Long-term administration of scopolamine interferes with nerve cell proliferation, differentiation and migration in adult mouse hippocampal dentate gyrus, but it does not induce cell death

Yan, Bing Chun; Park, Joon Ha; Chen, Bai Hui; Cho, Jeong‐Hwi; Kim, In Hye; Ahn, Ji Hyeon; Lee, Jae Chul; Hwang, In Koo; Cho, Jun Hwi; Lee, Yun Lyul; Kang, Il‐Jun; Won, Moo‐Ho

doi:10.4103/1673-5374.143415

Cited by 13 publications

(11 citation statements)

References 37 publications

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“…In addition, F-J B-positive cells, which are damaged cells, were not observed in any regions of the scopolamine-treated mice. This result was consistent with the results of previous studies ( 10 , 33 ). These findings indicated that treatment with scopolamine did not evoke neuronal death in the hippocampus.…”

Section: Resultssupporting

confidence: 94%

“…The results of the present study demonstrated that no neuronal loss was present in the mouse hippocampus following treatment with scopolamine for 4 weeks via NeuN immunohistochemistry and F-J B histofluorescence, proven histological methods for the examination of neuronal death or loss in the brain. Recently, it was reported that chronic treatment with scopolamine induced a significant reduction in neurogenesis of the hippocampal dentate gyrus in mice, closely associated with hippocampus-dependent learning and memory, without loss of neurons in the mouse dentate gyrus ( 33 ). This previous result indicated that chronic systemic treatment with scopolamine may induce cognitive deficits without neuronal loss in the mouse hippocampus.…”

Section: Discussionmentioning

confidence: 99%

“…Animals (n=70/group) were intraperitoneally injected with 1 mg/kg scopolamine (Sigma-Aldrich; Merck KGaA, Darmstadt, Germany) once daily for 4 weeks. The scopolamine dose was selected based on previously published studies ( 32 , 33 ). Scopolamine-treated animals were simultaneously administered 40 mg/kg vanillin (Sigma-Aldrich; Merck KGaA), which was suspended in 1 ml 10% Tween-80 solution.…”

Section: Methodsmentioning

confidence: 99%

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Vanillin improves scopolamine‑induced memory impairment through restoration of ID1 expression in the mouse hippocampus

et al. 2018

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4-Hydroxy-3-methoxybenzaldehyde (vanillin), contained in a number of species of plant, has been reported to display beneficial effects against brain injuries. In the present study, the impact of vanillin on scopolamine-induced alterations in cognition and the expression of DNA binding protein inhibitor ID-1 (ID1), one of the inhibitors of DNA binding/differentiation proteins that regulate gene transcription, in the mouse hippocampus. Mice were treated with 1 mg/kg scopolamine with or without 40 mg/kg vanillin once daily for 4 weeks. Scopolamine-induced cognitive impairment was observed from 1 week and was deemed to be severe 4 weeks following the administration of scopolamine. However, treatment with vanillin in scopolamine-treated mice markedly attenuated cognitive impairment 4 weeks following treatment with scopolamine. ID1-immunoreactive cells were revealed in the hippocampus of vehicle-treated mice, and were hardly detected 4 weeks following treatment with scopolamine. However, treatment with vanillin in scopolamine-treated mice markedly restored ID1-immunoreactive cells and expression 4 weeks subsequent to treatment. The results of the present study suggested that vanillin may be beneficial for cognitive impairment, by preventing the reduction of ID1 expression which may be associated with cognitive impairment.

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Section: Resultssupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Vanillin improves scopolamine‑induced memory impairment through restoration of ID1 expression in the mouse hippocampus

et al. 2018

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“…Structures immunoreactive for NeuN, GFAP, Iba-1, PECAM-1, and/or ZO-1 were increased × 20 * 10 for analysis and the figure of the NeuN immunohistochemistry was by enlarged × 4 * 10. The staining intensities of the structures immunoreactive for GFAP, Iba-1, PECAM-1, and ZO-1 were evaluated using OD, as described above ( 34 ).…”

Section: Methodsmentioning

confidence: 99%

Changes in the Blood-Brain Barrier Function Are Associated With Hippocampal Neuron Death in a Kainic Acid Mouse Model of Epilepsy

Yan

Gao

et al. 2018

Front. Neurol.

