ABSTRACT
Objective:To investigate the effect and the mechanism of electroacupuncture(EA)on corpus striatum white matter injury in rats with focal cerebral ischemia(FCI).Methods:Forty-four specific-pathogen-free Sprague-Dawley rats were divided into a normal group(n=10),a sham-operation group(sham group,n=10),and a modeling group(n=24)using the random number table method.The normal group was a blank control.In the sham group,only the vessels and vagus nerve were isolated without embolization.The FCI rat model in the modeling group was replicated using the middle cerebral artery occlusion embolization method.The 20 successfully modeled rats were randomly divided into a model group and an EA group,with 10 rats in each group.Rats in the model group did not receive further treatment.Rats in the EA group received EA stimulation at Baihui(GV20)and the left Zusanli(ST36)24 h after the successful modeling,30 min each time,once a day for 14 d.On the 14th day of the experiment,rats in each group were scored for neurological deficits and then sacrificed,and brain tissues containing corpus striatum around the ischemic focus were paraffin-embedded from 5 rats in each group.Luxol fast blue(LFB)staining was used to detect damage changes in the white matter.The positive immunoreactive expression of myelin basic protein(MBP),myelin-associated growth inhibitor A(Nogo-A)and its receptor(NgR)in rat corpus striatum tissue was detected by immunohistochemistry staining,and then the protein expression of MBP,Nogo-A,and NgR in the corpus striatum tissue around the ischemic focus was determined by Western blotting.Results:Compared with the normal group and the sham group,the model group had a significantly higher neurological deficit score(P＜0.05)and fiber bundle injuries in the corpus striatum white matter,evidenced by a significantly lower mean optical density value of corpus striatum LFB staining(P＜0.05),a significantly lower MBP expression level(P＜0.05),and significantly higher Nogo-A and NgR protein expression levels(P＜0.05).Compared with the model group,the neurological deficit score was significantly lower(P＜0.05),the mean optical density value of LFB staining was significantly higher(P＜0.05),the MBP expression level was increased(P＜0.05),and the expression levels of Nogo-A and NgR proteins were decreased(P＜0.05)in the EA group.Conclusion:EA reduces the ischemia-induced corpus striatum white matter injury and improves neurological deficits.The mechanism may be related to the inhibition of Nogo-A/NgR activation.
ABSTRACT
Objective:To explore the changes of brain activity in drug-resistant or drug-controlled medial temporal lobe epilepsy patients by the method of functional connectivity density (FCD), and to analyze their correlation with the course of the disease.Methods:According to the definition of drug-resistant epilepsy by the International League Against Epilepsy in 2010, 146 patients with medial temporal lobe epilepsy who were clearly diagnosed as unilateral hippocampal sclerosis in Jinling Hospital, Nanjing University School of Medicine from July 2009 to February 2019 were divided into drug control group ( n=73) and drug-resistant group ( n=73). The 3.0 T resting state functional magnetic resonance scan was performed on all subjects to compare the difference in FCD between the two groups, and calculate the correlation between the FCD value of the brain area and the course of the disease between the two groups of patients. Results:There was significant difference between the two groups in FCD. Compared with the drug control group, the drug-resistant group had significantly lower FCD values in the insula, lenticular nucleus, thalamus, hippocampus and precentral gyrus on the side of the epileptogenic focus. The FCD value of the precuneus on the side of the epileptogenic focus in the drug-resistant group was negatively correlated with the duration ( r=-0.30, P=0.01). Conclusions:The FCD of patients with drug-resistant medial temporal lobe epilepsy was lower than that of the drug control group. In addition, there may be progressive damage to the brain. The difference is helpful for exploring the pathophysiological mechanisms related to drug resistance in patients with medial temporal lobe epilepsy, and finding reliable neuroimaging markers related to drug resistance.
