemia and mailuoning administrated using electronmicroscope.Results The level of excitatory amino acid was promoted in right cerebral cortex after hypoxia-ischemia.The volume of excitatory amino acid was reduced sharply mailuoning administrated. Ultrastructure of neurons in the cerebral cortex showed serious injure after hypoxia-ischemia and ultrastructure of neurons in the cerebral cortex appeared slight damage.Conclusion Mailuoning may possess protective effects to the neurons after hypoxia-ischemia through supplying blood to neurons reducing release of excitatory amino acid.
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Objective:To investigate the level of excitatory amino acids in the cerebrospinal fluid and the effect of magnesium sulfate on the excitatory amino acids following traumatic brain injury. Methods:The Feeney′s model of the excitatory amino acids in the cerebrospinal fluid (glutamate and aspartate) were measured by amino acid analysis from rats in different time. Results:1. The glutamate and aspartate in the cerebrospinal fluid increased largely 2 hours after traumatic brain injury(P0.05).2.Magnesium inhibited strongly the releasing of the excitatory amino acids at 2h and 8h after the traumatic brain injury(P0.05).Conclusion:Plenty releasing of excitatory amino acid may play an important role at the phase of posttraumatic neuronal injury.Magnesium sulfate can inhibit early releasing of excitatory amino acids.Administering magnesium sulfate may be the optimal choice for treating traumatic brain injury.
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Objective To investigate the changes of excitatory amino acids of cerebrospinal fluid(CSF) in patients with acute cerebral infarction(ACI) and its clinical significance.Methods The CSF levels of excitatory amino acids including glutamate(Glu) and aspartate(Asp) in 30 cases with ACI and 20 control subjects with migraine were measured by high performance liquid chromatography.Results Glu and Asp levels in patients with ACI were significantly higher than those of the controls(all (P