scholarly journals Disruption of Hippocampal Neuregulin 1–ErbB4 Signaling Contributes to the Hippocampus-dependent Cognitive Impairment Induced by Isoflurane in Aged Mice

2014 ◽  
Vol 121 (1) ◽  
pp. 79-88 ◽  
Author(s):  
Xiao-Min Li ◽  
Fan Su ◽  
Mu-Huo Ji ◽  
Guang-Fen Zhang ◽  
Li-Li Qiu ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Enzyme Linked Immunosorbent Assay ◽  
Acid Decarboxylase ◽  
Neuregulin 1 ◽  
Aged Mice ◽  
Vehicle Injection ◽  
To Receive ◽  
The Brain

Abstract Background: A prolonged isoflurane exposure may lead to cognitive decline in rodents. Neuregulin 1 (NRG1)–ErbB4 signaling plays a key role in the modulation of hippocampal synaptic plasticity through regulating the neurotransmission. The authors hypothesized that hippocampal NRG1–ErbB4 signaling is involved in isoflurane-induced cognitive impairments in aged mice. Methods: Fourteen-month-old C57BL/6 mice were randomized to receive 100% O2 exposure, vehicle injection after 100% O2 exposure, vehicle injection after exposure to isoflurane carried by 100% O2, NRG1-β1 injection after exposure to isoflurane carried by 100% O2, and NRG1-β1 and an ErbB4 inhibitor AG1478 injection after exposure to isoflurane carried by 100% O2. Fear conditioning test was used to assess the cognitive function of mice 48-h postexposure. The brain tissues were harvested 48-h postexposure to determine the levels of NRG1, ErbB4, p-ErbB4, parvalbumin, and glutamic acid decarboxylase 67 in the hippocampus using Western blotting, enzyme-linked immunosorbent assay, and immunofluorescence. Results: The percentage of freezing time to context was decreased from 50.28 ± 11.53% to 30.82 ± 10.00%, and the hippocampal levels of NRG1, p-ErbB4/ErbB4, parvalbumin, and glutamic acid decarboxylase 67 were decreased from 172.79 ± 20.85 ng/g, 69.15 ± 12.20%, 101.68 ± 11.21%, and 104.71 ± 6.85% to 112.92 ± 16.65 ng/g, 42.26 ± 9.71%, 75.89 ± 10.26%, and 73.87 ± 16.89%, respectively, after isoflurane exposure. NRG1-β1 attenuated the isoflurane-induced hippocampus-dependent cognitive impairment and the declines in the hippocampal NRG1, p-ErbB4/ErbB4, parvalbumin, and glutamic acid decarboxylase 67. AG1478 inhibited the rescuing effects of NRG1-β1. Conclusion: Disruption of NRG1–ErbB4 signaling in the parvalbumin-positive interneurons might, at least partially, contribute to the isoflurane-induced hippocampus-dependent cognitive impairment after exposure to isoflurane carried by 100% O2 in aged mice.

scholarly journals Comparison of Measurements of Autoantibodies to Glutamic Acid Decarboxylase and Islet Antigen-2 in Whole Blood Eluates from Dried Blood Spots Using the RSR-Enzyme Linked Immunosorbent Assay Kits and In-House Radioimmunoassays

2010 ◽  
Vol 2010 ◽  
pp. 1-6 ◽  
Author(s):  
Anders Persson ◽  
Charlotte Becker ◽  
Ida Hansson ◽  
Anita Nilsson ◽  
Carina Törn
Keyword(s):  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Dried Blood Spots ◽  
Enzyme Linked Immunosorbent Assay ◽  
Acid Decarboxylase ◽  
Blood Spots ◽  
And Control ◽  
Islet Antigen ◽  
Prozone Effect

To evaluate the performance of dried blood spots (DBSs) with subsequent analyses of glutamic acid decarboxylase (GADA) and islet antigen-2 (IA-2A) with the RSR-ELISAs, we selected 80 children newly diagnosed with type 1 diabetes and 120 healthy women. DBSs from patients and controls were used for RSR-ELISAs while patients samples were analysed also with in-house RIAs. The RSR-ELISA-GADA performed well with a specificity of 100%, albeit sensitivity (46%) was lower compared to in RIA (56%;P=.008). No prozone effect was observed after dilution of discrepant samples. RSR-ELISA-IA-2A achieved specificity of 69% and sensitivity was lower (59%) compared with RIA (66%;P<.001). Negative or low positive patients and control samples in the RSR-ELISA-IA-2A increased after dilution. Eluates from DBS can readily be used to analyse GADA with the RSR-ELISA, even if low levels of autoantibodies were not detected. Some factor could disturb RSR-ELISA-IA-2A analyses.

scholarly journals GAB Aergic Innervation in Cerebral Blood Vessels: An Immunohistochemical Demonstration of L-Glutamic Acid Decarboxylase and GABA Transaminase

1991 ◽  
Vol 11 (1) ◽  
pp. 129-134 ◽  
Author(s):  
H. Imai ◽  
T. Okuno ◽  
J. Y. Wu ◽  
T. J-F. Lee
Keyword(s):  
Glutamic Acid ◽  
Glutamic Acid Decarboxylase ◽  
Cerebral Arteries ◽  
Immunohistochemical Method ◽  
Acid Decarboxylase ◽  
Cerebral Blood Vessels ◽  
Gaba Transaminase ◽  
Adjacent Part ◽  
Adventitial Layer ◽  
To Receive

The presence of GAB Aergic innervation in cerebral arteries of several species was investigated by an immunohistochemical method using antibodies against glutamic acid decarboxylase (GAD) and GABA transaminase (GABA-T). Both GAD and GABA-T immunoreactivities were found to be associated with large bundles and single fibers in the adventitial layer of arteries examined. The density and distribution pattern of both GAD-and GABA-T-immunoreactive fibers were found to be comparable at most regions examined. Both fibers were found to be most dense in the anterior cerebral artery and its adjacent part of the circle of Willis. Several peripheral arteries were found to receive very sparse or no GAD-and GABA-T-immunoreactive fibers. Superior cervical ganglionectomy did not appreciably affect the distribution of both fibers. Cold-storage denervation, however, resulted in a drastic decrease in both fibers. At ultrastructural levels, both GAD- and GABA-T-immunoreactive nerve profiles were found to be very close to the smooth muscle cells. These results demonstrate the presence of a potentially functional GAB Aergic innervation in cerebral circulation. On few occasions, GAD immunoreactivities were also found in some endothelial cells, suggesting that a nonneuronal GABA system may also be present in cerebral arteries.

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