Quetiapine attenuates cognitive impairment and decreases seizure susceptibility possibly through promoting myelin development in a rat model of malformations of cortical development

Ma, Lei; Feng, Yunjiang; Zhao, Rui; Li, Li; Kang, Xiaogang; Xiao, Lan; Jiang, Wen

doi:10.1016/j.brainres.2015.07.012

Cited by 14 publications

(15 citation statements)

References 56 publications

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“…Evidence for the latter includes the finding that children born preterm often display disrupted myelination and are at higher risk of developing epilepsy . Moreover, a study using a rat model of malformations in cortical development, which are linked to both epilepsy and developmental delay in humans, concluded that aberrant white matter development may be the underlying pathology supporting enhanced seizure vulnerability . The FAST/SLOW model, wherein no spontaneous seizures occur, precludes any involvement of seizure sequelae in relative rates of myelination or functional development and thereby identifies any observed deviations as inherent to the vulnerable or resistant state.…”

Section: Discussionmentioning

confidence: 99%

Delayed myelination and neurodevelopment in male seizure‐prone versus seizure‐resistant rats

et al. 2018

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Section: Discussionmentioning

confidence: 99%

Delayed myelination and neurodevelopment in male seizure‐prone versus seizure‐resistant rats

et al. 2018

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“…For example, it has been reported that QUE transiently disrupts avoidance behavior in a conditioned avoidance response task because it only transiently blocks D 2 receptors [44]. It has also been reported that QUE decreases object recognition deficits in a rat model of malformations of cortical development [26], stress-induced spatial working memory impairment [45], and reverses methamphetamine-induced cognitive deficits [46]. The benefits attributed to QUE could be due, in part to, to increased levels of DA in the frontal cortex.…”

Section: Discussionmentioning

confidence: 99%

“…The dose of HAL was chosen because it has been reported to be comparable to that used clinically to control psychosis [24] and has been used in several brain injury studies investigating functional outcome [12,13,15,19,25]. The dose of QUE was chosen based on the preclinical literature [26]. Treatments began 24 hr after CCI or sham surgery and were provided intraperitoneally once daily or once every other day (i.e., intermittently) for 19 days.…”

Section: Methodsmentioning

confidence: 99%

Intermittent treatment with haloperidol or quetiapine does not disrupt motor and cognitive recovery after experimental brain trauma

Weeks

Carlson

Radabaugh

et al. 2018

Behavioural Brain Research

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Traumatic brain injury (TBI)-induced agitation and aggression pose major obstacles to clinicians in the acute hospital and rehabilitation settings. Thus, management of these symptoms is crucial. Antipsychotic drugs (APDs) are a common treatment approach for alleviating these symptoms. However, previous preclinical TBI studies have indicated that daily and chronic administration of these drugs (e.g., haloperidol; HAL) can exacerbate cognitive and motor deficits. Quetiapine (QUE) is an atypical APD that differs from many typical APDs, such as HAL, in its relatively rapid dissociation from the D receptor. The goal of this study was to test the hypotheses that intermittent HAL and QUE would not hinder recovery of cognitive and motor function following TBI and that daily QUE would also not impair functional recovery, which would be in contrast to HAL. Seventy anesthetized male rats received either a controlled cortical impact or sham injury and were then randomly assigned to TBI and sham groups receiving HAL (0.5mg/kg) or QUE (10mg/kg) intraperitoneally once per day or once every other day and compared to each other and vehicle (VEH) controls. Motor function was assessed by beam balance/walk tests on post-operative days 1-5 and cognitive function was evaluated with a Morris water maze task on days 14-19. No differences were revealed among the sham groups in any task, and hence the data were pooled. No overall differences were detected among the TBI groups, regardless of treatment or administration paradigm [p>0.05], but all were impaired vs. SHAM controls [p<0.05]. The SHAM controls also performed significantly better in the cognitive test vs. all TBI groups [p<0.05]. Moreover, the TBI+continuous HAL group performed worse than the TBI+continuous VEH, TBI+continuous QUE, and TBI+intermittent QUE groups [p<0.05], which did not differ from one another. Overall, the data suggest that QUE does not exacerbate TBI-induced cognitive and motor deficits, which supports the hypothesis. QUE may prove useful as an alternative APD treatment for management of agitation and aggression after clinical TBI. HAL may also be safe, but only if used sparingly.

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“…For example, promoting myelination with quetiapine, an atypical antipsychotic known to enhance oligodendrocyte regeneration and myelin repair, 71 has been found to reduce seizure susceptibility and severity. 72 Therefore, the FAST/SLOW rat model serves as a useful tool to facilitate investigations into neurodevelopmental contributions to seizure vulnerability. The most common neuropathologic change associated with acquired limbic epilepsy in animal models and humans is mossy fiber sprouting, a form of hippocampal synaptic reorganization associated with network hyperexcitability.…”

Section: Neuroanatomic Differencesmentioning

confidence: 99%

An animal model of genetic predisposition to develop acquired epileptogenesis: The FAST and SLOW rats

et al. 2019

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Epidemiological data and gene association studies suggest a genetic predisposition to developing epilepsy after an acquired brain insult, such as traumatic brain injury. An improved understanding of genetic determinants of vulnerability is imperative for early disease diagnosis and prognosis prediction, with flow‐on benefits for the development of targeted antiepileptogenic treatments as well as optimal clinical trial design. In the laboratory, one approach to investigate why some individuals are more vulnerable to acquired epilepsy than others is to examine unique rodent models exhibiting either vulnerability or resistance to epileptogenesis. This review focuses on the most well‐characterized of these models, the FAST (seizure‐prone) and SLOW (seizure‐resistant) rat strains, which were derived by selective breeding for differential amygdala electrical kindling rates. We describe how these strains differ in their seizure profiles, neuroanatomy, and neurobehavioral phenotypes, both at baseline and after a brain insult, with this knowledge proving fruitful to identify common pathological abnormalities associated with seizure susceptibility and psychiatric comorbidities. It is important to note that accruing data on strain differences in multiple biological processes provides insight into why some individuals may be more vulnerable to epileptogenesis, although future studies are evidently needed to identify the precise molecular and genetic risk factors. Together, the FAST and SLOW rat strains, and other similar experimental models, are invaluable neurobiological tools to investigate the effect of genetic background on acquired epilepsy risk, as well as the poorly understood relationship between epilepsy development and associated comorbidities.

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Quetiapine attenuates cognitive impairment and decreases seizure susceptibility possibly through promoting myelin development in a rat model of malformations of cortical development

Cited by 14 publications

References 56 publications

Delayed myelination and neurodevelopment in male seizure‐prone versus seizure‐resistant rats

Delayed myelination and neurodevelopment in male seizure‐prone versus seizure‐resistant rats

Intermittent treatment with haloperidol or quetiapine does not disrupt motor and cognitive recovery after experimental brain trauma

An animal model of genetic predisposition to develop acquired epileptogenesis: The FAST and SLOW rats

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