Topiramate promotes neurological recovery in a new model of traumatic brain injury in rats

Kouzounias, K.; Kimiskidis, Vasilios Κ.; Siozos, T.; Violaris, Konstantinos; Kostomitsopoulos, Nikolaos; Karayannakos, P.E.; Sotirakoglou, Κyriaki; Nanassis, K.

doi:10.1016/j.neuroscience.2011.03.069

Cited by 11 publications

(10 citation statements)

References 36 publications

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“…Mao et al (2012), Yang et al (1998) reported the benefits of TPM in improving neurological function in animal models exposed to ischemic brain injury. In addition, a similar effect of TPM treatment was discovered in a previous study on traumatic brain injury in rats (Kouzounias et al, 2011). Similar to the aforementioned brain injuries, EBI after SAH can also lead to neurological deficits, as demonstrated in numerous in vivo experiments (Chen et al, 2014a(Chen et al, , 2013Dai et al, 2014).…”

Section: Discussionsupporting

confidence: 75%

“…Moreover, EBI is the primary cause of mortality and morbidity in SAH patients, and the time point of 24 h post-SAH has been reported to be appropriate for the study of EBI (Bederson et al, 2009;Mayberg et al, 1994;Yatsushige et al, 2006). Some researchers have also reported the protective effects of TPM on a series of neural injuries, such as cerebral ischemia/reperfusion injury, epilepsy, cervical spinal cord injury, traumatic brain injury (TBI), chronic constriction injury and SAH-induced hippocampal injury, via multiple mechanisms (Benoliel et al, 2006;Gensel et al, 2012;Hoover et al, 2004;Kouzounias et al, 2011;Kudin et al, 2004;Mao et al, 2012;Seckin et al, 2009;Yang et al, 1998Yang et al, , 2000. Our present study shows the protective effect of TPM on EBI after SAH.…”

Section: Discussionmentioning

confidence: 99%

“…5B. The doses, administration route and time point of TPM (purchased from Janssen pharmaceutical LTD., Xi'an, Shanxi, China) were selected according to previous studies (Kouzounias et al, 2011;Kudin et al, 2004;Mao et al, 2012). …”

Section: Study Design and Drug Administrationmentioning

confidence: 99%

“…Topiramate (TPM) is a broadspectrum antiepileptic drug (AED) that exerts its anticonvulsant effect by enhancing γ-aminobutyric acid (GABA)ergic activity and by inhibiting kainite receptors, α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) glutamate receptors and voltage-sensitive sodium and calcium channels (Borowicz et al, 2003;Guerrini and Parmeggiani, 2006;Seckin et al, 2009). Prior research has verified the neuroprotective effects of TPM in excitotoxic brain damage, traumatic brain injury, periventricular leukomalacia and cerebral ischemiareperfusion injury models in vivo (Follett et al, 2004;Gensel et al, 2012;Kouzounias et al, 2011;Mao et al, 2012;Seckin et al, 2009;Sfaello et al, 2005). Seckin et al (2009) also showed that the post-injury administration of TPM can attenuate delayed hippocampal apoptosis and basilar artery vasospasm in an experimental SAH rabbit model.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Topiramate attenuates early brain injury following subarachnoid haemorrhage in rats via duplex protection against inflammation and neuronal cell death

Tian

Guo

et al. 2015

Brain Research

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Section: Discussionsupporting

confidence: 75%

Section: Discussionmentioning

confidence: 99%

Section: Study Design and Drug Administrationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Topiramate attenuates early brain injury following subarachnoid haemorrhage in rats via duplex protection against inflammation and neuronal cell death

Tian

Guo

et al. 2015

Brain Research

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“…The consistent ability of topiramate to attenuate cognitive impairment and neuronal injury in rat SE models coincides with reports showing that topiramate treatment promotes neurological recovery in rats following TBI induced by lateral fluid percussion or by the weight-drop technique [47,48]. Interestingly, this effect may, at least partially, reflect an ability of topiramate to reduce glutamate release after TBI [49].…”