ABSTRACT
RESUMO Objetivos: Pouco se sabe sobre a atuação dos esteroides androgênicos anabolizantes (EAA) no cérebro humano e, por isso, resolvemos estudar a perda neuronal causada pelo uso e abuso de EAA em camundongos. Métodos: Utilizamos 60 camundongos da linhagem Swiss, sendo 30 machos e 30 fêmeas, divididos em três grupos: 20 animais foram tratados com Deposteron® (cipionato de testosterona); outros 20 animais foram tratados com Winstrol Depot® (stanozolol); os últimos 20 animais foram tratados com solução salina. Todos foram submetidos à natação por 15 minutos. Finalizado o tratamento, os animais foram sacrificados pelo método de inalação de Halotano. Os encéfalos foram retirados e armazenados em solução de formaldeído a 4% por 24 horas. De cada encéfalo foram retiradas amostras homotípicas da região média do cérebro em cortes frontais para que pudéssemos avaliar as áreas estabelecidas para este estudo. Resultados: As análises da estimativa dos perfis celulares mostraram que houve uma diminuição do número de perfis no núcleo pálido dos animais machos tratados com Winstrol Depot®. Conclusão: Esses resultados nos permitem inferir que o uso inadequado e sem orientação médica de EAA pode levar a degenerações celulares.
ABSTRACT Objectives: Little is known about the action of anabolic-androgenic steroids (AAS) on the human brain and, therefore, we decided to study the neuronal loss caused by use and abuse of AAS in mice. Methods: We used 60 Swiss mice, 30 males and 30 females, divided into three groups: 20 animals treated with Deposteron® (testosterone cypionate); another 20 animals were treated with Winstrol Depot® (stanozolol); the last 20 animals were treated with saline solution. All the animals were submitted to swimming for 15 minutes. After the treatment, the animals were euthanized by halothane inhalation (Halotano) method. The brains were removed and stored in 4% formal-dehyde solution for 24 hours. From each brain, homotypic samples were taken from the middle region of the brain in frontal cuts so that we could evaluate the areas established for this study. Results: Analyzes of the estimated cell profiles showed that there was a decrease in the number of profiles in the pallidal nucleus of the male animals treated with Winstrol Depot®. Conclusion: These results allow us to infer that inadequate and non-medical use of AAS can lead to cellular degeneration.
RESUMEN Objetivos: Poco se sabe acerca del efecto de la acción de los esteroides anabólicos androgénicos (EAA) en el cerebro humano y, por este motivo, decidimos estudiar la pérdida neuronal causada por el uso y abuso de EAA en ratones. Métodos: Utilizamos 60 ratones de linaje Swiss, siendo 30 machos y 30 hembras, divididos en tres grupos: 20 animales fueron tratados con Deposteron® (cipionato de testosterona); otros 20 animales fueron tratados con Winstrol Depot® (stanozolol); los últimos 20 animales fueron tratados con solución salina. Todos fueron sometidos a natación durante 15 minutos. Terminado el tratamiento, los animales fue-ron sacrificados por el método de inhalación de Halotano. Los cerebros fueron retirados y almacenados en solución de formaldehído al 4% durante 24 horas. De cada cerebro fueron retiradas muestras homotípicas de la región media del cerebro en cortes frontales, así que pudimos evaluar las áreas establecidas para este estudio. Resultados: El análisis de la estimación de los perfiles celulares mostró que hubo una disminución en el número de perfiles en el globo pálido de los animales machos tratados con Winstrol Depot®. Conclusión: Estos resultados permiten inferir que el uso inadecuado y sin orientación médica de EAA puede conducir a la degeneración celular.
