The neuro-behavioral profile in rats after subarachnoid hemorrhage

Boyko, Matthew; Azab, Abed N.; Kuts, Ruslan; Gruenbaum, Benjamin F.; Gruenbaum, Shaun E.; Melamed, Israel; Brotfain, Evgeni; Shapira, Yoram; Cesnulis, Evaldas; Zlotnik, Alexander

doi:10.1016/j.brainres.2012.10.061

Cited by 31 publications

(35 citation statements)

References 41 publications

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“…Both the DB and PB groups had recovered to normal rotarod performance by the time of MWM testing and there was no effect of either SAH model on escape latency in the visual platform test. Similarly, Boykin et al [19] found no motor deficits in the DB model at 3 weeks post-SAH. MWM deficits have largely been associated with CA1 injury, which was present in both models.…”

Section: Discussionmentioning

confidence: 85%

“…In contrast, DB rats spent more time in the enclosed arms than any other group, consistent with increased anxiety. Boyko et al [19] reported that plus maze responses were dependent upon insult severity in the cisterna magna injection model. Single-blood injection caused a major decrease in open arm entries and time spent in the open arms at 3 weeks, consistent with our observation.…”

Section: Discussionmentioning

confidence: 99%

“…& David S. Warner warne002@mc.duke.edu; david.warner@duke.edu injection model, created by injection of autologous blood into the dorsal posterior fossa on two separate days, consistently causes long-term cognitive deficits [9,10,19]. The prechiasmatic blood (PB) model, which requires a single stereotactic injection of autologous blood into the anterior fossa, has been shown to produce both short-and long-term cognitive deficits [11,20].…”

Section: Introductionmentioning

confidence: 99%

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Long-Term Cognitive Deficits After Subarachnoid Hemorrhage in Rats

et al. 2016

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Background Cognitive dysfunction can be a long-term complication following subarachnoid hemorrhage (SAH). Preclinical models have been variously characterized to emulate this disorder. This study was designed to directly compare long-term cognitive deficits in the context of similar levels of insult severity in the cisterna magna double-blood (DB) injection versus prechiasmatic blood (PB) injection SAH models. Methods Pilot work identified blood injectate volumes necessary to provide similar mortality rates (20-25 %). Rats were then randomly assigned to DB or PB insults. Saline injection and naïve rats were used as controls. Functional and cognitive outcome was assessed over 35 days. Results DB and PB caused similar transient rotarod deficits. PB rats exhibited decreased anxiety behavior on the elevated plus maze, while anxiety was increased in DB. DB and PB caused differential deficits in the novel object recognition and novel object location tasks. Morris water maze performance was similarly altered in both models (decreased escape latency and increased swimming speed). SAH caused histologic damage in the medial prefrontal cortex, perirhinal cortex, and hippocampal CA1, although severity of injury in the respective regions differed between DB and PB. Conclusion Both SAH models caused long-term cognitive deficits in the context of similar insult severity. Cognitive deficits differed between the two models, as did distribution of histologic injury. Each model offers unique properties and both models may be useful for study of SAH-induced cognitive deficits.

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Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Long-Term Cognitive Deficits After Subarachnoid Hemorrhage in Rats

et al. 2016

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“…The open field test was performed as described previously [21]. The standard open field test is commonly used to assess locomotor, exploratory and anxiety-like behavior in laboratory animals, and behavioral responses to novelty.…”

Section: Methodsmentioning

confidence: 99%

Establishment of an animal model of depression contagion

Boyko

Kutz

Grinshpun

et al. 2015

Behavioural Brain Research

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Background Depression is a common and important cause of morbidity, and results in a significant economic burden. Recent human studies have demonstrated that that depression is contagious, and depression in family and friends might cumulatively increase the likelihood that a person will exhibit depressive behaviors. The mechanisms underlying contagion depression are poorly understood, and there are currently no animal models for this condition. Methods Rats were divided into 3 groups: depression group, contagion group, and control group. After induction of depression by 5 weeks of chronic unpredictable stress, rats from the contagion group were housed with the depressed rats (1 naïve rat with 2 depressed rats) for 5 weeks. Rats were then subjected to sucrose preference, open field, and forced swim tests. Results The sucrose preference was significantly reduced in the depressed rats (p < 0.01) and contagion depression rats (p < 0.01). Climbing time during forced swim test was reduced in the depression and contagion depression groups (p < 0.001), whereas immobility time was significantly prolonged in only the depression group (p < 0.001). Rats in both the depression (p < 0.05) and depression contagion group (p < 0.005) had decreased total travel distance and decreased mean velocity in the open field test, whereas the time spent in the central part was significantly shorter in only the depression group (p < 0.001). Conclusions In this study, for the first time we demonstrated depression contagion in an animal model. A reliable animal model may help better understand the underlying mechanisms of contagion depression, and may allow for future investigations of the studying therapeutic modalities.

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“…Clinical evaluations of patients after SAH commonly reveal cognitive deficits, and this information is critical to providing for proper care (Wong et al, 2013). However, cognitive function, fatigue, and emotional disturbances are seldom evaluated in preclinical experiments (Boyko et al, 2013; Tso and Loch Macdonald, 2013). Additionally, for many patients with SAH and their relatives, the activities of daily living is as important as, or even more important than, the life prolonged.…”

Section: Sah Backgroundmentioning

confidence: 99%

Controversies and evolving new mechanisms in subarachnoid hemorrhage

Chen

Feng

Sherchan

et al. 2014

Progress in Neurobiology

314

263

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Despite decades of study, subarachnoid hemorrhage (SAH) continues to be a serious and significant health problem in the United States and worldwide. The mechanisms contributing to brain injury after SAH remain unclear. Traditionally, most in vivo research has heavily emphasized the basic mechanisms of SAH over the pathophysiological or morphological changes of delayed cerebral vasospasm after SAH. Unfortunately, the results of clinical trials based on this premise have mostly been disappointing, implicating some other pathophysiological factors, independent of vasospasm, as contributors to poor clinical outcomes. Delayed cerebral vasospasm is no longer the only culprit. In this review, we summarize recent data from both experimental and clinical studies of SAH and discuss the vast array of physiological dysfunctions following SAH that ultimately lead to cell death. Based on the progress in neurobiological understanding of SAH, the terms “early brain injury” and “delayed brain injury” are used according to the temporal progression of SAH-induced brain injury. Additionally, a new concept of the vasculo-neuronal-glia triad model for SAH study is highlighted and presents the challenges and opportunities of this model for future SAH applications.

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The neuro-behavioral profile in rats after subarachnoid hemorrhage

Cited by 31 publications

References 41 publications

Long-Term Cognitive Deficits After Subarachnoid Hemorrhage in Rats

Long-Term Cognitive Deficits After Subarachnoid Hemorrhage in Rats

Establishment of an animal model of depression contagion

Controversies and evolving new mechanisms in subarachnoid hemorrhage

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