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Glutamate receptor 1 Glutamate receptor 2 Glutamate [NMDA] receptor subunit epsilon-1 Glutamate [NMDA] receptor subunit zeta-1 Glutamate [NMDA] receptor subunit epsilon-3 Glutamate [NMDA] receptor subunit epsilon-2 Glutamate [NMDA] receptor subunit epsilon-4 Glutamate [NMDA] receptor subunit 3A Glutamate [NMDA] receptor subunit 3B Sodium channel subunit beta-1 Potassium voltage-gated channel subfamily D member 2 Kv channel- interacting protein 2 Voltage- dependent P/Q-type calcium channel subunit alpha-1A Voltage- dependent L-type calcium channel subunit beta-1 Voltage- dependent calcium channel subunit alpha-2/delta-2 Voltage- dependent T-type calcium channel subunit alpha-1H Voltage- dependent T-type calcium channel subunit alpha-1G Multidrug resistance- associated protein 4 Solute carrier family 22 member 11 Aldo-keto reductase family 1 member C3 Sodium channel protein type 10 subunit alpha Glutamate Licarbazepine K+ K+ Ca+ Ca+ Glutamate Na+ Na+ Ca+ Ca+ Ca+ Ca+ Na+ Na+ Licarbazepine Licarbazepine Oxcarbazepine Oxcarbazepine Oxcarbazepine Depolarization axon width = 9 Presynaptic Neuron Post-synaptic Neuron Since no action potential arrives to the nerve terminal, calcium entry does not occur and neurotransmitters like glutamate are not released from synaptic vesicles into the synapse. Licarbazepine blocks the channel, preventing the entry of sodium into the neuron. Membrane Potential (mV) 0 40 -70 Hyperpolarization Repolarization Peak action potential Resting potential The depolarization phase of the action potential is inhibited, therefore, the action potential cannot be geenrated. ACTION POTENTIAL Time (ms) Endoplasmic Reticulum Hepatocyte Oxcarbazepine is converted to Licarbazepine which is responsible for the pharmacological action. Synaptic Vesicle The post synaptic neuron is unable to depolarize due to the inhibition of neurotransmitter release. Oxcarbazepine is administered as an oral tablet
Mitochondria Endoplasmic Reticulum GRIA1 GRIA2 GRIN2A GRIN1 GRIN2C GRIN2B GRIN2D GRIN3A GRIN3B SCN1B KCND2 KCNIP2 CACNA1A CACNB1 CACNA2D2 CACNA1H CACNA1G ABCC4 SLC22A11 AKR1C3 SCN10A Glutamate Licarbazepine Potassium Potassium Calcium Calcium Glutamate Sodium Sodium Calcium Calcium Calcium Calcium Sodium Sodium Licarbazepine Licarbazepine Oxcarbazepine Oxcarbazepine Oxcarbazepine
GRIA1 GRIA2 GRIN2A GRIN1 GRIN2C GRIN2B GRIN2D GRIN3A GRIN3B SCN1B KCND2 KCNIP2 CACNA1A CACNB1 CACNA2D2 CACNA1H CACNA1G ABCC4 SLC22A11 AKR1C3 SCN10A Gluta MHD K+ K+ Ca+ Ca+ Gluta Na+ Na+ Ca+ Ca+ Ca+ Ca+ Na+ Na+ MHD MHD Oxcarb Oxcarb Oxcarb Depolarization axon width = 9 Presynaptic Neuron Post-synaptic Neuron Since no action potential arrives to the nerve terminal, calcium entry does not occur and neurotransmitters like glutamate are not released from synaptic vesicles into the synapse. Licarbazepine blocks the channel, preventing the entry of sodium into the neuron. Membrane Potential (mV) 0 40 -70 Hyperpolarization Repolarization Peak action potential Resting potential The depolarization phase of the action potential is inhibited, therefore, the action potential cannot be geenrated. ACTION POTENTIAL Time (ms) Endoplasmic Reticulum Hepatocyte Oxcarbazepine is converted to Licarbazepine which is responsible for the pharmacological action. Synaptic Vesicle The post synaptic neuron is unable to depolarize due to the inhibition of neurotransmitter release. Oxcarbazepine is administered as an oral tablet
Mitochondria Endoplasmic Reticulum GRIA1 GRIA2 GRIN2A GRIN1 GRIN2C GRIN2B GRIN2D GRIN3A GRIN3B SCN1B KCND2 KCNIP2 CACNA1A CACNB1 CACNA2D2 CACNA1H CACNA1G ABCC4 SLC22A11 AKR1C3 SCN10A Gluta MHD K+ K+ Ca2+ Ca2+ Gluta Na+ Na+ Ca2+ Ca2+ Ca2+ Ca2+ Na+ Na+ MHD MHD Oxcarb Oxcarb Oxcarb