Evidence of the antiepileptic potential of amiloride with neuropharmacological benefits in rodent models of epilepsy and behavior

Ali, Atif; Ahmad, Feroz; Pillai, K. K.; Vohora, Divya

doi:10.1016/j.yebeh.2004.01.005

Cited by 84 publications

(66 citation statements)

References 26 publications

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“…Additionally, amiloride can cross the blood-brain barrier and has proven beneficial in the treatment of several neuropathological conditions including brain ischemia (Xiong et al, 2004), multiple sclerosis (Friese et al, 2007;Vergo et al, 2011), seizures (Ali et al, 2004(Ali et al, , 2005(Ali et al, , 2007N'Gouemo, 2008), Parkinson's disease (Arias et al, 2008), gliomas (Sipos et al, 2000), and in an in vitro model of spinal cord dorsal column compression injury (Agrawal and Fehlings, 1996). However, the therapeutic potential of amiloride has not been tested in a clinically relevant animal model of contusion spinal cord injury (SCI).…”

mentioning

confidence: 99%

Amiloride Improves Locomotor Recovery after Spinal Cord Injury

Durham-Lee

Mokkapati²,

Johnson³

et al. 2011

Journal of Neurotrauma

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Amiloride is a drug approved by the United States Food and Drug Administration, which has shown neuroprotective effects in different neuropathological conditions, including brain injury or brain ischemia, but has not been tested in spinal cord injury (SCI). We tested amiloride's therapeutic potential in a clinically relevant rat model of contusion SCI inflicted at the thoracic segment T10. Rats receiving daily administration of amiloride from 24 h to 35 days after SCI exhibited a significant improvement in hindlimb locomotor ability at 21, 28, and 35 days after injury, when compared to vehicle-treated SCI rats. Rats receiving amiloride treatment also exhibited a significant increase in myelin oligodendrocyte glycoprotein (MOG) levels 35 days after SCI at the site of injury (T10) when compared to vehicle-treated controls, which indicated a partial reverse in the decrease of MOG observed with injury. Our data indicate that higher levels of MOG correlate with improved locomotor recovery after SCI, and that this may explain the beneficial effects of amiloride after SCI. Given that amiloride treatment after SCI caused a significant preservation of myelin levels, and improved locomotor recovery, it should be considered as a possible therapeutic intervention after SCI.

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confidence: 99%

Amiloride Improves Locomotor Recovery after Spinal Cord Injury

Durham-Lee

Mokkapati²,

Johnson³

et al. 2011

Journal of Neurotrauma

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“…Grip strength in all the animals was measured for evaluation of neuromuscular strength, as described by Ali et al [15]. The neuromuscular strength tests were carried out between 9:00 a.m. and 4:00 p.m. under standard laboratory conditions.…”

Section: Grip Strength Studymentioning

confidence: 99%

Protection by Vanadium, a Contemporary Treatment Approach to Both Diabetes and Focal Cerebral Ischemia in Rats

Liu

Zhao

et al. 2011

Biol Trace Elem Res

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There is now substantial epidemiological evidence that diabetes is a risk factor for cerebrovascular disease. The protection by vanadium from focal cerebral ischemia in diabetic rats was studied in this paper. Rats with streptozotocin-induced diabetes were subjected to middle cerebral artery occlusion followed by 4 weeks of administration of 0.6 mg/ml sodium orthovanadate in drinking water. Vanadium significantly improved the outcome in diabetic rats after cerebral ischemia and reperfusion in terms of neurobehavioral function. Vanadium reduces brain damage in streptozotocin-induced diabetic rats by imitating action of insulin.

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“…Babinski and colleagues first reported a change of ASIC1a and ASIC2b expression in the hippocampal area following pilocarpine-induced epilepticus (Biagini et al, 2001), suggesting that the channels containing ASIC1a and ASIC2b subunits might play a role in the pathology of epilepsy. Later on, a number of studies showed that amiloride, a commonly used non-selective ASIC blocker, has an anticonvulsant property in vivo in pilocarpine and pentylenetetrazole models of seizures (Ali et al, 2004(Ali et al, , 2006N'Gouemo, 2008), suggesting that ASIC activation might be proconvulsant. However, since amiloride also inhibits a number of other channels and ion exchange systems, these findings do not define ASICs as a specific target for amiloride to achieve its anti-epileptic action.…”

Section: Asic Activation and Epileptic Seizure Activitymentioning

confidence: 99%