Effects of levetiracetam on blood-brain barrier disturbances following hyperthermia-induced seizures in rats with cortical dysplasia

Ahıshalı, Bülent; Kaya, Mehmet; Orhan, Nurcan; Arıcan, Nadir; Ekizoğlu, Oğuzhan; Elmas, İmdat; Küçük, Mutlu; Kemikler, Gönül; Kalayci, Rivaze; Gürses, Candan

doi:10.1016/j.lfs.2010.09.014

Cited by 23 publications

(18 citation statements)

References 51 publications

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“…Marchi et al [46] reported a disruption in BBB permeability after Li-PIL administration that is sufficient to elicit seizures, an effect that aids in the neutrophil infiltration. The reduction in MPO by LEV could be linked to its ability to maintain the BBB integrity [47], where LEV preserves the morphological and functional properties of the BBB together with the reduction of pinocytotic activity during epileptic seizures [48]. …”

Section: Discussionmentioning

confidence: 99%

Additional Antiepileptic Mechanisms of Levetiracetam in Lithium-Pilocarpine Treated Rats

2013

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Several studies have addressed the antiepileptic mechanisms of levetiracetam (LEV); however, its effect on catecholamines and the inflammatory mediators that play a role in epilepsy remain elusive. In the current work, lithium (Li) pretreated animals were administered LEV (500 mg/kg i.p) 30 min before the induction of convulsions by pilocarpine (PIL). Li-PIL-induced seizures were accompanied by increased levels of hippocampal prostaglandin (PG) E2, myeloperoxidase (MPO), tumor necrosis factor-α, and interleukin-10. Moreover, it markedly elevated hippocampal lipid peroxides and nitric oxide levels, while it inhibited the glutathione content. Li-PIL also reduced hippocampal noradrenaline, as well as dopamine contents. Pretreatment with LEV protected against Li-PIL-induced seizures, where it suppressed the severity and delayed the onset of seizures in Li-PIL treated rats. Moreover, LEV reduced PGE2 and MPO, yet it did not affect the level of both cytokines in the hippocampus. LEV also normalized hippocampal noradrenaline, dopamine, glutathione, lipid peroxides, and nitric oxide contents. In conclusion, alongside its antioxidant property, LEV anticonvulsive effect involves catecholamines restoration, as well as inhibition of PGE2, MPO, and nitric oxide.

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Section: Discussionmentioning

confidence: 99%

Additional Antiepileptic Mechanisms of Levetiracetam in Lithium-Pilocarpine Treated Rats

2013

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“…Levetiracetam (LEV) may constitute a novel approach for BBB protection [206]. Clinical studies have evidenced the effects of levetiracetam (LEV) in various pain conditions, such as postmastectomy pain syndrome, trigeminal neuralgia, chronic general or central pain in MS, lumbar radiculopathy, chronic daily headache, polyneuropathy, and central poststroke pain [207–212].…”

Section: Potential Strategies Targeting Bbb or Bscb For Chronic Pamentioning

confidence: 99%

Neurovascular Unit in Chronic Pain

Radu

Bramantı

Osculati

et al. 2013

Mediators of Inflammation

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Chronic pain is a debilitating condition with major socioeconomic impact, whose neurobiological basis is still not clear. An involvement of the neurovascular unit (NVU) has been recently proposed. In particular, the blood-brain barrier (BBB) and blood-spinal cord barrier (BSCB), two NVU key players, may be affected during the development of chronic pain; in particular, transient permeabilization of the barrier is suggested by several inflammatory- and nerve-injury-based pain models, and we argue that the clarification of molecular BBB/BSCB permeabilization events will shed new light in understanding chronic pain mechanisms. Possible biases in experiments supporting this theory and its translational potentials are discussed. Moving beyond an exclusive focus on the role of the endothelium, we propose that our understanding of the mechanisms subserving chronic pain will benefit from the extension of research efforts to the NVU as a whole. In this view, the available evidence on the interaction between analgesic drugs and the NVU is here reviewed. Chronic pain comorbidities, such as neuroinflammatory and neurodegenerative diseases, are also discussed in view of NVU changes, together with innovative pharmacological solutions targeting NVU components in chronic pain treatment.

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“…A third group of proteins involved in tight junction formation is made up by junction adhesion molecules which also contain intra-and extracellular domains [28][29][30]. Decreased expression of several tight junction proteins occurs in brain tissue of patients with epilepsy as well as in epileptic animals and is associated with increased BBB permeability [31][32][33][34][35][36].…”

Section: Blood-brain Barrier -Morphology and Transport Mechanismsmentioning

confidence: 99%

The blood–brain barrier—Gatekeeper to neuronal homeostasis: Clinical implications in the setting of stroke

Schoknecht

David

Heinemann

2015

Seminars in Cell & Developmental Biology

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Effects of levetiracetam on blood-brain barrier disturbances following hyperthermia-induced seizures in rats with cortical dysplasia

Cited by 23 publications

References 51 publications

Additional Antiepileptic Mechanisms of Levetiracetam in Lithium-Pilocarpine Treated Rats

Additional Antiepileptic Mechanisms of Levetiracetam in Lithium-Pilocarpine Treated Rats

Neurovascular Unit in Chronic Pain

The blood–brain barrier—Gatekeeper to neuronal homeostasis: Clinical implications in the setting of stroke

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