ABSTRACT
Objective To observe non-displaceable binding potential (BPND) changes of striatal dopamine D2 receptors(SDDR) in patients with first-episode major depressive disorder (MDD) using 11C-Raclopride PET/CT,and to analyze the relationship between BPND and Hamilton rating scale for depression (HAM-D).Methods From December 2014 to December 2015,patients with first-episode MDD and age/gender-matched healthy controls underwent brain MRI and 11C-Raclopride PET/CT in this prospective study.BPND of bilateral SDDR was calculated by molecular imaging and kinetic analysis toolbox (MIAKAT).BPND changes of bilateral SDDR and their relationship with HAM-D score were analyzed.Paired t test,two-sample t test and Pearson correlation analysis were used.Results A total of 20 MDD patients (8 males,12 females,average age: (32.80±9.76) years) and 20 healthy controls (9 males,11 females,average age:(29.25±6.93) years) were enrolled in this study.The 11C-Raclopride uptake in brain tissue of the MDD group and control group were mainly distributed in bilateral striatum,and very few 11C-Raclopride was distributed in bilateral cerebral cortex and cerebellum.In MDD group,the BPND level of bilateral SDDR had no statistical differences(t values: 0.69,0.35,both P>0.05),and similar results were found in the control group(t values: 0.28,0.24,both P>0.05).Compared with the control group,however,the MDD group had lower BPND level of bilateral SDDR(t values: 3.13-4.41,all P<0.05).The BPND of bilateral caudate nucleus and/or putamen D2 receptors was correlated with HAM-D total score,anxiety/somatization factor score,cognitive impairment factor score,retardation factor score and sleep disturbance factor score(r values: from-0.688 to-0.453,all P<0.05).Conclusions The binding potential of SDDR in patients with first-episode MDD is declined,and the BPND level of SDDR is correlated with symptoms of depression.The abnormality of SDDR may be an important molecular mechanism of the abnormality of midbrain-striatal dopamine reward circuits in MDD patients.
ABSTRACT
Objective@#To elucidate the effect of taurine on neurotoxicity induced by Mn by investigating activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase and content of Mn and active calmodulin in manganese exposed rats.@*Methods@#156 male SD rats were randomly divided into 1 control group, 3 manganese exposed groups (10, 15, and 20 mg/kg respectively) , and 9 taurine intervened groups based on orthogonal design (doses of taurine intervention were 100, 150, and 200 mg/kg respectively) , with 12 rats in each group. After 12 weeks of exposure, all rats were decapitated and corpus striatums were removed, activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase and content of Mn and active calmodulin were analyzed.@*Results@#The corpus striatum Mn content of the 3 dose groups exposed to Mn and 9 taurine intervened groups were significantly higher than that of the control group (P<0.05) . Active calmodulin content in 10 mg/kg manganese exposed group was significantly higher than that of the control group (P<0.05) . 150 and 200 mg/kg of taurine could decrease active calmodulin content of the group exposed to 10 mg/kg of Mn (P<0.05) . The corpus striatum activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase of the 3 dose groups exposed to Mn were significantly lower than that of the control group (P<0.05) . 150 mg/kg of taurine could increase activities of Na+-K+-ATPase of the group exposed to 10 mg/kg of Mn (P<0.05) . 150 and 200 mg/kg of taurine could respectively improve activities of Ca2+-Mg2+-ATPase of the group exposed to 15, 10 mg/kg of Mn (P<0.05) .@*Conclusion@#Mn can decrease the rats corpus striatum activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase, effect level of active calmodulin in relation to dose of Mn, to a certain extent, taurine could regulate activities of Na+-K+-ATPase and Ca2+-Mg2+-ATPase and improve the level of active calmodulin.
ABSTRACT
Objective To assess the effects of 7,8-dihydroxyflavone (7,8-DHF) on the striatum (ST) in normal cynomolgus monkeys using 99Tcm-TRODAT-1 imaging.Methods A total of six healthy female cynomolgus monkeys were included in this study.Three of them were fed with normal food (control group),and the other three were given oral administration of 7,8-DHF in addition to normal food (experimental group).The SPECT/CT imaging was performed at different time after 99Tcm-TRODAT-1 injection.The ROI of ST was drawn on images of 3 consecutive transverse slices that could be visualized best.The cerebellum (CB) was taken as the background reference area.The radioactivity uptake ratios of ST/CB at 1,3,4 and 5 h were calculated respectively.Paired-t test was used to analyze the data.Results ST radioactive uptake ratios showed continuing increase on the delay images.ST/CB uptake ratios of the control group at 1,3,4 and 5 h were 1.43±0.04,1.82±0.06,2.04±0.12,2.42±0.23,respectively,and those of the experimental group were 1.35±0.08,2.40±0.09,2.74±0.13 and 3.25±0.15 respectively.There was no significant difference between the two groups at 1 h (t =2.57,P＞0.05),while ST/CB uptake ratios of the experimental group at 3,4 and 5 h were significantly higher (t values:2.77,2.87 and 2.92,all P＜0.05).Conclusion 99Tcm-TRODAT-1 SPECT/CT imaging can be used to assess the DAT activation effect by 7,8-DHF on ST of cynomolgus monkeys.
