hyperexcitability

NS309 is a nonselective activator of small- and intermediate-conductance Ca2+-activated K+ (SK/KCa2 and IK/KCa3.1) channels (EC50s range from 0.12-1.2 µM for SK channels and 10-90 nM for IK channels). It can also activate voltage-gated Kv11.1 channels (hE

Phenytoin (5,5-Diphenylhydantoin) is a hydantoin derivative and a non-sedative antiepileptic agent with anticonvulsant activity. It potentially acts by promoting sodium efflux from neurons in the motor cortex, reducing post-tetanic potentiation at synapses. This prevents cortical seizure foci from spreading to adjacent areas and stabilizes the threshold against hyperexcitability. Additionally, it appears to reduce muscle spindle sensitivity to stretch, causing muscle relaxation.

Rhosin hydrochloride is a specific inhibitor of the RhoA subfamily Rho GTPases and inhibits the RhoA-GEF interaction. Rhosin hydrochloride can significantly induce cell apoptosis without affecting cell cycle progression. [1]

RL648_81 is a selective activator of KCNQ2 3 channels (EC50 = 190 nM). RL648_81 can be used in studies about neuronal hyperexcitability neurologic disorders.

Olodanrigan (EMA401), a highly selective AT2R antagonist, inhibition of augmented AngII AT2R induced p38 and p42 p44 MAPK activation, and hence inhibition of DRG neuron hyperexcitability and sprouting of DRG neurons. EMA401 blocks p38, p42 p44 mitogen-activated protein kinase (MAPK) activation, neurite outgrowth in adult rat DRG neurons, and sensitization of adult rat and human DRG neurons induced by AngII. It inhibits capsaicin responses in cultured hDRG neurons.

Phenytoin (Standard) is the standard substance of Phenytoin, and it is applicable for quantitative analysis, quality control, and related research in biochemical experiments. Phenytoin (5,5-Diphenylhydantoin) is a hydantoin derivative and a non-sedative antiepileptic agent with anticonvulsant activity. Phenytoin potentially acts by promoting sodium efflux from neurons located in the motor cortex reducing post-tetanic potentiation at synapses. The reduction of potentiation prevents cortical seizure foci spreading to adjacent areas, stabilizing the threshold against hyperexcitability. In addition, this agent appears to reduce sensitivity of muscle spindles to stretch causing muscle relaxation.