Nicotinic Acetylcholine Receptors are Associated with Ketamine-induced Neuronal Apoptosis in the Developing Rat Retina

Gao, Li; Han, Junde; Bai, Jie; Dong, Jing; Zhang, Sen; Zhang, Mazhong; Zheng, Jijian

doi:10.1016/j.neuroscience.2018.01.057

Cited by 6 publications

(3 citation statements)

References 37 publications

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“…Immunohistochemistry was performed according to experimental methods described previously. 6,9 After drug treatment, the retinas were dissected from the eyeballs in an ice-cold bath of ACSF and fixed in 4% paraformaldehyde for 24 hours. The fixed retinas were then incubated with ethanol and xylene, after which they were infiltrated with paraffin.…”

Section: Immunohistochemistrymentioning

confidence: 99%

“…7,8 General anesthetics promote central nervous system inhibition via activation of the gamma-aminobutyric acid type A receptor (GABAA-R) and/or blockade of the N-methyl-D-aspartic acid receptor (NMDAR). 9 During early neuronal development, both GABAA-R activation and long-term NMDAR blockade can cause intracellular calcium disturbances and neuronal apoptosis. 8,10 In addition to these effects caused by the receptors, general anesthesia may also induce neuronal apoptosis by influencing the extracellular environment including brain-derived neurotrophic factor, inflammatory mediators, cell-extracellular matrix (ECM), etc [11][12][13] During early postnatal development, the ECM plays crucial roles in proliferation, migration, and differentiation of neural cells and form loose ECM fiber-like structures, which occurs in parallel with synaptic development.…”

Section: Introductionmentioning

confidence: 99%

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Laminin degradation by matrix metalloproteinase 9 promotes ketamine‐induced neuronal apoptosis in the early developing rat retina

Zhang

Sun

et al. 2020

CNS Neurosci Ther

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Aims During early development, laminin degradation contributes to the death of neurons. This study aims to investigate the role and regulation of laminin in ketamine‐induced apoptosis. Methods We performed terminal deoxynucleotidyl transferase biotin‐dUTP nick end labeling (TUNEL) and immunohistochemical assays to investigate the roles of the non‐integrin laminin receptor, matrix metalloproteinase 9 (MMP9) in ketamine‐induced neuronal apoptosis. In situ zymography, Western blot, and immunofluorescence were used to explore the relationships between laminin, MMP9 activity, and Zn2+. Experiments were performed using whole‐mount retinas dissected from Sprague Dawley rats. Results The TUNEL and immunohistochemical assays indicated that ketamine‐induced neuronal apoptosis in early developing rat retina. Blockade of non‐integrin laminin receptor promoted ketamine‐induced apoptosis, while non‐integrin laminin receptor activation attenuated ketamine‐induced apoptosis. Ketamine‐induced laminin degradation, possibly by enhancing the activity of MMP9. MMP9 inhibition reduced ketamine‐induced apoptosis by reducing laminin degradation. Downregulation of Zn2+ attenuated the increased MMP9 activity, laminin degradation caused by ketamine and significantly reduced ketamine‐induced neuronal apoptosis. Conclusion Laminin degradation by MMP9 promoted ketamine‐induced neuronal apoptosis in early developing rat retina. The non‐integrin laminin receptor may be a pathway involved in ketamine‐induced apoptosis. Zn2+ downregulation may play a protective role against ketamine‐induced neuronal apoptosis through inhibiting MMP9 activity.

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Section: Immunohistochemistrymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Laminin degradation by matrix metalloproteinase 9 promotes ketamine‐induced neuronal apoptosis in the early developing rat retina

Zhang

Sun

et al. 2020

CNS Neurosci Ther

Self Cite

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“…Although the precise mechanism of general anesthesiainduced neurotoxicity during the early development is unclear, neuronal apoptosis is one of the most basic characteristic induced by general anesthetics through impairing neurotrophy signaling, blockade of synchronized network activity, neuroinflammation and remodeling of the extracellular matrix (ECM) [4,[10][11][12][13][14][15], etc. As one of the most commonly used general anesthetics in children before, our previous study demonstrated that ketamine aggravated neuronal apoptosis by MMP9 upregulation and ECM degradation during the early development of rat retina.…”

Section: Introductionmentioning

confidence: 99%

Albumin alleviated esketamine-induced neuronal apoptosis of rat retina through downregulation of Zn2+-dependent matrix metalloproteinase 9 during the early development

Zhang

Feng

et al. 2022

BMC Neurosci

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Aims Esketamine upregulates Zn2+-dependent matrix metalloproteinase 9 (MMP9) and increases the neuronal apoptosis in retinal ganglion cell layer during the early development. We aimed to test whether albumin can alleviate esketamine-induced apoptosis through downregulating Zn2+-dependent MMP9. Methods We investigate the role of Zn2+ in esketamine-induced neuronal apoptosis by immunofluorescence. MMP9 protein expression and enzyme activity were investigated by zymography in situ., western blot and immunofluorescence. Whole-mount retinas from P7 Sprague-Dawley rats were used. Results We demonstrated that esketamine exposure increased Zn2+ in the retinal GCL during the early development. Zn2+-dependent MMP9 expression and enzyme activity up-regulated, which eventually aggravated apoptosis. Albumin effectively down-regulated MMP9 expression and activity via binding of free zinc, ultimately protected neurons from apoptosis. Meanwhile albumin treatment promoted activated microglia into multi-nucleated macrophagocytes and decreased the inflammation. Conclusion Albumin alleviates esketamine-induced neuronal apoptosis through decreasing Zn2+ accumulation in GCL and downregulating Zn2+-dependent MMP9.

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Transcriptome analysis provides insights into the function of the cholinergic system in pearl oyster transplantation immunity

et al. 2021

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Nicotinic Acetylcholine Receptors are Associated with Ketamine-induced Neuronal Apoptosis in the Developing Rat Retina

Cited by 6 publications

References 37 publications

Laminin degradation by matrix metalloproteinase 9 promotes ketamine‐induced neuronal apoptosis in the early developing rat retina

Laminin degradation by matrix metalloproteinase 9 promotes ketamine‐induced neuronal apoptosis in the early developing rat retina

Albumin alleviated esketamine-induced neuronal apoptosis of rat retina through downregulation of Zn2+-dependent matrix metalloproteinase 9 during the early development

Transcriptome analysis provides insights into the function of the cholinergic system in pearl oyster transplantation immunity

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