Section: Topiramatesupporting

confidence: 85%

The Potential of Antiseizure Drugs and Agents that Act on Novel Molecular Targets as Antiepileptogenic Treatments

2014

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A major goal of contemporary epilepsy research is the identification of therapies to prevent the development of recurrent seizures in individuals at risk, including those with brain injuries, infections, or neoplasms; status epilepticus; cortical dysplasias; or genetic epilepsy susceptibility. In this review we consider the evidence largely from preclinical models for the antiepileptogenic activity of a diverse range of potential therapies, including some marketed antiseizure drugs, as well as agents that act by immune and inflammatory mechanisms; reduction of oxidative stress; activation of the mammalian target of rapamycin or peroxisome proliferatoractivated receptors γ pathways; effects on factors related to thrombolysis, hematopoesis, and angiogenesis; inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reducatase; brainderived neurotrophic factor signaling; and blockade of α2 adrenergic and cannabinoid receptors. Antiepileptogenesis refers to a therapy of which the beneficial action is to reduce seizure frequency or severity outlasting the treatment period. To date, clinical trials have failed to demonstrate that antiseizure drugs have such disease-modifying activity. However, studies in animal models with levetiracetam and ethosuximide are encouraging, and clinical trials with these agents are warranted. Other promising strategies are inhibition of interleukin 1β signaling by drugs such as VX-765; modulation of sphingosine 1-phosphate signaling by drugs such as fingolimod; activation of the mammalian target of rapamycin by drugs such as rapamycin; the hormone erythropoietin; and, paradoxically, drugs such as the α2 adrenergic receptor antagonist atipamezole and the CB1 cannabinoid antagonist SR141716A (rimonabant) with proexcitatory activity. These approaches could lead to a new paradigm in epilepsy drug therapy where treatment for a limited period prevents the occurrence of spontaneous seizures, thus avoiding lifelong commitment to symptomatic treatment.

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Long-lasting recognition memory impairment and alterations in brain levels of cytokines and BDNF induced by maternal deprivation: effects of valproic acid and topiramate

et al. 2014

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Exposure to stressful events early in life may have permanent deleterious consequences on nervous system function and increase the susceptibility to psychiatric conditions later in life. Maternal deprivation, commonly used as a source of neonatal stress, impairs memory in adult rats and reduces hippocampal brain-derived neurotrophic factor (BDNF) levels. Inflammatory cytokines, such as interleukins (IL) and tumor necrosis factor-α (TNF-α) have been shown to be increased in the peripheral blood of patients with psychiatric disorders. The aim of the present study was to investigate the effects of maternal separation on the levels of IL-10 and TNF-α, and BDNF in the hippocampus and prefrontal cortex of adult rats. We also evaluated the potential ameliorating properties of topiramate and valproic acid on memory deficits and cytokine and BDNF changes associated with maternal deprivation. The results indicated that, in addition to inducing memory deficits, maternal deprivation increased the levels of IL-10 in the hippocampus, and TNF-α in the hippocampus and in the cortex, and decreased hippocampal levels of BDNF, in adult life. Neither valproic acid nor topiramate were able to ameliorate memory deficits or the reduction in BDNF induced by maternal separation. The highest dose of topiramate was able to reduce IL-10 in the hippocampus and TNF-α in the prefrontal cortex, while valproate only reduced IL-10 levels in the hippocampus. These findings may have implications for a better understanding of the mechanisms associated with alterations observed in adult life induced by early stressful events, and for the proposal of novel therapeutic strategies.

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Topiramate promotes neurological recovery in a new model of traumatic brain injury in rats

Cited by 11 publications

References 36 publications

Topiramate attenuates early brain injury following subarachnoid haemorrhage in rats via duplex protection against inflammation and neuronal cell death

Topiramate attenuates early brain injury following subarachnoid haemorrhage in rats via duplex protection against inflammation and neuronal cell death

The Potential of Antiseizure Drugs and Agents that Act on Novel Molecular Targets as Antiepileptogenic Treatments

Long-lasting recognition memory impairment and alterations in brain levels of cytokines and BDNF induced by maternal deprivation: effects of valproic acid and topiramate

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