Anticonvulsant activity of BmK AS, a sodium channel site 4-specific modulator

Zhao, Rong; Weng, Chun-Chun; Qi, Feng; Chen, Lulan; Zhang, Xu-Ying; Wang, Yun; Ji, Yonghua

doi:10.1016/j.yebeh.2010.12.006

Cited by 20 publications

(15 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Neuron is an excitable cell, in which the action potential is an important feature property of its excitability and transmitting of the excitation. Abnormal action potential firing such as epileptiform burst firing, caused by varies reasons such as convulsant stimulation [17], [22], would induce abnormal epileptiform activity dependent cellular cascade change even to trigger cell apoptosis [22], [32]. We indeed observed in our current study that, without estrogen receptor stimulation during the culture process in phenol red free medium, cultured hippocampal neurons were having high probability to have epileptiform burst firing.…”

Section: Discussionsupporting

confidence: 63%

U-Shape Suppressive Effect of Phenol Red on the Epileptiform Burst Activity via Activation of Estrogen Receptors in Primary Hippocampal Culture

Liu

Chen

et al. 2013

PLoS ONE

Self Cite

View full text Add to dashboard Cite

Phenol red is widely used in cell culture as a pH indicator. Recently, it also has been reported to have estrogen-like bioactivity and be capable of promoting cell proliferation in different cell lines. However, the effect of phenol red on primary neuronal culture has never been investigated. By using patch clamp technique, we demonstrated that hippocampal pyramidal neurons cultured in neurobasal medium containing no phenol red had large depolarization-associated epileptiform bursting activities, which were rarely seen in neurons cultured in phenol red-containing medium. Further experiment data indicate that the suppressive effect of the phenol red on the abnormal epileptiform burst neuronal activities was U-shape dose related, with the most effective concentration at 28 µM. In addition, this concentration related inhibitory effect of phenol red on the epileptiform neuronal discharges was mimicked by 17-β-estradiol, an estrogen receptor agonist, and inhibited by ICI-182,780, an estrogen receptor antagonist. Our results suggest that estrogen receptor activation by phenol red in the culture medium prevents formation of abnormal, epileptiform burst activity. These studies highlight the importance of phenol red as estrogen receptor stimulator and cautions of careful use of phenol red in cell culture media.

show abstract

Section: Discussionsupporting

confidence: 63%

U-Shape Suppressive Effect of Phenol Red on the Epileptiform Burst Activity via Activation of Estrogen Receptors in Primary Hippocampal Culture

Liu

Chen

et al. 2013

PLoS ONE

Self Cite

View full text Add to dashboard Cite

show abstract

“…Some venom toxins with anticonvulsant potential act on these voltage-dependent ion channels. The alpha-type neurotoxins BmK IT2 and BmK AS are sodium channels modulators (Zhao et al 2008(Zhao et al , 2011, and the ω-conotoxins GVIA and MVIIA are N-type calcium channel antagonists (Gasior et al 2007).…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2015

View full text Add to dashboard Cite

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.

show abstract

“…The recurrent seizure assessment was based on the latency for spontaneous seizure behavior, the seizure score, and the seizure number. The seizure score in an animal was calculated based on the maximal behavioral seizure grade observed [15, 16]. …”

Section: Methodsmentioning

confidence: 99%

Downregulated GABA and BDNF-TrkB Pathway in Chronic Cyclothiazide Seizure Model

et al. 2014

Self Cite

View full text Add to dashboard Cite

Cyclothiazide (CTZ) has been reported to simultaneously enhance glutamate receptor excitation and inhibit GABAA receptor inhibition, and in turn it evokes epileptiform activities in hippocampal neurons. It has also been shown to acutely induce epileptic seizure behavior in freely moving rats. However, whether CTZ induced seizure rats could develop to have recurrent seizure still remains unknown. In the current study, we demonstrated that 46% of the CTZ induced seizure rats developed to have recurrent seizure behavior as well as epileptic EEG with a starting latency between 2 weeks and several months. In those chronic seizure rats 6 months after the seizure induction by the CTZ, our immunohistochemistry results showed that both GAD and GAT-1 were significantly decreased across CA1, CA3, and dentate gyrus area of the hippocampus studied. In addition, both BDNF and its receptor TrkB were also decreased in hippocampus of the chronic CTZ seizure rats. Our results indicate that CTZ induced seizure is capable of developing to have recurrent seizure, and the decreased GABA synthesis and transport as well as the impaired BDNF-TrkB signaling pathway may contribute to the development of the recurrent seizure. Thus, CTZ seizure rats may provide a novel animal model for epilepsy study and anticonvulsant drug testing in the future.

show abstract

Anticonvulsant activity of BmK AS, a sodium channel site 4-specific modulator

Cited by 20 publications

References 32 publications

U-Shape Suppressive Effect of Phenol Red on the Epileptiform Burst Activity via Activation of Estrogen Receptors in Primary Hippocampal Culture

U-Shape Suppressive Effect of Phenol Red on the Epileptiform Burst Activity via Activation of Estrogen Receptors in Primary Hippocampal Culture

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

Downregulated GABA and BDNF-TrkB Pathway in Chronic Cyclothiazide Seizure Model

Contact Info

Product

Resources

About