Mouse cerebral magnetic resonance imaging fails to visualize brain volume changes after experimental subarachnoid hemorrhage

Atangana, Etienne Ndzie; Homburg, David; Vajkoczy, Peter; Schneider, Ulf C.

doi:10.1007/s00701-014-2276-5

Cited by 10 publications

(8 citation statements)

References 33 publications

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“…Lastly, the endovascular perforation model of SAH in mice may lack the extent and/or distribution of neuronal injury, death, or dysfunction necessary to manifest neurobehavioral deficits beyond the acute period when general cerebral dysfunction is marked. Cell death has been documented in the ipsilateral parietal cortex 37 and ipsilateral basal cortex 38 in this model, but we and others previously failed to detect cell or volume loss in the hippocampus 19, 39 . In contrast, ipsilateral hippocampal atrophy and apoptosis are both observed following SAH in humans 40, 41 .…”

Section: Discussioncontrasting

confidence: 66%

Minimal Long-Term Neurobehavioral Impairments after Endovascular Perforation Subarachnoid Hemorrhage in Mice

Fanizzi

Sauerbeck

Gangolli

et al. 2017

Sci Rep

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Cognitive deficits are among the most severe and pervasive consequences of aneurysmal subarachnoid hemorrhage (SAH). A critical step in developing therapies targeting such outcomes is the characterization of experimentally-tractable pre-clinical models that exhibit multi-domain neurobehavioral deficits similar to those afflicting humans. We therefore searched for neurobehavioral abnormalities following endovascular perforation induction of SAH in mice, a heavily-utilized model. We instituted a functional screen to manage variability in injury severity, then assessed acute functional deficits, as well as activity, anxiety-related behavior, learning and memory, socialization, and depressive-like behavior at sub-acute and chronic time points (up to 1 month post-injury). Animals in which SAH was induced exhibited reduced acute functional capacity and reduced general activity to 1 month post-injury. Tests of anxiety-related behavior including central area time in the elevated plus maze and thigmotaxis in the open field test revealed increased anxiety-like behavior at subacute and chronic time-points, respectively. Effect sizes for subacute and chronic neurobehavioral endpoints in other domains, however, were small. In combination with persistent variability, this led to non-significant effects of injury on all remaining neurobehavioral outcomes. These results suggest that, with the exception of anxiety-related behavior, alternate mouse models are required to effectively analyze cognitive outcomes after SAH.

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Section: Discussioncontrasting

confidence: 66%

Minimal Long-Term Neurobehavioral Impairments after Endovascular Perforation Subarachnoid Hemorrhage in Mice

Fanizzi

Sauerbeck

Gangolli

et al. 2017

Sci Rep

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“…Moreover, no hemispherical or hippocampal volume changes were detected in SAH mice in a study by Atangana et al using MRI, suggesting that current models of SAH may not induce significant radiological and functional deficits in hippocampus volume and neurocognitive tests respectively in SAH mice. 90 Further research is needed to improve surgical SAH induction methods and assessment of neurocognitive deficits at different time points.…”

Section: Cognitive Tests Morris Water Mazementioning

confidence: 99%

Neurobehavioral testing in subarachnoid hemorrhage: A review of methods and current findings in rodents

Turan

Miller

Heider

et al. 2016

J Cereb Blood Flow Metab

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The most important aspect of a preclinical study seeking to develop a novel therapy for neurological diseases is whether the therapy produces any clinically relevant functional recovery. For this purpose, neurobehavioral tests are commonly used to evaluate the neuroprotective efficacy of treatments in a wide array of cerebrovascular diseases and neurotrauma. Their use, however, has been limited in experimental subarachnoid hemorrhage studies. After several randomized, double-blinded, controlled clinical trials repeatedly failed to produce a benefit in functional outcome despite some improvement in angiographic vasospasm, more rigorous methods of neurobehavioral testing became critical to provide a more comprehensive evaluation of the functional efficacy of proposed treatments. While several subarachnoid hemorrhage studies have incorporated an array of neurobehavioral assays, a standardized methodology has not been agreed upon. Here, we review neurobehavioral tests for rodents and their potential application to subarachnoid hemorrhage studies. Developing a standardized neurobehavioral testing regimen in rodent studies of subarachnoid hemorrhage would allow for better comparison of results between laboratories and a better prediction of what interventions would produce functional benefits in humans.

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“…However, hippocampal atrophy may not be present in all neuroimaging investigations of experimental SAH. For instance, a recent MRI study by Atangana et al (2015) did not detect hippocampal atrophy in their experimental model of SAH. This discrepancy between our findings and the results of Atangana et al (2015) study could be ascribed to the less severe course of tissue injury in their study.…”

Section: Discussionmentioning

confidence: 94%

Hippocampal Atrophy Following Subarachnoid Hemorrhage Correlates with Disruption of Astrocyte Morphology and Capillary Coverage by AQP4

Anzabi

Ardalan

Iversen

et al. 2018

Front. Cell. Neurosci.

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Despite successful management of ruptured intracranial aneurysm following subarachnoid hemorrhage (SAH), delayed cerebral ischemia (DCI) remains the main cause of high mortality and morbidity in patients who survive the initial bleeding. Astrocytes play a key role in neurovascular coupling. Therefore, changes in the neurovascular unit including astrocytes following SAH may contribute to the development of DCI and long-term complications. In this study, we characterized morphological changes in hippocampal astrocytes following experimental SAH, with special emphasis on glia-vascular cross-talk and hippocampal volume changes. Four days after induction of SAH or sham-operation in mice, their hippocampal volumes were determined by magnetic resonance imaging (MRI) and histological/stereological methods. Glial fibrillary acid protein (GFAP) immunostained hippocampal sections were examined by stereological techniques to detect differences in astrocyte morphology, and global spatial sampling method was used to quantify the length density of Aquaporin-4 (AQP4) positive capillaries. Our results indicated that hippocampal volume, as measured both by MRI and by histological approaches, was significantly lower in SAH animals than in the sham-operated group. Accordingly, in this animal model of SAH, hippocampal atrophy existed already at the time of DCI onset in humans. SAH induced retraction of GFAP positive astrocyte processes, accompanied by a significant reduction in the length density of AQP4 positive capillaries as well as narrowing of hippocampal capillaries. Meanwhile, astrocyte volume was higher in SAH mice compared with the sham-operated group. Morphological changes in hippocampal astrocytes seemingly disrupt glia-vascular interactions early after SAH and may contribute to hippocampal atrophy. We speculate that astrocytes and astrocyte-capillary interactions may provide targets for the development of therapies to improve the prognosis of SAH.

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Mouse cerebral magnetic resonance imaging fails to visualize brain volume changes after experimental subarachnoid hemorrhage

Cited by 10 publications

References 33 publications

Minimal Long-Term Neurobehavioral Impairments after Endovascular Perforation Subarachnoid Hemorrhage in Mice

Minimal Long-Term Neurobehavioral Impairments after Endovascular Perforation Subarachnoid Hemorrhage in Mice

Neurobehavioral testing in subarachnoid hemorrhage: A review of methods and current findings in rodents

Hippocampal Atrophy Following Subarachnoid Hemorrhage Correlates with Disruption of Astrocyte Morphology and Capillary Coverage by AQP4

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