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The kainic acid (KA)-induced epilepsy experimental model is widely used to study the mechanisms underlying this disorder. Recently, the blood-brain barrier (BBB) has become an innovative alternative treatment target for epilepsy patients. KA causes neuronal injury and BBB damage in this experimental epilepsy model but the mechanisms underlying epilepsy-related neuronal injury, autophagy, and BBB damage remain unclear. Therefore, the present study investigated the relationships among neuronal injury, the expressions of autophagy-related proteins, and changes in BBB-related proteins during the acute phase of epilepsy to further understand the mechanisms and pharmacotherapy of epilepsy. NeuN immunohistochemistry and Fluoro-Jade B (FJ-B) staining in the hippocampal CA3 region revealed that neuronal death induced by intraventricular injections of 10 μg/kg KA was greater than that induced by 3 μg/kg KA. In addition, there were transient increases in the levels of microtubule-associated protein light chain 3-II (LC3I/II) and Beclin-1, which are autophagy-related proteins involved in neuronal death, in this region 24 h after the administration of 10 μg/kg KA. There were also morphological changes in BBB-related cells such as astrocytes, endothelial cells (ECs), and tight junctions (TJs). More specifically, there was a significant increase in the activation of astrocytes 72 h after the administration of 10 μg/kg KA as well as continuous increases in the expressions of platelet endothelial cell adhesion molecule-1 (PECAM-1) and BBB-related TJ proteins (Zonula occludens-1 and Claudin-5) until 72 h after KA treatment. These results suggest that the overexpression of autophagy-related proteins and astrocytes and transient increases in the expressions of BBB-related TJ proteins may be closely related to autophagic neuronal injury. These findings provide a basis for the identification of novel therapeutic targets for patients with epilepsy.

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“…Mice were intraperitoneally injected with 1 mg/kg of SCO (Sigma-Aldrich; Merck KGaA, Darmstadt, Germany), once daily, for 1, 2, 3 and 4 weeks ( n =14 at each point in time). Dose of SCO was selected based on previous studies ( 30 , 31 ). The control mice ( n =14 at each point in time) were injected with the same volume of saline (pH 7.4).…”

Section: Methodsmentioning

confidence: 99%

Effects of chronic scopolamine treatment on cognitive impairment and neurofilament expression in the mouse hippocampus

et al. 2017

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Neurofilaments (NFs) including neurofilament-200 kDa (NF-H), neurofilament-165 kDa (NF-M) and neurofilament-68 kDa (NF-L) are major protein constituents of the brain, and serve important roles in the regulation of axonal transport. NF alteration is a key feature in the pathogenesis of neurological disorders involving cognitive dysfunction. In the present study, cognitive impairments were investigated, via assessments using the Morris water maze and passive avoidance tests, in mice following chronic systemic treatment with 1 mg/kg scopolamine (SCO) for 4 weeks. SCO-induced cognitive impairments were significantly observed 1 week following the SCO treatment, and these cognitive deficits were maintained for 4 weeks. However, the NF immunoreactivities and levels were altered differently according to the hippocampal subregion following SCO treatment. NF-H immunoreactivity and levels were markedly altered in all hippocampal subregions, and were significantly increased 1 week following the SCO treatment; thereafter, the immunoreactivity and levels significantly decreased with time. NF-M immunoreactivity and levels gradually decreased in the hippocampus and were significantly decreased 4 weeks following SCO treatment. NF-L immunoreactivity and levels gradually decreased in the hippocampus, and were significantly decreased 2 and 4 weeks following SCO treatment. In conclusion, the results of the present study demonstrated that chronic systemic treatment with SCO induced cognitive impairment from 1 week following SCO treatment, and NF expression was diversely altered according to the hippocampal subregion from 1 week following SCO treatment. These results suggest that SCO-induced changes in NF expression may be associated with cognitive impairment.

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Long-term administration of scopolamine interferes with nerve cell proliferation, differentiation and migration in adult mouse hippocampal dentate gyrus, but it does not induce cell death

Cited by 13 publications

References 37 publications

Vanillin improves scopolamine‑induced memory impairment through restoration of ID1 expression in the mouse hippocampus

Vanillin improves scopolamine‑induced memory impairment through restoration of ID1 expression in the mouse hippocampus

Changes in the Blood-Brain Barrier Function Are Associated With Hippocampal Neuron Death in a Kainic Acid Mouse Model of Epilepsy

Effects of chronic scopolamine treatment on cognitive impairment and neurofilament expression in the mouse hippocampus

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