Inhibition of Acetylcholinesterase Modulates NMDA Receptor Antagonist Mediated Alterations in the Developing Brain

Bendix, Ivo; Serdar, Meray; Herz, Josephine; Haefen, Clarissa von; Nasser, Fatme; Rohrer, Benjamin; Endesfelder, Stefanie; Felderhoff‐Mueser, Ursula; Spies, Claudia; Sifringer, Marco

doi:10.3390/ijms15033784

Cited by 4 publications

(6 citation statements)

References 69 publications

(71 reference statements)

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“…Similarly, a previous study showed that the enzymatic activity of MMP2 increased after treatment with the non-competitive NMDA receptor antagonist MK801 in newborn rats. 39 analysis in the latter study. 39 Taken together, the ketamine-induced laminin degradation observed in our study may be due to the enhanced activity of MMP9.…”

Section: Discussionmentioning

confidence: 60%

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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: Discussionmentioning

confidence: 60%

“…39 analysis in the latter study. 39 Taken together, the ketamine-induced laminin degradation observed in our study may be due to the enhanced activity of MMP9.…”

Section: Discussionmentioning

confidence: 60%

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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“…An important finding that gives support is that cells with increased AChE activity can easily switch to an apoptotic state by caspases cleavage [68]. Another important fact of its involvement with cellular death processes is that AChE inhibitors in pathological state slow down neurodegeneration by increasing BDNF levels [35]. In the present study, we found an increase in AChE activity and decrease of its immunocontent in cerebellum.…”

Section: Discussionmentioning

confidence: 68%

“…It has been shown that in the hippocampus, BDNF production is directly influenced by acetylcholine levels [33]. In this context, several studies have shown that acetylcholinesterase (AChE) inhibition increases BDNF levels by prolonging acetylcholine action on its receptors [34,35]. The crosstalk between the cholinergic system and BDNF production suggests an important role of the cholinergic system in cell survival [36].…”

Section: Introductionmentioning

confidence: 98%

D-Galactose Causes Motor Coordination Impairment, and Histological and Biochemical Changes in the Cerebellum of Rats

et al. 2016

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Classical galactosemia is an inborn error of carbohydrate metabolism in which patients accumulate high concentration of galactose in the brain. The most common treatment is a galactose-restricted diet. However, even treated patients develop several complications. One of the most common symptoms is motor coordination impairment, including affected gait, balance, and speech, as well as tremor and ataxia. In the present study, we investigated the effects of intracerebroventricular galactose administration on motor coordination, as well as on histological and biochemical parameters in cerebellum of adult rats. Wistar rats received 5 μL of galactose (4 mM) or saline by intracerebroventricular injection. The animals performed the beam walking test at 1 and 24 h after galactose administration. Histological and biochemical parameters were performed 24 h after the injections. The results showed motor coordination impairment at 24 h after galactose injection. Galactose also decreased the number of cells in the molecular and granular layers of the cerebellum. The immunohistochemistry results suggest that the cell types lost by galactose are neurons and astrocytes in the spinocerebellum and neurons in the cerebrocerebellum. Galactose increased active caspase-3 immunocontent and acetylcholinesterase activity, decreased acetylcholinesterase immunocontent, glutathione, and BDNF levels, as well as caused protein and DNA damage. Our results suggest that galactose induces histological and biochemical changes in cerebellum, which can be associated with motor coordination impairment.

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“…Many previous studies have reported that BDNF may confer protective effects against various neurotoxic conditions in the brain, via reduction of the AChE levels or activity [64–66]. In addition, emerging evidence suggests that regulation of AChE activity by BDNF is related to hippocampal neurogenesis [61, 67–69]. For example, huperzine A, an AChE inhibitor, increases BDNF mRNA and protein levels, while cholinergic denervation or muscarinic antagonist treatment, such as atropine, decreases the hippocampal BDNF mRNA levels [70].…”

Section: Discussionmentioning

confidence: 99%

Essential oils from two Allium species exert effects on cell proliferation and neuroblast differentiation in the mouse dentate gyrus by modulating brain-derived neurotrophic factor and acetylcholinesterase

Jung

Lee

Yoo

et al. 2016

BMC Complement Altern Med

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BackgroundIn the present study, we investigated the effects of oil products from two Allium species: Allium sativum (garlic) and Allium hookeri (Chinese chives) on cell proliferation and neuroblast differentiation in the mouse dentate gyrus.MethodsUsing corn oil as a vehicle, the essential oil from garlic (10 ml/kg), or Chinese chives (10 ml/kg) was administered orally to 9-week-old mice once a day for 3 weeks. One hour following the last treatment, a novel object recognition test was conducted and the animals were killed 2 h after the test.ResultsIn comparison to the vehicle-treated group, garlic essential oil (GO) treatment resulted in significantly increased exploration time and discrimination index during the novel object recognition test, while Chinese chives essential oil (CO) reduced the exploration time and discrimination index in the same test. In addition, the number of Ki67-immunoreactive proliferating cells and doublecortin-immunoreactive neuroblasts significantly increased in the dentate gyrus of GO-treated animals. However, administration of CO significantly decreased cell proliferation and neuroblast differentiation. Administration of GO significantly increased brain-derived neurotrophic factor (BDNF) levels and decreased acetylcholinesterase (AChE) activity in the hippocampal homogenates. In contrast, administration of CO decreased BDNF protein levels and had no significant effect on AChE activity, compared to that in the vehicle-treated group.ConclusionsThese results suggest that GO significantly improves novel object recognition as well as increases cell proliferation and neuroblast differentiation, by modulating hippocampal BDNF protein levels and AChE activity, while CO impairs novel object recognition and decreases cell proliferation and neuroblast differentiation, by reducing BDNF protein levels in the hippocampus.

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Inhibition of Acetylcholinesterase Modulates NMDA Receptor Antagonist Mediated Alterations in the Developing Brain

Cited by 4 publications

References 69 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

D-Galactose Causes Motor Coordination Impairment, and Histological and Biochemical Changes in the Cerebellum of Rats

Essential oils from two Allium species exert effects on cell proliferation and neuroblast differentiation in the mouse dentate gyrus by modulating brain-derived neurotrophic factor and acetylcholinesterase

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