Animal Models of Hydrocephalus

Curzio, Domenico L. Di

doi:10.4236/ojmn.2018.81004

Cited by 19 publications

(23 citation statements)

References 102 publications

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“…Hydrocephalus, a common defect frequently occurring in infants, is characterized by the increased head size, impaired vision, poor coordination, seizures, poor appetite, and urinary incontinence. Hydrocephalus is usually accompanied by disrupted neural cell determination in the SVZ, reduced subcommissural organ, shrunken corticospinal tract, or deficiency in corpus callosum (54). In mice, the most prominent phenotypes are dome-shaped skull and enlarged ventricles caused by the accumulation of CSF, due to either the obstruction of the ventricular system or defects in the ECs.…”

Section: Discussionmentioning

confidence: 99%

MT1-MMP deficiency leads to defective ependymal cell maturation, impaired ciliogenesis, and hydrocephalus

Jiang¹,

Zhou²,

Xin³

et al. 2020

JCI Insight

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Section: Discussionmentioning

confidence: 99%

MT1-MMP deficiency leads to defective ependymal cell maturation, impaired ciliogenesis, and hydrocephalus

Jiang¹,

Zhou²,

Xin³

et al. 2020

JCI Insight

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“…Hydrocephalus is a common neurological condition in which cerebrospinal fluid (CSF) flow dynamics are altered, leading to enlargement of ventricular cavities in the brain. There is still no definitive cure for this disease [1]. The histopathologic consequences of hydrocephalus depend on the age of onset, rate of ventricular enlargement, and the aetiology [2].…”

Section: Introductionmentioning

confidence: 99%

Changes in Neuronal Density of the Sensorimotor Cortex and Neurodevelopmental Behaviour in Neonatal Mice with Kaolin-Induced Hydrocephalus

Femi-Akinlosotu

Shokunbi

2020

Pediatr Neurosurg

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Introduction: Hydrocephalus is a disorder in which the circulation of cerebrospinal fluid is altered in a manner that leads to its accumulation in the ventricles and subarachnoid space. Its impact on the neuronal density and networks in the overlying cerebral cortex in a time-dependent neonatal hydrocephalic process is largely unknown. We hypothesize that hydrocephalus will affect the cytoarchitecture of the cerebral cortical mantle of neonatal hydrocephalic mice, which will in turn modify sensorimotor processing and neurobehaviour. Objective: The purpose of this study is to probe the effect of hydrocephalus on 3 developmental milestones (surface righting reflex, cliff avoidance reflex, and negative geotaxis) and on cortical neuronal densities in neonatal hydrocephalic mice. Methods: Hydrocephalus was induced in 1-day-old mice by intracisternal injection of sterile kaolin suspension. The pups were tested for reflex development and sensorimotor ability using surface righting reflex (PND 5, 7, and 9), cliff avoidance (PND 6), and negative geotaxis (PND 10 and 12) prior to their sacrifice on PND 7, 14, and 21. Neuronal density and cortical thickness in the sensorimotor cortex were evaluated using atlas-based segmentation of the neocortex and boundary definition in 4-μm paraffin-embedded histological sections with hematoxylin and eosin as well as cresyl violet stains. Results: Surface righting and cliff avoidance activities were significantly impaired in hydrocephalic pups but no statistically significant difference was observed in negative geotaxis in both experimental and control pups. The neuronal density of the sensorimotor cortex was significantly higher in hydrocephalic mice than in age-matched controls on PND 14 and 21 (373.20 ± 21.54 × 10−6 μm2 vs. 157.70 ± 21.88 × 10−6 μm2; 230.0 ± 44.1 × 10−6 μm2 vs. 129.60 ± 3.72 × 10−6 μm2, respectively; p < 0.05). This was accompanied by reduction in the cortical thickness (µm) in the hydrocephalic mice on PND 7 (2,409 ± 43.37 vs. 3,752 ± 65.74, p < 0.05), PND 14 (2,035 ± 322.10 vs. 4,273 ± 67.26, p < 0.05), and PND 21 (1,676 ± 33.90 vs. 4,945 ± 81.79, p < 0.05) compared to controls. Conclusion: In this murine model of neonatal hydrocephalus, the quantitative changes in the cortical neuronal population may play a role in the observed changes in neurobehavioural findings.

