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1.
Neuroscience Bulletin ; (6): 992-1006, 2018.
Article in English | WPRIM | ID: wpr-775482

ABSTRACT

Inhibitory GABAergic interneurons are fundamental elements of cortical circuits and play critical roles in shaping network activity. Dysfunction of interneurons can lead to various brain disorders, including epilepsy, schizophrenia, and anxiety. Based on the electrophysiological properties, cell morphology, and molecular identity, interneurons could be classified into various subgroups. In this study, we investigated the density and laminar distribution of different interneuron types and the co-expression of molecular markers in epileptic human cortex. We found that parvalbumin (PV) and somatostatin (SST) neurons were distributed in all cortical layers except layer I, while tyrosine hydroxylase (TH) and neuropeptide Y (NPY) were abundant in the deep layers and white matter. Cholecystokinin (CCK) neurons showed a high density in layers IV and VI. Neurons with these markers constituted ~7.2% (PV), 2.6% (SST), 0.5% (TH), 0.5% (NPY), and 4.4% (CCK) of the gray-matter neuron population. Double- and triple-labeling revealed that NPY neurons were also SST-immunoreactive (97.7%), and TH neurons were more likely to express SST (34.2%) than PV (14.6%). A subpopulation of CCK neurons (28.0%) also expressed PV, but none contained SST. Together, these results revealed the density and distribution patterns of different interneuron populations and the overlap between molecular markers in epileptic human cortex.


Subject(s)
Adolescent , Adult , Child , Female , Humans , Male , Middle Aged , Young Adult , Brain Chemistry , Genetics , Physiology , Cerebral Cortex , Metabolism , Pathology , Cholecystokinin , Metabolism , Epilepsy , Pathology , Gene Expression Regulation , Physiology , Interneurons , Metabolism , Neuropeptide Y , Metabolism , Parvalbumins , Metabolism , Phosphopyruvate Hydratase , Metabolism , Somatostatin , Metabolism , Tyrosine 3-Monooxygenase , Metabolism
2.
Chinese Journal of Applied Clinical Pediatrics ; (24): 1820-1822, 2018.
Article in Chinese | WPRIM | ID: wpr-733345

ABSTRACT

Objective To evaluate the effect of vagus nerve stimulation (VNS)on post-encephalitic intrac-table epilepsy and the improvement of postoperative cognitive function and quality of life.Methods The patients with post-encephalitic epilepsy in Sanbo Brain Hospital,Capital Medical University from January 2008 to December 2016 were selected.A single center and retrospective study method was used to evaluate the cognitive function,social function of preoperative and postoperative and postoperative seizure classification.The follow-up time points included preopera-tive,posto-perative in 6 months,1 year after operation and postoperative annual review.Results A total of 43 patients were followed up,including 19 females and 24 males,with an average age of (9.37 ± 4.18)years old.The time of fol-low-up was (43.90 ± 33.04)months.According to Engel classification:GradeⅠ3 cases (7.0%),gradeⅡ3 ca-ses (7. 0%),grade Ⅲ14 cases (32.6%),grade Ⅳ21 cases (48.8%).According to McHugh classification:GradeⅠ8 cases (18.6%),grade Ⅱ12 cases (28%),gradeⅢ11 cases (25.5%),gradeⅣ6 cases (14.0%),gradeⅤ4 cases (9.3%).Speech improvement of postoperative:significant improvement in 3 cases (7.0%),slightly improved in 17 cases (39.6%);interpersonal communication improvement of postoperative:significantly increased 7 cases (16. 4%), slightly improved 16 cases(37.2%);learning/working ability improvement of postoperative:significantly improved 6 cases (14. 0%),slightly increased 14 cases(32. 6%).The postoperative VIQ (6.21 ±5.02)scores,PIQ (7.28 ±6.10)scores,FIQ (2.93 ±3.74)scores and MQ were (4.81 ± 2.98)scores higher than preoperative.Conclusions VNS can effectively im-prove the seizures of post-encephalitic epilepsy as well as the children's quality of life,cognition and social function.

3.
Chinese Journal of Pathophysiology ; (12): 1505-1509, 2015.
Article in Chinese | WPRIM | ID: wpr-477239

ABSTRACT

AIM:TostudythefunctionofmicroRNA(miR)-19aandmiR-92abyseed-targetinginhibitionin multiple myeloma cells and their signal pathways .METHODS:The experiments were divided into t-antimiR-19a group, t-antimiR-92a group, scramble control group and blank control group .The growth-inhibitory potencies were measured by MTT assay.The ability of cell colony formation was measured by cell colony formation assay .The ability of cell invasion was measured by Transwell experiment .The miR-19a and miR-92a target gene signal pathways were integrated by miRFo-cus software.RESULTS:MTT assay showed that t-antimiR-19a and t-antimiR-92a significantly inhibited the viability of multiple myeloma cells , and the best concentration and time were 0.5μmol/L and 48 h, respectively .The colony number in t-antimiR-19a/92a group was less than that in scramble control group .The transfection with t-antimiR-19a or t-antimiR-92a effectively decreased the cell invasion , as the relative invasion cell number was significantly decreased compared with scramble control group.miR-19a and miR-92a were involved in mTOR signaling, cell cycle and other cancer pathways . CONCLUSION:miR-19a and miR-92a cluster might be a potential target for therapeutic intervention in multiple myelo-ma.

4.
Chinese Pharmacological Bulletin ; (12)1987.
Article in Chinese | WPRIM | ID: wpr-552601

ABSTRACT

AIM To observe effects of IBMX on cGMP and GFAP production in gerbil hippocampus after recirculation following ischemia. METHODS Bilateral occlusion of common carotid arteries and immunofluorescent stain methods in gerbil hippocampal tissue slice were used. RESULTS Recirculation following ischemia leads to a rise in hippocampus cGMP and GFAP concentration. cGMP and GFAP positive cells mainly distributed in rediatum layer and molecular layer in the CA 1 subfield, Most of cGMP positive cells are astrocytes under double immunofluorescent stain. Most of cGMP strong positive cells are also those of GFAP strong positive cells. IBMX increased cGMP and GFAP production. CONCLUSION cGMP is possible to play an important role in the activation or regulation of GFAP in the hippocampus.

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