The epileptic seizures induced by BmK I, a modulator of sodium channels

Bai, Zhan-Tao; Zhao, Rong; Zhang, Xu-Ying; Chen, Jin; Liu, Tong; Ji, Yonghua

doi:10.1016/j.expneurol.2005.09.006

Cited by 24 publications

(27 citation statements)

References 61 publications

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“…A seizure episode was defined as the time window from the beginning of seizure onset to the recovery from the seizure. The seizure score in an animal was calculated based on the maximal behavioral seizure grade observed (Bai et al ., 2006, Zhao et al ., 2008). Behavioral seizure of grade IV and V are considered to represent kindled motor seizures as previously reported by Lothman and Williamson (1994).…”

Section: Surgerymentioning

confidence: 99%

Cyclothiazide induces seizure behavior in freely moving rats

Kong¹,

Qian²,

Liu³

et al. 2010

Brain Research

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We have previously demonstrated that cyclothiazide (CTZ) is a potent convulsant drug inducing robust epileptiform activity in hippocampal neurons both in vitro and in vivo. Here we further establish an animal model for CTZ-induced behavioral seizures in freely moving rats. Microinjection of CTZ into left ventricle dose-dependently induced robust seizure behaviors within three hours after administration. At doses of 0.75 μmol, CTZ induced Racine score IV-V seizure behaviors in 71% (n=14) of the rats tested. In addition, CTZ also induced epileptiform EEG activity accompanying behavioral seizures. The convulsant action of CTZ on both behavior and EEG was blocked by pre-treatment with clinical anticonvulsant drug diazepam (n=5). In conclusion, our results demonstrate that CTZ is capable of inducing behavioural seizures in intact animals. Since CTZ acts on both GABAergic and glutamatergic systems, this new animal epilepsy model will be useful for anticonvulsant drug testing and general epilepsy research.

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Section: Surgerymentioning

confidence: 99%

Cyclothiazide induces seizure behavior in freely moving rats

Kong¹,

Qian²,

Liu³

et al. 2010

Brain Research

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“…Further, compounds isolated from venoms can also elicit seizures in rodents. For example, the BmK I, an alpha-like scorpion neurotoxin isolated from the venom of Buthus martensi Karsch, induced seizures in rats by intrahippocampal administration (Bai et al 2006). Moreover, the TsTX-I, a scorpion neurotoxin isolated from T. serrulatus venom, promoted short and long epileptic-like discharges when injected in the hippocampus of rats (Teixeira et al 2010).…”

Section: Introductionmentioning

confidence: 98%

“…Epilepsy is an episodic disorder of the nervous system resulting from the excessive synchronous and sustained discharge of a group of neurons (Bai et al 2006). This disorder affects at least 50 million people worldwide, and approximately 20-30% of the patients develop a chronic epilepsy, in which the seizures persist despite careful monitored treatment with antiepileptic drugs (Löscher 1997).…”

Section: Introductionmentioning

confidence: 99%

Pro- and Anticonvulsant Effects of the Ant Dinoponera quadriceps (Kempf) Venom in Mice

et al. 2015

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Epilepsy affects at least 50 million people worldwide, and the available treatment is associated with various side effects. Approximately 20-30% of the patients develop seizures that persist despite careful monitored treatment with antiepileptic drugs. Thus, there is a clear need for the development of new antiepileptic drugs, and the venoms can be an excellent source of probes. In this context, while there are studies on venoms from snakes, scorpions, and spiders, little is known regarding venom from ants. The aim of this study was to investigate the potential pro- and anticonvulsant effects of the venom from the ant Dinoponera quadriceps (Kempf) in Swiss mice. After the injection of the crude venom (DqTx-5, 50, and 500 mg/mL) in the lateral ventricle of mice, we observed a reduction of exploration and grooming behaviors, as well as an increase in immobility duration. In addition, the crude venom induced procursive behavior and tonic-clonic seizures at the highest concentration. Conversely, the preadministration of the denatured venom (AbDq) at the concentration of 2 mg/mL protected the animals against tonic-clonic seizures (66.7%) and death (100%) induced by administration of bicuculline. Taken together, the findings demonstrate that D. quadriceps venom might be potential source of new pro- and anticonvulsants molecules.

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“…Moreover, it was found that the efficacy of BmK venom in treating pain and epilepsy depends upon the type of BmK of scorpion venom and how the agent interacts with the sodium channel (Tan et al, 2001;Chen & Ji, 2002;Bai et al, 2003Bai et al, , 2006Zhang et al, 2003). Therefore, elucidation of the functional and structural interactions between scorpion neurotoxins and sodium channels may provide a promising target for the design of drugs in treatment of pain and epilepsy.…”

Section: Effects Of Bmknjx11 a Bioactive Polypeptide Purified From Bmentioning

confidence: 97%

Effects ofBmKNJX11, A Bioactive Polypeptide Purified fromButhus martensiKarsch, on Sodium Channels in Rat Dorsal Root Ganglion Neurons

Wang

Cheng

et al. 2009

Journal of Toxicology and Environmental Health, Part A

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A long-chain polypeptide BmKNJX11 was purified from the venom of Asian scorpion Buthus martensi Karsch (BmK) by a combination of gel filtration, ion-exchange chromatography, and reverse-phase high-performance liquid chromatography. The molecular mass was found to be 7036.85 Da by electrospray ionization mass spectrometry. The first 15 N-terminal amino acid sequence of BmKNJX11 was determined to be GRDAY IADSE NCTYT by Edman degradation. With whole cell recording, BmKNJX11 inhibited tetrodotoxin-sensitive voltage-gated sodium channels (TTX-S VGSC) in freshly isolated rat dorsal root ganglion (DRG) neurons in a concentration- and voltage-dependent manner. At a concentration of 40 mug/ml BmKNJX11 lowered the activation threshold and produced negative shifting of TTX-S sodium current (I(Na)) activation curve. In addition, BmKNJX11 induced shifting of the steady-state inactivation curve to the left, delayed the recovery of TTX-S I(Na) from inactivation, and also reduced the fraction of available sodium channels. These results suggested that BmKNJX11 might exert effects on VGSC by binding to a specific site. Considering that TTX-S VGSC expressed in DRG neurons play a critical role in nociceptive transmission, the interaction of BmKNJX11 with TTX-S VGSC might lead to a change in excitability of nociceptive afferent fibers, which may be involved in the observed peripheral pain expression.

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The epileptic seizures induced by BmK I, a modulator of sodium channels

Cited by 24 publications

References 61 publications

Cyclothiazide induces seizure behavior in freely moving rats

Cyclothiazide induces seizure behavior in freely moving rats

Pro- and Anticonvulsant Effects of the Ant Dinoponera quadriceps (Kempf) Venom in Mice

Effects ofBmKNJX11, A Bioactive Polypeptide Purified fromButhus martensiKarsch, on Sodium Channels in Rat Dorsal Root Ganglion Neurons

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