ABSTRACT
Objective To investigate changes of striatal DAT following hypoxic ischemic (HI)brain injury in newborn piglets using 11C-N-2-carbomethoxy-3-(4-fluorophenyl)-tropane (CFT) PET/CT,and to evaluate the value of 11C-CFT PET/CT in brain injury.Methods Newborn piglets with HI brain injury (n =20) were taken as a model group,and five piglets were used as a control group.Radioligand 11CCFT (55.5-74.0 MBq) was injected through the jugular vein,and PET/CT imaging was performed to observe the changes of striatal DAT in newborn piglets.The ST/occipital lobe (OC) ratio was calculated.Model group was divided into 0-6 h,20-24 h,44-48 h and 68-72 h sub-groups after HI in accordance with the imaging time.The piglets were sacrificed immediately after 11C-CFT PET/CT scanning,and then the brains were removed for pathological analysis.Data analysis was performed with one-way analysis of variance and Pearson linear correlation analysis.Results After intravenous injection of 11C-CFT,the radioactivity accumulation in cortical,striatum,and cerebellum was shown clearly in the control and model groups.The radioactivity accumulation was lower in the white matter.The radioactivity in cortical and cerebellum exhibited decreased with time,while the striatum was still clear.After HI,the ST/OC activity ratio in the striatum was initially increased,and the ratio of 0-6 h group (1.34 ± 0.04) was statistically significant compared with that of thecontrol group (1.18 ± 0.06 ; F =4.658,P ＜ 0.05),followed by a gradual decrease.ST/OC ratios of other HI subgroups were 1.27 ±0.01,1.27 ±0.10 and 1.18 ±0.05,respectively.There was a positive correlation between the number of DAT positive neurons ((13 ± 3),(13 ± 4),(8 ±3) and (4 ±4)/high power field) and 11C-CFT ST/OC activity ratios (r =0.844,P ＜0.05).Conclusion 11C-CFT PET/CT study can accurately reflect the changes of DAT in the striatum,and the amount of DAT is related to the severity of the ischemic insult in a newborn piglet model of HI.
ABSTRACT
La aciduria glutárica tipo I se produce por deficiencia de la enzima glutaril-CoA deshidrogenasa involucrada en el catabolismo de la L-lisina, L-hidroxilisina y L-triptófano lo que ocasiona acumulación de los ácidos glutárico y 3 hidroxiglutárico responsables del compromiso neurológico severo característico de esta enfermedad. La sospecha y diagnóstico de las enfermedades metabólicas constituyen un reto para el personal de salud dada su baja incidencia. En el caso de la aciduria glutárica tipo I se trata de una enfermedad para la cual se poseen los recursos técnicos para el diagnóstico y tratamiento nutricional, su instauración previa a la aparición de encefalopatía aguda, que ocasionan daños irreversibles en el sistema nervioso central, mejora el pronóstico y disminuye el grado de discapacidad. En esta publicación se reportan 5 casos con diagnóstico clínico y bioquímico de aciduria glutárica tipo I que ilustran el espectro clínico y el proceso diagnóstico y de tratamiento en el medio colombiano. Los pacientes se encuentran en seguimiento por los servicios de Neuropediatría.
Glutaric aciduria type i is a disorder resulting trom the deficiency ot the glutaryl-CoA dehydrogenase, enzyme involved in the catabolism ot L-lysine, L-hydroxy-lysine y L-tryptophan causing the accumulation ot its derivatives glutaric acid and 3-hydroxy-glutaric acid which are responsible tor the severe neurological involvement observed in this disease. The diagnosis ot metabolic disorders represents a challenge tor health-care services given its low incidence. Glutaric aciduria type I is a disease tor which there are available technical resources tor diagnosis as well as the nutritional therapy that when set prior to acute encephalopathy, who results in irreversible damage ot central nervous system, can improve the prognosis and decrease the disability ot patients. This publication report 5 cases with clinical and biochemical diagnosis ot glutaric aciduria type i that show the clinical spectrum the diagnostic and treatment approach ot this pathology in Colombia. All the patients are being followed by neuropediatrics services.