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“…Kaolin injection into the cisterna magna to induce hydrocephalus is a well-characterized technique that has been used in several animal models, including rodents and large animals [ 20 , 27 , 35 , 37 , 39 , 40 , 60 – 64 ]. Its use has the advantage of being a less invasive, inexpensive, and consistent technique to produce ventriculomegaly [ 36 ]. Although some variability across age groups was present in the hydrocephalic animals, no correlations were found with ventricular volume, ventricular zone disruption, oligodendrocytes, cell proliferation in the ASVZ, or inflammation, except for cell death in the PVWM adjacent to the body of the lateral ventricles.…”

Section: Discussionmentioning

confidence: 99%

“…A commonly used method for inducing experimental hydrocephalus is the injection of kaolin (aluminum silicate) into the cisterna magna [ 27 , 35 – 40 ], which obstructs CSF flow as a result of a local inflammatory reaction and fibrous scarring [ 7 , 35 , 36 ]. This method has been developed mostly in non-gyrencephalic animals [ 41 ].…”

Section: Introductionmentioning

confidence: 99%

Acquired hydrocephalus is associated with neuroinflammation, progenitor loss, and cellular changes in the subventricular zone and periventricular white matter

García-Bonilla

Castañeyra-Ruiz

Zwick

et al. 2022

Fluids Barriers CNS

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Background Hydrocephalus is a neurological disease with an incidence of 80–125 per 100,000 births in the United States. Neuropathology comprises ventriculomegaly, periventricular white matter (PVWM) alterations, inflammation, and gliosis. We hypothesized that hydrocephalus in a pig model is associated with subventricular and PVWM cellular alterations and neuroinflammation that could mimic the neuropathology described in hydrocephalic infants. Methods Hydrocephalus was induced by intracisternal kaolin injections in 35-day old female pigs (n = 7 for tissue analysis, n = 10 for CSF analysis). Age-matched sham controls received saline injections (n = 6). After 19–40 days, MRI scanning was performed to measure the ventricular volume. Stem cell proliferation was studied in the Subventricular Zone (SVZ), and cell death and oligodendrocytes were examined in the PVWM. The neuroinflammatory reaction was studied by quantifying astrocytes and microglial cells in the PVWM, and inflammatory cytokines in the CSF. Results The expansion of the ventricles was especially pronounced in the body of the lateral ventricle, where ependymal disruption occurred. PVWM showed a 44% increase in cell death and a 67% reduction of oligodendrocytes. In the SVZ, the number of proliferative cells and oligodendrocyte decreased by 75% and 57% respectively. The decrease of the SVZ area correlated significantly with ventricular volume increase. Neuroinflammation occurred in the hydrocephalic pigs with a significant increase of astrocytes and microglia in the PVWM, and high levels of inflammatory interleukins IL-6 and IL-8 in the CSF. Conclusion The induction of acquired hydrocephalus produced alterations in the PVWM, reduced cell proliferation in the SVZ, and neuroinflammation.

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Animal Models of Hydrocephalus

Cited by 19 publications

References 102 publications

MT1-MMP deficiency leads to defective ependymal cell maturation, impaired ciliogenesis, and hydrocephalus

MT1-MMP deficiency leads to defective ependymal cell maturation, impaired ciliogenesis, and hydrocephalus

Changes in Neuronal Density of the Sensorimotor Cortex and Neurodevelopmental Behaviour in Neonatal Mice with Kaolin-Induced Hydrocephalus

Acquired hydrocephalus is associated with neuroinflammation, progenitor loss, and cellular changes in the subventricular zone and periventricular white matter

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