Mouth breathing increases the pentylenetetrazole-induced seizure threshold in mice: A role for ATP-sensitive potassium channels

Niaki, Seyed Esfandiar Akhavan; Shafaroodi, Hamed; Ghasemi, Mehdi; Shakiba, Bijan; Fakhimi, Ali; Dehpour, Ahmad Reza

doi:10.1016/j.yebeh.2008.04.013

Cited by 25 publications

(8 citation statements)

References 48 publications

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“…(14). In addition, it has been recently reported that K ATP channel openers, such as cromakalim and diazoxide, increase clonic seizures induced by pentylenetetrazole in mice (9,29). The role of K channel openers in seizure has been shown in several clinical and animal studies.…”

Section: Treatmentmentioning

confidence: 99%

RETRACTED ARTICLE: Cromakalim, a Potassium Channel Opener, Ameliorates Organophosphate- and Carbamate-Induced Seizures in Mice

et al. 2017

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Background: Organophosphates (OPs) and carbamates are acetylcholine esterase inhibitors (AChEIs), which can cause seizure and death. The anticonvulsant properties of potassium channel openers, including cromakalim, have been determined in previous studies. Methods: In the present experiment, the possible effects of cromakalim on convulsion and death, induced by OPs and carbamates, were studied in mice. Dichlorvos as an OP compound (50 mg/kg) and physostigmine as a carbamate (2 mg/kg) were used to induce seizure in animals.

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Section: Treatmentmentioning

confidence: 99%

RETRACTED ARTICLE: Cromakalim, a Potassium Channel Opener, Ameliorates Organophosphate- and Carbamate-Induced Seizures in Mice

et al. 2017

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“…Indeed, adaptation to mouth breathing has been observed in children with upper airway obstruction (Trosman and Trosman, 2017). Although mice are described as obligate nose breathers (Harkema and Morgan, 1996), adaptation to mouth breathing (Agrawal et al, 2008;Niaki et al, 2008) or gasping (Khurana and Thach, 1996) has been observed in the event of nasal obstruction. Assuming that adaptation occurs in Bmp7 ncko mice, further experiments will be necessary to distinguish adaptation to mechanical and/or central control of breathing.…”

Section: Disease Models and Mechanisms • Dmm • Accepted Manuscriptmentioning

confidence: 99%

Neural crest-specific loss ofBmp7leads to midfacial hypoplasia, nasal airway obstruction and disordered breathing, modeling obstructive sleep apnea

Baddam

Biancardi

Roth

et al. 2021

Disease Models &Amp; Mechanisms

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Pediatric obstructive sleep apnea (OSA), a relatively common sleep-related breathing disorder (SRBD) affecting approximately 1-5% of children, is often caused by anatomical obstruction and/or collapse of the nasal and/or pharyngeal airways. The resulting sleep disruption and intermittent hypoxia lead to various systemic morbidities. Predicting the development of OSA from craniofacial features alone is currently not possible and a controversy remains if upper airway obstruction facilitates reduced midfacial growth or vice-versa. Currently, there is no rodent model that recapitulates both the development of craniofacial abnormalities and upper airway obstruction to address these questions. Here, we describe that mice with a neural crest-specific deletion of Bmp7 (Bmp7ncko) present with shorter, more acute angled cranial base, midfacial hypoplasia, nasal septum deviation, turbinate swelling and branching defects, and nasal airway obstruction. Interestingly, several of these craniofacial features develop after birth during periods of rapid midfacial growth and precede the development of an upper airway obstruction. We identified that in this rodent model, no single feature appeared to predict upper airway obstruction, but the sum of those features resulted in a reduced breathing frequency, apneas and overall reduced oxygen consumption. Metabolomics analysis of serum from peripheral blood identified increased levels of hydroxyproline, a metabolite upregulated under hypoxic conditions. As this model recapitulates many features observed in OSA, it offers unique opportunities for studying how upper airway obstruction affects breathing physiology and leads to systemic morbidities.

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“…K ATP channels locate at either the plasma membrane (sK ATP ) or the inner mitochondrial membrane (mitoK ATP ). Basic studies have indicated that mitoK ATP channel openers can be effective in prevention of neural death in cerebral ischemia [1,2], AD [3] and epilepsy [4,5]. However, the mechanisms of neuroprotection still are not completely understood.…”

Section: Introductionmentioning

confidence: 99%

Effects of Nicorandil in Neuroprotective Activation of PI3K/AKT Pathways in a Cellular Model of Alzheimer's Disease

et al. 2013

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Nicorandil, an ATP-sensitive potassium (K_ATP) channel opener, is known to have protective effects on ischemic injury in heart and brain. One of the most important protective mechanisms is the anti-apoptotic effect on cardiomyocytes and neurons. This study explored the anti-apoptotic effect of nicorandil against neurotoxicity in SH-SY5Y cells overexpressing the Swedish mutant APP (APPsw) and the possible mechanisms involved. We used SH-SY5Y cells transiently transfected with APPsw as a cellular model of Alzheimer's disease. Cells were treated with nicorandil (0.1, 0.5, 1 mM) for 24 h with and without glibenclamide (10 μM), a K_ATP channel inhibitor. The cells were then collected for MTT, apoptosis assay, and Western blot. In addition, we also investigated the potential involvement of the PI3K/Akt pathway in nicorandil-mediated neuroprotection of APPsw cells. Our results showed that nicorandil dose-dependently increased cell viability and reduced the rate of apoptosis as measured by MTT assay and annexin V/PI staining. Western blot showed that nicorandil could upregulate Bcl-2 levels and downregulate Bax and caspase-3 expression. Further studies showed that nicorandil increased the levels of phospho-Akt and upregulated element-binding protein activity by PI3K activation. Applying a PI3K inhibitor, LY294002 blocked the protection. All these findings suggest that nicorandil might be a potential treatment option for Alzheimer's disease.

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Mouth breathing increases the pentylenetetrazole-induced seizure threshold in mice: A role for ATP-sensitive potassium channels

Cited by 25 publications

References 48 publications

RETRACTED ARTICLE: Cromakalim, a Potassium Channel Opener, Ameliorates Organophosphate- and Carbamate-Induced Seizures in Mice

RETRACTED ARTICLE: Cromakalim, a Potassium Channel Opener, Ameliorates Organophosphate- and Carbamate-Induced Seizures in Mice

Neural crest-specific loss ofBmp7leads to midfacial hypoplasia, nasal airway obstruction and disordered breathing, modeling obstructive sleep apnea

Effects of Nicorandil in Neuroprotective Activation of PI3K/AKT Pathways in a Cellular Model of Alzheimer's Disease

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