ABSTRACT
Objective To investigate the effect of repetitive transcranial magnetic stimulation (rTMS) on dopaminergic neurons in substantia nigra and nigrostriate fibers in the striatum in cases of Parkinson's disease (PD).Methods Forty male C57BL/6J mice were randomly divided into a control group,a PD model group,a sham-rTMS (srTMS) group and an rTMS group with 10 mice in each group.A PD model was established by subcutaneous injection of a solution of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP),and the mice were treated with rTMS or sham rTMS for 14 days.Tyrosine hydroxylase (TH) expression in the substantia and striatum were detected using an immunohistochemical technique,and the corrected optical densities (CODs) of TH in the striatum were analysed using an image analysis system.The Nissl bodies were detected by Nissl staining.The morphological disposition of nerve fibers in the striatum was detected using Warthin-Starry staining.Results The fraction of neurons expressing TH decreased significantly more in the substantia nigras of mice in the rTMS group than in the control group,the PD group and the srTMS group.In the control group the neural plasm of dopaminergic neurons was full of dark blue and granular Nissl bodies.Many Nissl bodies were lost in the PD and srTMS groups,and the remaining Nissl bodies were colored lightly.Few Nissl bodies were lost in the rTMS group.Positive TH reactions in the striatum were significantly decreased in the rTMS group compared to the control group.The average COD was also significantly lower.But positive TH reactions in the striata of the rTMS group mice were significantly greater than in the PD and srTMS groups,and the average COD was significantly higher.In the control group,the disposition of nerve fibers in the striatum was typically fasciculated,concentrated and ordered; in PD and srTMS groups,many fibers were lost,and the remaining nerve fibers were rare,ruptured and scattered ; in the rTMS group fewer nerve fibers were lost and the disposition of the remaining fibers was more fasciculated,concentrated and ordered than in the PD and srTMS groups.Conclusion rTMS may play a role in treating Parkinson's disease by protecting dopaminergic neurons as well as nigrostriate fibers and by improving the synthesis and transport of dopamine.
ABSTRACT
Objective To investigate the correlation between the expression of P-SAPK/JNK and neuronal apoptosis in the striatum during permanent middle cerebral artery occlusion (pMCAO) in rats.Methods Fifty-four male Sprague-Dawley rats were randomly divided into sham operation group and pMCAO 1-,3-,6-,12-,and 24-hour groups (n =9 in each group).Apoptotic neurons in the striatum during cerebral ischemia were detected by TUNEL assay,the nuclear translocation of P-SAPK/JNK in the striatum by immunohistochemical staining expressions of P-SAPK/JNK protein by Western blot.Results The numbers TUNEL- and P-SAPK/JNK-positive cells in the striatum at 1 hour after pMCAO increased significantly (P =0.000 1),and reached the peak at 6 hours.The numbers of TUNEL-positive cells decreased at 12 hours,however,it still higher than the sham operation group (P =0.000 2).Western blot analysis showed that the expression of P-SAPK/JNK after pMCAO increased significantly,and the time-course change was in accord with the result of immunohistochemical staining Neuronal apoptosis in the striatum was significantly positively correlated with the expression of P-SAPK/ JNK (r =0.984,P =0.000 4).Conclusions Cerebral ischemia may induce neuronal apoptosis in the striatum through the activation of P-SAPK/JNK.
