Antiepileptogenic and anticonvulsant activity of interleukin-1β in amygdala-kindled rats

Sayyah, Mohammad; Beheshti, Siamak; Shokrgozar, Mohammad Ali; Eslamifar, Ali; Deljoo, Z.; Khabiri, Alireza; Rohani, Ali Haeri

doi:10.1016/j.expneurol.2004.08.032

Cited by 48 publications

(33 citation statements)

References 37 publications

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“…However, data from the current study suggests that the neuroprotective effects of IL-1 inhibition may be injury specific and may not be a process that can be generalized. While IL-1β has been implicated in neurodegeneration, there are also observations indicating that, under certain conditions, IL-1 can contribute beneficial effects (Brenneman et al, 1992), including regulation of ischemic tolerance in CA1 hippocampal neurons (Ohtsuki et al, 1996), anti-convulsive properties such as, slowing the rate of amygdala kindling (Sayyah et al, 2005), and the induction of various neurotrophic factors. In addition, previous evidence reveals that IL-1 demonstrates properties signifying its role as a modulator of memory functions, including effects on long term potentiation and synaptic transmission (Bellinger et al, 1993), as well as, regulating N-methyl-D-aspartate (NMDA) receptors (Ma et al, 2002) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors (Lai et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

The type 1 interleukin 1 receptor is not required for the death of murine hippocampal dentate granule cells and microglia activation

Harry¹,

Funk²,

d’Hellencourt³

et al. 2008

Brain Research

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Alterations in the inflammatory process, neuronal death, and glia response have been observed under manipulation of the interleukin-1 (IL-1) cytokine and subsequent signaling through the type 1 IL-1 receptor (IL-1R1). To investigate the influence of IL-1R1 activation in the pathophysiology of a chemical-induced injury to the murine hippocampus, we examined the level and pattern of neuronal death and neuroinflammation in 25-day-old male mice exposed to trimethyltin hydroxide (2.0 mg/ kg, i.p.). In IL-1R1 null (IL-1R1−/−) mice, the pattern and severity of dentate granule cell death was similar as compared to wild type mice. In both groups of mice, mRNA levels for TNFα and MIP-1α were elevated and the early activation of microglia, including their ability to progress to a phagocytic phenotype, was maintained. Compared to WT mice, IL-1R1−/− mice displayed a limited glial fibrillary acidic protein (GFAP) astrocytic response, as well as a preferential induction in mRNA levels of Fas signaling components. Cumulatively, these results indicate that IL-1R1 activation is not necessary for TMT-induced death of dentate granule neurons or local activation of microglia; however, IL-1R1 signaling is involved in mediating the structural response of astrocytes to injury and may also regulate apoptotic mechanisms by influencing Fas signaling components.

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Section: Discussionmentioning

confidence: 99%

The type 1 interleukin 1 receptor is not required for the death of murine hippocampal dentate granule cells and microglia activation

Harry¹,

Funk²,

d’Hellencourt³

et al. 2008

Brain Research

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“…26 Although most studies demonstrate proconvulsive effects of IL-1b, this cytokine has an anti-convulsant effect in amygdala-kindled rats. 27 These differential results might be dose-dependent. 28 Similarly, the roles of IL-6 and TNF-a remain controversial since there are studies demonstrating either proand anti-convulsive effects or neuroprotection and neurotoxicity.…”

Section: Role Of Cytokines In Animal Models Of Epilepsymentioning

confidence: 87%

Insights into inflammation and epilepsy from the basic and clinical sciences

Silveira

Oliveira

Teixeira

2012

Journal of Clinical Neuroscience

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“…A number of studies demonstrate both anticonvulsant and antidepressant action of other active substances and mediators, for instance: pro-inflammatory cytokines [46,47], neurotrophins (mainly BDNF) [48], allopregnanolone [49], nitric oxide [50].…”

Section: Gaba (γ-Aminobutyric Acid)mentioning

confidence: 99%

Pharmacokinetic/pharmacodynamic considerations for epilepsy – depression comorbidities

Banach

Popławska

Błaszczyk³

et al. 2016

Expert Opinion on Drug Metabolism & Toxicology

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The preclinical data may provide valuable clues on how to combine these two groups of drugs - antidepressant drugs neutral or potentiating the anticonvulsant action of antiepileptics are recommended in this regard. Avoidance of antidepressants clearly decreasing the convulsive threshold or decreasing the anticonvulsant efficacy of antiepileptic drugs (f.e. bupropion or mianserin) in patients with epilepsy is recommended.

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Antiepileptogenic and anticonvulsant activity of interleukin-1β in amygdala-kindled rats

Cited by 48 publications

References 37 publications

The type 1 interleukin 1 receptor is not required for the death of murine hippocampal dentate granule cells and microglia activation

The type 1 interleukin 1 receptor is not required for the death of murine hippocampal dentate granule cells and microglia activation

Insights into inflammation and epilepsy from the basic and clinical sciences

Pharmacokinetic/pharmacodynamic considerations for epilepsy – depression comorbidities

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