Minocycline reduces reactive gliosis in the rat model of hydrocephalus

Xu, Hao; Tan, Guowei; Zhang, Shaolin; Zhu, Hongwei; Feng, Lin; Huang, Cai-quan; Zhang, Feifei; Wang, Zhanxiang

doi:10.1186/1471-2202-13-148

Cited by 29 publications

(21 citation statements)

References 43 publications

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“…The ability of astrocytes to cause cerebral vasodilation and its antioxidant properties make it a candidate to compensate for the increased intra-cerebral pressure and generation of reactive oxygen species which are synonymous with kaolin-induced hydrocephalus. Reactive gliosis is a known manifestation of hydro- cephalus which is amenable to shunting thereby associating it with the ventriculomegaly of hydrocephalus [19,20] . Of note, in our study, the increase in the density of glial cell was significant across the experimental subsets at 4 weeks of induction.…”

Section: Discussionmentioning

confidence: 99%

Cortical Oligodendrocytes in Kaolin-Induced Hydrocephalus in Wistar Rat: Impact of Degree and Duration of Ventriculomegaly

Ayannuga

Naicker

2017

Ann Neurosci

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Background: Oligodendrocytes are critical to the function of the brain. They generate the myelin sheath which ensures saltatory conduction, which is a more energy saving and efficient means of axonal impulse transmission. Ventriculomegaly results in neuronal degeneration and astrogliosis. Purpose: The effect of the degree of ventriculomegaly on oligodendrocyte in kaolin-induced hydrocephalus and the timeline have not been extensively documented, hence this study. Methods: A total of 81 rats that were 3 weeks old were divided into 4 groups each consisting of control and experimental subgroups. Kaolin suspension was intracisternally injected to induce hydrocephalus and the animal sacrificed post-induction at 1, 2, 3, and 4 weeks. Two 1-mm-thick coronal slices at optic chiasma level were fixed in 10% buffered formal-saline and Karnovsky's fixative for light and transmission electron microscopy (TEM), respectively. The former slices were processed and stained with hematoxylin and eosin for glial density, cortical thickness, and oligodendrocyte evaluations. Subcortical white matter region of the latter were processed by conventional techniques for TEM. Results: Compared with their corresponding control rats, thickness of the dorsolateral cortex was significantly reduced across the 2-4 week post-induction (WPI), glial density was significantly increased in the mild and moderate ventriculomegaly subgroups 1 WPI but only in mild ventriculomegaly subset 2 WPI. In the 4 WPI group, there was significant increase in glial density across the 3 ventriculomegaly subsets. Early hydropic changes of oligodendrocytes were noted in the inner pyramidal layer mostly in the 4 WPI experimental rats. Dilation of the endoplasmic reticulum precedes that of mitochondria, while mitochondrial crista disruption was noted in the 3 and 4 WPI rats. The nuclear membrane of the oligodendrocytes was progressively deformed from the 2nd to 4th WPI. Conclusion: This study reported degenerative changes of oligodendrocytes and its organelles in kaolin-induced hydrocephalus. Degeneration was worse with duration and in the deep cortical layers.

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Section: Discussionmentioning

confidence: 99%

Cortical Oligodendrocytes in Kaolin-Induced Hydrocephalus in Wistar Rat: Impact of Degree and Duration of Ventriculomegaly

Ayannuga

Naicker

2017

Ann Neurosci

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“…Multiple models for ICP measurement (Chavko et al, 2007; Kawoos et al, 2014; Lin and Liu, 2010; Silasi et al, 2009) or elevation (Bragin et al, 2013; Morrow et al, 1990; Park et al, 2011; Samuels et al, 2012; Xu et al, 2012) have been developed in rats. These studies have each been limited by a short duration of ICP elevation, a poorly predictable system for ICP elevation, brief ICP monitoring, a need for concurrent anesthesia, or some combination.…”

Section: Discussionmentioning

confidence: 99%

Elevated intracranial pressure causes optic nerve and retinal ganglion cell degeneration in mice

Nusbaum

Frankfort

2015

Experimental Eye Research

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The purpose of this study was to develop a novel experimental system for the modulation and measurement of intracranial pressure (ICP), and to use this system to assess the impact of elevated ICP on the optic nerve and retinal ganglion cells (RGCs) in CD1 mice. This system involved surgical implantation of an infusion cannula and a radiowave based pressure monitoring probe through the skull and into the subarachnoid space. The infusion cannula was used to increase ICP, which was measured by the probe and transmitted to a nearby receiver. The system provided robust and consistent ICP waveforms, was well tolerated, and was stable over time. ICP was elevated to approximately 30 mmHg for one week, after which we assessed changes in optic nerve structure with transmission electron microscopy in cross section and RGC numbers with antibody staining in retinal flat mounts. ICP elevation resulted in optic nerve axonal loss and disorganization, as well as RGC soma loss. We conclude that the controlled manipulation of ICP in active, awake mice is possible, despite their small size. Furthermore, ICP elevation results in visual system phenotypes of optic nerve and RGC degeneration, suggesting that this model can be used to study the impact of ICP on the visual system. Potentially, this model can also be used to study the relationship between ICP and IOP, as well diseases impacted by ICP variation such as glaucoma, idiopathic intracranial hypertension, and the spaceflight-related visual impairment intracranial pressure syndrome.

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“…Minocycline is reported to be effective in reducing the gliosis and delaying the development of HCP in rat model [40]. And decorin may be beneficial for the long-term of HCP [7].…”

Section: Treatmentmentioning

confidence: 99%

Hydrocephalus after Subarachnoid Hemorrhage: Pathophysiology, Diagnosis, and Treatment

Chen

Luo

Reis

et al. 2017

BioMed Research International

125

131

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Hydrocephalus (HCP) is a common complication in patients with subarachnoid hemorrhage. In this review, we summarize the advanced research on HCP and discuss the understanding of the molecular originators of HCP and the development of diagnoses and remedies of HCP after SAH. It has been reported that inflammation, apoptosis, autophagy, and oxidative stress are the important causes of HCP, and well-known molecules including transforming growth factor, matrix metalloproteinases, and iron terminally lead to fibrosis and blockage of HCP. Potential medicines for HCP are still in preclinical status, and surgery is the most prevalent and efficient therapy, despite respective risks of different surgical methods, including lamina terminalis fenestration, ventricle-peritoneal shunting, and lumbar-peritoneal shunting. HCP remains an ailment that cannot be ignored and even with various solutions the medical community is still trying to understand and settle why and how it develops and accordingly improve the prognosis of these patients with HCP.

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Minocycline reduces reactive gliosis in the rat model of hydrocephalus

Cited by 29 publications

References 43 publications

Cortical Oligodendrocytes in Kaolin-Induced Hydrocephalus in Wistar Rat: Impact of Degree and Duration of Ventriculomegaly

Cortical Oligodendrocytes in Kaolin-Induced Hydrocephalus in Wistar Rat: Impact of Degree and Duration of Ventriculomegaly

Elevated intracranial pressure causes optic nerve and retinal ganglion cell degeneration in mice

Hydrocephalus after Subarachnoid Hemorrhage: Pathophysiology, Diagnosis, and Treatment

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