ABSTRACT
Objective To explore the neural mechanism underlying the craving of heroin addicts induced by picture-cue and the correlation between the brain activation degree in nucleus accumbens (NAc)/the ventral striatum and the scores of patients' self-report craving. Methods Twelve active heroin addicts and 12 matched healthy controls underwent fMRI scan while viewing drug-related pictures and neutral pictures presented in a block design paradigm after anatomical scanning in GE 3.0 T scanner. The fMRI data were analyzed with SPM 5. The change of craving scores was tested by Wilcoxon signed rank test. The Pearson correlation between the activation of NAc/the ventral striatum and the heroin craving score was tested by SPSS 13.0. Results The craving scores of heroin addicts ranged from 0 to 3.70(median 0.15) before exposed to drug cue and 0 to 5.10(median 3.25) after viewing drug-related pictures and showed statistical significance(Z = -2.666, P < 0.05). There were 16 activated brain areas when heroin dependent patients exposed to visual drug-related cue vs. neutral visual stimuli. The activation brain regions belonged to two parts, one was limbic system (amygdale, hippocampus, putamen, anterior cingulate cortex and caudate), another was brain cortex (middle frontal cortex, inferior frontal cortex, precentral gyrus, middle temporal cortex, inferior temporal cortex, fusiform gyrus, precuneus and middle occipital gyrus). The MR signal activation magnitude of heroin addicts ranged from 0.19 to 3.50. The result displayed a significant positive correlation between the cue-induced fMRI activation in NAc/the ventral striatum and heroin craving severity (r=0.829, P < 0.05). Conclusion Heroin shared the same neural circuitry in part with other drugs of abuse for cue-induced craving, including brain reward circuitry, visualspatial attention circuit and working memory region. In addition, the dysfunction of NAc/the ventral striatum may attribute to heroin-related cue induced craving.
ABSTRACT
Because there are the fiber connections between striatum and substantia nigra, the striatal infarction may result in the secondary degeneration of the substantia nigra. In recent years, there have been a series of characteristics on secondary lesions of the substantia nigra, pathophysiological mechanisms, and the studies of how to detect the patients with striatal infarction in vivo. This article reviews the advances in this field.
ABSTRACT
@# Objective To study the oxidative stress and apoptosis relative protein expression in rat striatum during the pathogenesis of Parkinson's disease (PD) induced by 6-hydroxydopamine (6-OHDA). Methods 6-OHDA was stereotacticly injected into the right striatum of the rats at two sites to produce PD models. Activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), contents of reduced glutathione (GSH) and malondialdehyde (MDA) in the injured and normal striatum were measured using assay kits; and levels of Bax and Bcl-2 were detected by Western blotting in injured striatum. Results In 10 successful PD rats, compared with either the sham group or the normal group, activities of SOD and GSH-Px and contents of GSH in the right striatum significantly decreased while contents of MDA increased obviously (P<0.05); And levels of Bax significantly increased while expression of Bcl-2 obviously decreased. Conclusion Oxidative stress plays a key role in the pathogenesis of PD. Furthermore, Bax and Bcl-2 were involved in the regulation of apoptosis under oxidative stress induced by 6-OHDA.
ABSTRACT
Objective To examine whether the marginal division of the striatum(MrD)is involved in the associative learning and memory function of human brain with the help of functional magnetic resonance imaging(fMRI)technique.Methods Sixteen right-handed normal volunteers participated in a test of paired-word associative learning and memory,while the fMRI data were recorded.Control tasks were performed for the block-design.Statistcs parameter mapping 99 was used to analyze the data and to obtain the activated brain regions.Results When the threshold was set as P＜0.005.using a one-sample T-test,the left occipital lobe and the superior and middle gyrus of the left frontal lobe were activated remarkably during the encoding process of the paired-word associative learning and memory task,with the maximum intensity T value being 13.87 and 9.36.respectively.The left MrD was also obviously activated during this stage(T value was 5.46).But during the retrieval process,the left parietal lobe was prominently activated(T value was 8.73).Conclusion The resuhs of this study reveal that the subcortical structures such as MrD as well as the cerebral cortex are involved in the associative learning and memory of paired-word in human brain.
ABSTRACT
BACKGROUND: Overlapping clinical features of idiopathic Parkinson's disease (IPD) and multiple system atrophy (MSA) make it difficult to conduct an accurate differential diagnosis. We performed a quantitative F18- fluorodeoxyglucose PET (FDG PET) and measured the striatal and cerebellar glucose metabolism to evaluate the efficacy of a FDG PET study in the differential diagnosis between IPD and MSA. METHODS: This study included 19 patients with IPD, 28 patients with MSA (MSA-P : MSA-C = 19 : 9) and 12 age matched normal controls. A FDG PET study was performed in all subjects and the original PET image was corrected with the radioactivity curve obtained by repetitive sampling of the radial arterial blood. RESULTS: The measurements of striatal and cerebellar glucose metabolisms of the patients with MSA-P were significantly lower than those of the patients with IPD (P<0.001). However, the measurement of the caudate nucleus provided the most reliable clue for the differential diagnosis between IPD and MSA-P (sensitivity 94.7% and specificity 94.7%). In the patients with MSA-C, the glucose metabolism of the cerebellar vermis (P<0.001), cerebellar cortex (P<0.001) and putamen (P<0.05) was significantly lower than those of the patients with IPD. CONCLUSIONS: Quantitative FDG PET is a useful and reliable method in making a differential diagnosis between IPD and MSA.
