Effects of antiepileptic drugs on GABA release from rat and human neocortical synaptosomes

@article{Kammerer2011EffectsOA,
  title={Effects of antiepileptic drugs on GABA release from rat and human neocortical synaptosomes},
  author={Miriam Kammerer and Michael P. Rassner and Thomas M. Freiman and Thomas J. Feuerstein},
  journal={Naunyn-Schmiedeberg's Archives of Pharmacology},
  year={2011},
  volume={384},
  pages={47-57}
}
In epilepsy, allegedly, a neurotransmitter imbalance between the inhibitory GABA and the excitatory glutamate prevails. Therefore, some antiepileptic drugs (AEDs) are thought to increase GABA release. Because little is known about corresponding presynaptic effects of AEDs in the human brain, this study investigated the effects of carbamazepine, lamotrigine, phenytoin, gabapentin, pregabalin, levetiracetam, and valproate on 3H-GABA release from human neocortical synaptosomes preincubated with 3H… 

Figures and Tables from this paper

Altered transporter‐mediated neocortical GABA release in Rasmussen encephalitis
TLDR
3H‐GABA was released from neocortical synaptosomes through transporter reversal following intrasynaptosomal Na+ accumulation by veratridine that prevents inactivation of Na+ channels that resembles maximal frequency of action potentials corresponding to epileptic seizures.
The Effects of Ginsenoside Compound K Against Epilepsy by Enhancing the γ-Aminobutyric Acid Signaling Pathway
TLDR
Findings suggested that GCK exerted anti-epileptic effects by promoting the hippocampal GABA release and enhancing the GABAAR-mediated inhibitory synaptic transmission.
Inhibition of Excitatory Synaptic Transmission in Hippocampal Neurons by Levetiracetam Involves Zn2+-Dependent GABA Type A Receptor–Mediated Presynaptic Modulation
TLDR
Results clearly show that LEV removes the Zn2+-induced suppression of GABAA-mediatedpresynaptic inhibition, resulting in a presynaptic decrease in glutamate-mediated excitatory transmission, providing a novel mechanism by which LEV may inhibit neuronal activity.
The Impact of Gabapentin Administration on Brain GABA and Glutamate Concentrations: A 7T 1H-MRS Study
Gamma-aminobutyric acid (GABA) and glutamate are implicated in numerous neuropsychiatric and substance abuse conditions, but their spectral overlap with other resonances makes them a challenge to
Bupropion attenuates kainic acid-induced seizures and neuronal cell death in rat hippocampus
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 94 REFERENCES
Effects of antiepileptic drugs on glutamate release from rat and human neocortical synaptosomes
TLDR
The depression of 3H-glutamate release by carbamazepine, lamotrigine, and phenytoin may be due to inhibited synaptosomal Na+ or Ca2+ influx.
Effects of gabapentin and pregabalin on K+-evoked 3H-GABA and 3H-glutamate release from human neocortical synaptosomes
TLDR
An inhibition of glutamate release by gabapentin and pregabalin as main anticonvulsant principle is not supported by experiments, suggesting an anticonVulsant mode of action of both drugs may be the reduction of a proconvulsant exocytotic GABA release.
Effects of anticonvulsants on veratridine- and KCl-evoked glutamate release from rat cortical synaptosomes
A summary of mechanistic hypotheses of gabapentin pharmacology
Pregabalin Reduces the Release of Synaptic Vesicles from Cultured Hippocampal Neurons
TLDR
Results indicate that pregabalin treatment, at concentrations that are therapeutically relevant, slightly but significantly reduces the emptying of neurotransmitter vesicles from presynaptic sites in living neurons.
A calcium antagonistic effect of the new antiepileptic drug lamotrigine
Similar potency of carbamazepine, oxcarbazepine, and lamotrigine in inhibiting the release of glutamate and other neurotransmitters
TLDR
The hypothesis that inhibition of glutamate release is the mechanism of anticonvulsant action of lamotrigine (or carbamazepine and oxcarbazepine) is doubtful, because the drugs are markedly less potent in inhibiting the more physiologic release elicited by electrical stimulation.
A reevaluation of veratridine as a tool for studying the depolarization-induced release of neurotransmitters from nerve endings
TLDR
It is suggested that the inhibitory effect of Ca2+ on the overall release of amino acids is due to the antagonism exerted by the divalent cation on the veratridine action at the Na+ channel, whereas the depolarization itself would have slight or no importance in the case of catecholamines.
Gabapentin and vigabatrin increase GABA in the human neocortical slice
...
1
2
3
4
5
...