scholarly journals Role of γ-aminobutyric acid B (GABAB) receptors in the regulation of kainic acid-induced cell death in mouse hippocampus

2005 ◽  
Vol 37 (6) ◽  
pp. 533-545 ◽  
Author(s):  
Han-Kyu Lee ◽  
Young-Jun Seo ◽  
Seong-Soo Choi ◽  
Min-Soo Kwon ◽  
Eon-Jeong Shim ◽  
...  
Keyword(s):  
Cell Death ◽  
Kainic Acid ◽  
Gabab Receptors ◽  
Aminobutyric Acid ◽  
Mouse Hippocampus

scholarly journals Bark Constituents from Mushroom-detoxifiedRhus vernicifluaSuppress Kainic Acid-induced Neuronal Cell Death in Mouse Hippocampus

2010 ◽  
Vol 14 (5) ◽  
pp. 279 ◽  
Author(s):  
Jong-Seon Byun ◽  
Yoon Hee Han ◽  
Sung-Jun Hong ◽  
Sung-Mi Hwang ◽  
Yong-Soo Kwon ◽  
...  
Keyword(s):  
Cell Death ◽  
Kainic Acid ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Mouse Hippocampus

scholarly journals Role of microglial IKKβ in kainic acid-induced hippocampal neuronal cell death

Brain ◽  
2008 ◽  
Vol 131 (11) ◽  
pp. 3019-3033 ◽  
Author(s):  
Ik-Hyun Cho ◽  
Jinpyo Hong ◽  
Eun Cheng Suh ◽  
Jae Hwan Kim ◽  
Hyunkyoung Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Kainic Acid ◽  
Neuronal Cell Death ◽  
Neuronal Cell

scholarly journals Glycyrrhizin Attenuates Kainic Acid-Induced Neuronal Cell Death in the Mouse Hippocampus

2013 ◽  
Vol 22 (2) ◽  
pp. 107-115 ◽  
Author(s):  
Lidan Luo ◽  
Yinchuan Jin ◽  
Il-Doo Kim ◽  
Ja-Kyeong Lee
Keyword(s):  
Cell Death ◽  
Kainic Acid ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Mouse Hippocampus

Role of nicotinic acetylcholine receptors in the regulation of kainic acid-induced hippocampal cell death in mice

2004 ◽  
Vol 64 (4) ◽  
pp. 309-317 ◽  
Author(s):  
Han-Kyu Lee ◽  
Seong-Soo Choi ◽  
Eun-Jung Han ◽  
Jin-Young Lee ◽  
Min-Soo Kwon ◽  
...  
Keyword(s):  
Cell Death ◽  
Kainic Acid ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Nicotinic Acetylcholine ◽  
Hippocampal Cell

Ethyl pyruvate attenuates kainic acid-induced neuronal cell death in the mouse hippocampus

2006 ◽  
Vol 84 (7) ◽  
pp. 1505-1511 ◽  
Author(s):  
Ik-Hyun Cho ◽  
Seung-Woo Kim ◽  
Jung-Bin Kim ◽  
Tae-Kyung Kim ◽  
Kang-Woo Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Kainic Acid ◽  
Ethyl Pyruvate ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Mouse Hippocampus

scholarly journals Sex difference in the contribution of GABAB receptors to tibial neuromodulation of bladder overactivity in cats

2017 ◽  
Vol 312 (3) ◽  
pp. R292-R300 ◽  
Author(s):  
Thomas W. Fuller ◽  
Xuewen Jiang ◽  
Utsav Bansal ◽  
Vladimir Lamm ◽  
Bing Shen ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Sex Difference ◽  
Pudendal Nerve ◽  
Bladder Capacity ◽  
Gabab Receptors ◽  
Aminobutyric Acid ◽  
Intravesical Administration ◽  
Subtype B ◽  
Pudendal Neuromodulation