Subject(s)
Humans , Caudate Nucleus , Cerebellar Cortex , Cerebellum , Corpus Striatum , Diagnosis, Differential , Fluorodeoxyglucose F18 , Glucose , Metabolism , Multiple System Atrophy , Parkinson Disease , Positron-Emission Tomography , Putamen , Radioactivity , Sensitivity and SpecificityABSTRACT
Objective To study the altered expression of dopamine transporter (DAT) in substantia nigra and striatum in postmortem human brain of Parkinson’s disease (PD). Methods Immunoautoradiography was used to reveal DAT distribution in postmortem human brain. Results Strongly labeling signal of DAT was mainly found in the substantia nigra, the putamen and the caudate nucleus in controls. In contrast, it was drastically reduced in the putmen and the dorsolateral caudate nuclus in PD brains, but the ventromedial part of the caudate nucleus showed a significant sparing adjacent to the border of the lateral ventricle. In the substantia nigra, the ventral and the lateral parts of the substantia nigra showed an obvious decreasing of DAT and the reducing degree of DAT labeling signals in those regions is smaller than that in the putamen and the caudate nucleus. Quantitative analysis revealed that 90.9% and 66.7% of the labeling intensity of DAT were decreased in the putamen and the caudate nucleus as comparing with the corresponding controls respectively (P
ABSTRACT
Objective:To study the dynamic distribution of BaP in the corpus striatum by r-counting and light microscopic autoradiography,then to explore the neurotoxic mechanism of BaP.Methods:100 SD male rats were divided into control group(n=40)and test group(n=60),experimental animals were given a single intravenous injection of 3.7?105 Bq/kg of 14CBaP while the same doses of Normal Saline were given to the control group.The rats were sacrificed at 1h,1 d,2 d,3 d and 7 d after the administration of radiolabelled BaP.During the experiment,some toxicological symptoms were observed and the ratios of brain-weight/body-weight were detected.Light microscopic autoradiography and r-counting were used to observe the dynamic distribution of BaP in the corpus striatum.Results:The change of toxicological symptoms are observed and the decrease ratios of brain-weight/body-weight are detected.R-counting shows that the percentage dose/g of 14CBaP in striatum is significant higher than in hippocampus and cortex at 1d and 2 d after administration.Light microscopic autoradiography shows that the silver granules in striatum reach the peak in 1d and sharp decrease in 2 d,which can be found even at 7d.Conclusion:BaP can penetrate the blood-brain barrier and distribute in corpus striatum,inducing CNS toxicity in SD rat.
ABSTRACT
OBJECTIVES: This study was undertaken to identify the effect of oxidative stress on the pathology of manganese intoxication through an analysis of manganese concentrations, superoxide dismutase (SOD) activities, malondialdehyde (MDA) concentrations, and the compositional changes of fatty acids from the corpus striatum of the rat brain. METHODS: Ten Sprague-Dawley rats were equally divided into two groups. Five rats in the experimental group were administered MnCl2 intraperitoneally for 4 weeks (4 mg/kg once daily, 5 days per week) and another five rats from the control group were given normal saline. Twenty-four hours after the last injection, the rats were decapitated and, the corpus striatum was isolated from the brain. RESULTS: In the corpus striatums of the experimental group, manganese concentrations increased significantly by 139 % (p<0.01). The SOD activities decreased significantly by 81 % (p<0.01) and the MDA concentrations increased significantly by 138 % (p<0.01) as compared to the control group. Among fatty acids, total n-6 polyunsaturated fatty acids (PUFAs) increased significantly by 325 % (p<0.01) as compared with the control group. Arachidonic acids (AA) increased by 341 % (p<0.01), and these increases were composed mostly of n-6 polyunsaturated fatty acids (PUFA). Among n-3 PUFAs, with the exception of linolenic acids, eicosapentanoic acid (EPA) decreased significantly by 72 % (p<0.05) and docosahexanoic acids (DHA) decreased by 67 % (p<0.05) as compared with the control group. CONCLUSIONS: Our results suggest that the oxygen free radicals produced by manganese may cause compositional changes of fatty acids in the corpus striatum of the rat brain. The characteristics of the fatty acids'compositional changes by manganese were a decrease of EPAs and DHAs (n-3 PUFAs), and an increase of AAs (n-6 PUFAs). These changes coupled with the decrease of SOD activity and the increase of MDA, suggest that manganese neurotoxicity is caused by lipid peroxidation mediated with oxygen free radicals, particularly superoxide radicals.
