The neurobiology of antiepileptic drugs

No abstract is available for this paper.

• Publication year

  2004

• Venue

  Nature Reviews Neuroscience

• Publication date

  2004-07-01

• Fields of study

  Medicine

• Identifiers
  DOI 10.1038/nrn1430PMID 15208697
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Gating Effects of Mutations in the Cav3.2 T-type Calcium Channel Associated with Childhood Absence Epilepsy*

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• Cortical-area specific block of genetically determined absence seizures by ethosuximide.

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• Increased neuronal firing in computer simulations of sodium channel mutations that cause generalized epilepsy with febrile seizures plus.

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• Use-dependent inhibition of the N-methyl-D-aspartate currents by felbamate: a gating modifier with selective binding to the desensitized channels.

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• Topiramate selectively protects against seizures induced by ATPA, a GluR5 kainate receptor agonist.

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• Topiramate selectively protects against seizures induced by ATPA, a GluR5 kainate receptor agonist.

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• Ionotropic Glutamate Receptors as Therapeutic Targets

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• Is the persistent sodium current a specific target of anti-absence drugs?

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• The neurobiology of antiepileptic drugs for the treatment of nonepileptic conditions

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• Molecular basis of inherited epilepsy.

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• The synaptic vesicle protein SV2A is the binding site for the antiepileptic drug levetiracetam.

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• Valproate and sodium currents in cultured hippocampal neurons

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• Genetic variation of CACNA1H in idiopathic generalized epilepsy

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• Mechanisms of sodium channel inactivation.

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• GABA transporters and GABA-transaminase as drug targets.

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• The genetics of human epilepsy.

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• Low-Threshold Calcium Currents in Central Nervous System Neurons

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• Dynamic GABAA Receptor Subtype-Specific Modulation of the Synchrony and Duration of Thalamic Oscillations

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• Molecular physiology of low-voltage-activated t-type calcium channels.

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• Vigabatrin induces tonic inhibition via GABA transporter reversal without increasing vesicular GABA release.

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• Selective Antagonism of GluR5 Kainate-Receptor-Mediated Synaptic Currents by Topiramate in Rat Basolateral Amygdala Neurons

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• Increased Persistent Sodium Currents in Rat Entorhinal Cortex Layer V Neurons in a Post–Status Epilepticus Model of Temporal Lobe Epilepsy

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• Association between genetic variation of CACNA1H and childhood absence epilepsy

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• Differential interactions of lamotrigine and related drugs with transmembrane segment IVS6 of voltage-gated sodium channels.

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• Anticonvulsant pharmacology of voltage‐gated Na+ channels in hippocampal neurons of control and chronically epileptic rats

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• Molecular and functional changes in voltage-dependent Na(+) channels following pilocarpine-induced status epilepticus in rat dentate granule cells.

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• Selective Blockade of N‐Type Calcium Channels by Levetiracetam

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• Molecular basis of an inherited epilepsy.

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• Subthreshold sodium current from rapidly inactivating sodium channels drives spontaneous firing of tuberomammillary neurons.

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• Preferential action of gabapentin and pregabalin at P/Q‐type voltage‐sensitive calcium channels: Inhibition of K+‐evoked [3H]‐norepinephrine release from rat neocortical slices

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• Gabapentin and vigabatrin increase GABA in the human neocortical slice.

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• Molecular Determinants of Voltage-dependent Gating and Binding of Pore-blocking Drugs in Transmembrane Segment IIIS6 of the Na+ Channel α Subunit*

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• D1/D5 Dopamine Receptor Activation Differentially Modulates Rapidly Inactivating and Persistent Sodium Currents in Prefrontal Cortex Pyramidal Neurons

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• Mutant GABA(A) receptor gamma2-subunit in childhood absence epilepsy and febrile seizures.

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• Gabapentin Decreases Membrane Calcium Currents in Injured as Well as in Control Mammalian Primary Afferent Neurons

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• Paradoxical reduction of synaptic inhibition by vigabatrin.

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• Association between the α1a calcium channel gene CACNA1A and idiopathic generalized epilepsy

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• Levetiracetam does not modulate neuronal voltage-gated Na+ and T-type Ca2+ currents.

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• Lack of the burst firing of thalamocortical relay neurons and resistance to absence seizures in mice lacking α1G T-type Ca2+ channels

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• Enhanced inactivation and acceleration of activation of the sodium channel associated with epilepsy in man

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• Epilepsy, hyperalgesia, impaired memory, and loss of pre- and postsynaptic GABA(B) responses in mice lacking GABA(B(1)).

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• Block of cloned human T-type calcium channels by succinimide antiepileptic drugs.

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• Calcium Channel α2δ Subunits—Structure and Gabapentin Binding

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• Human epilepsy associated with dysfunction of the brain P/Q-type calcium channel.

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• Calcium channel alpha(2)delta subunits-structure and Gabapentin binding.

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• Mutant GABAA receptor γ2-subunit in childhood absence epilepsy and febrile seizures

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• Activation of Expressed KCNQ Potassium Currents and Native Neuronal M-Type Potassium Currents by the Anti-Convulsant Drug Retigabine

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• Effects of Gabapentin on Brain GABA, Homocarnosine, and Pyrrolidinone in Epilepsy Patients

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