This study investigated the role of γ-aminobutyric acid subtype B (GABAB) receptors in tibial and pudendal neuromodulation of bladder overactivity induced by intravesical administration of dilute (0.5%) acetic acid (AA) in α-chloralose-anesthetized cats. To inhibit bladder overactivity, tibial or pudendal nerve stimulation (TNS or PNS) was applied at 5 Hz and two or four times threshold (T) intensity for inducing toe or anal sphincter twitch. TNS at 2T or 4T intensity significantly ( P < 0.05) increased the bladder capacity to 173.8 ± 16.2 or 198.5 ± 24.1%, respectively, of control capacity. Meanwhile, PNS at 2T or 4T intensity significantly ( P < 0.05) increased the bladder capacity to 217 ± 18.8 and 221.3 ± 22.3% of control capacity, respectively. CGP52432 (a GABAB receptor antagonist) at intravenous dosages of 0.1–1 mg/kg completely removed the TNS inhibition in female cats but had no effect in male cats. CGP52432 administered intravenously also had no effect on control bladder capacity or the pudendal inhibition of bladder overactivity. These results reveal a sex difference in the role of GABAB receptors in tibial neuromodulation of bladder overactivity in cats and that GABAB receptors are not involved in either pudendal neuromodulation or irritation-induced bladder overactivity.

scholarly journals Lymphocytes Protect Cortical Neurons Against Excitotoxicity Mediated by Kainic Acid, an in vitro Model for Neurodegeneration

2015 ◽  
Vol 11 (2) ◽  
pp. 132-138 ◽  
Author(s):  
R Shrestha ◽  
O Millington ◽  
J Brewer ◽  
T Bushell
Keyword(s):  
T Cells ◽  
Cell Death ◽  
Kainic Acid ◽  
Cortical Neurons ◽  
In Vitro Model ◽  
Harmful Effect ◽  
Activated T Cells ◽  
Vitro Model

Background Neurodegenerative disease is a progressive loss of neurons from the central nervous system (CNS). Various conditions have been implicated for such conditions including ageing, inflammation, stress and genetic predisposition. Recently, studies have linked neurodegeneration with inflammation. Some studies have suggested the harmful effect of immune response while others have argued its neuroprotective role in neurodegeneration of the CNS. However, the precise role of inflammation and immune cells in such condition is still not clear. Objective To investigate the role of lymphocytes in neurodegeneration of the CNS and determine the underlying mechanism. Method We have used 4-7 days old mouse pups (C57Bl6) to prepare organotypic slice cultures which were cultured for 13-15 days prior to experiment. To induced cell death kainic acid was used and considered as an in vitro model for neurodegeneration. Lymphocytes were obtained from peripheral lymph nodes of 5-10 weeks old adult mouse which were used in the current study. Propidium iodide was used as a fluorescent dye to determine cell death in brain slice cultures. Result Lymphocytes do not induce cell death in slice cultures in the absence of any toxic insult whereas, after applying toxic insult to the slice cultures using kainic acid, lymphocytes show neuroprotection against such insult. Similarly, purified non-activated and purified activated T cells along with T cells depleted lymphocyte preparation also exhibit neuroprotection against kainic acid-induced cell death. We further, have demonstrated that the observed neuroprotection is contact-independent and soluble mediators released from lymphocytes are responsible for the observed neuroprotection. Moreover, our study has revealed that soluble mediators exhibiting neuroprotection act via astrocytes. Conclusion Lymphocyte preparations are neuroprotective and the observed neuroprotection is contact-independent. Soluble mediators released from lymphocytes are responsible for the observed neuroprotection. DOI: http://dx.doi.org/10.3126/kumj.v11i2.12488 Kathmandu University Medical Journal Vol.11(2) 2013: 132-138

scholarly journals Fcγ receptors contribute to pyramidal cell death in the mouse hippocampus following local kainic acid injection

Neuroscience ◽  
2010 ◽  
Vol 166 (3) ◽  
pp. 819-831 ◽  
Author(s):  
S. Suemitsu ◽  
M. Watanabe ◽  
E. Yokobayashi ◽  
S. Usui ◽  
T. Ishikawa ◽  
...  
Keyword(s):  
Cell Death ◽  
Kainic Acid ◽  
Pyramidal Cell ◽  
Fcγ Receptors ◽  
Acid Injection ◽  
Mouse Hippocampus ◽  
Kainic Acid Injection

Fluoxetine attenuates kainic acid-induced neuronal cell death in the mouse hippocampus

2009 ◽  
Vol 1281 ◽  
pp. 108-116 ◽  
Author(s):  
Yinchuan Jin ◽  
Chae-Moon Lim ◽  
Seung-Woo Kim ◽  
Ju-Young Park ◽  
Ji-Seon Seo ◽  
...  
Keyword(s):  
Cell Death ◽  
Kainic Acid ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Mouse Hippocampus
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