Subject(s)
Animals , Rats , alpha-Linolenic Acid , Arachidonic Acid , Arachidonic Acids , Brain , Corpus Striatum , Eicosapentaenoic Acid , Fatty Acids , Fatty Acids, Omega-3 , Fatty Acids, Unsaturated , Free Radicals , Linolenic Acids , Lipid Peroxidation , Malondialdehyde , Manganese , Oxidative Stress , Oxygen , Pathology , Rats, Sprague-Dawley , Superoxide Dismutase , SuperoxidesABSTRACT
Decreased number of the Neuropeptide-Y[NPY] immunoreactive neurons in the corpus striatum and primary motor cortex of aged rat was detected by the immunohistochemical method. The animals were categorized into control and aged group and we used 10 Sprague-Dawley rat weighing 250-300gm for control group. 10 Sprague-Dawley rat weighing over 600gm for aged group. The number of NPY-immunoreactive neurons in corpus striatum and primary motor cortex were counted under the light microscope and the following results were obtained. 1. The NPY-immunoreactive neurons were evenly distributed in corpus striatum and in the primaty motor cortex, the NPY-immunoreactive neurons were concentrated within the layer II, III and layer V, VI. The typical NPY-immunoreactive perikarya was multipolar shape. 2. Decreased number of NPY-immunoreactive neurons were detected in some areas of corpus striatum and primary mortor cortex of the aged rat. 3. Decrease of NPY-immunoreactive neurons were most prominent in the caudate-putamen and there were moderate decrease of NPY-immunoreactive neurons in the primary motor cortex, mild decrease of NPY-immunoreactive neurons in the nucleus accumbens but the NPY-immunoreactive neurons were not observed in the globus pallidus in both control and aged rat. NPY is supposed to act as a neurotransmitter of local circuit neurons in the striatum and may exert its potent vasoconstrictor effects on cerebral vessels which influences on the microcirculation of cerebral cortex and striatum. So our results seems to provide an important data on change of the function in the striatum and primary motor cortex of aged rat brain.
Subject(s)
Animals , Rats , Aging , Brain , Cerebral Cortex , Corpus Striatum , Globus Pallidus , Microcirculation , Motor Cortex , Neurons , Neuropeptide Y , Neuropeptides , Neurotransmitter Agents , Nucleus Accumbens , Rats, Sprague-DawleyABSTRACT
The ultrastructure of the excitotoxic lesion similar to that occurring in the degenerative neuronal disease was produceby stereotaxic injections of 1 nmol and 10 mnol of kainic acid nto the corpus striatum of adult rat brain There were rnarked swellings in the neuronal dendrites at injected sites. Neurotubules and neurofilarnents were disrupted as and amorphous materials and scattered throughout the interior of distended dendrites. Internal cristae and membranes of mitochondria were destroyed with the loss of integrity of intracellular organelles. Disruption of cellular and nuclear membranes occurered in severe cases. But there was no apparent pathologic change in the other structure, ie, synapses, presynaptic and postsynaptic parts, axons and glial cells. The synapses between dendrites and axon terminals were not destroyed despite of marked distension of dendrites. The local administration of excitatory amino acid into the brain caused the destruction of dendrites and neuronal cell bodies, but axons and axon terminals were intact With the lapse of time, axons and axon terminals from the destroyed neuron degenerate Therelore stereotaxic injection of excitatory amino acid into the brain may provldes a method of investigating neuronal connectivity.