Mefloquine selectively increases asynchronous acetylcholine release from motor nerve terminals

@article{McArdle2006MefloquineSI,
  title={Mefloquine selectively increases asynchronous acetylcholine release from motor nerve terminals},
  author={Joseph J. McArdle and Lawrence C. Sellin and Kathleen M. Coakley and Joseph G. Potian and Kormakur Hognason},
  journal={Neuropharmacology},
  year={2006},
  volume={50},
  pages={345-353}
}

Mefloquine enhances nigral gamma-aminobutyric acid release via inhibition of cholinesterase.

Data suggest that mefloquine enhances GABA release through its inhibition of cholinesterase, which allows accumulation of endogenously released acetylcholine, which activates neuronal nicotinic receptors on GABAergic nerve terminals.

Mefloquine Enhances Nigral γ-Aminobutyric Acid Release via Inhibition of Cholinesterase

Data suggest that mefloquine enhances GABA release through its inhibition of cholinesterase, which allows accumulation of endogenously released acetylcholine, which activates neuronal nicotinic receptors on GABAergic nerve terminals.

Review of the mechanism underlying mefloquine-induced neurotoxicity

The aim of this study was to review the literature on the neurotoxic mechanisms of action of mefloquine to better understand its potential toxicity in the central nervous system, highlighting the mechanisms that lead to its psychiatric disorders.

Acute and chronic effects of botulinum neurotoxin a on the mammalian neuromuscular junction

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Mefloquine effects on ventral tegmental area dopamine and GABA neuron inhibition: A physiologic role for connexin‐36 GAP junctions

It is suggested that blocking Cx36 GJs increases VTA DA neuron inhibition, and that GJs play in key role in regulating inhibition of VTADA neurons.

Effect of Zidovudine and its Interaction with Rocuronium on Neuromuscular Transmission

Zidovudine affects the neuromuscular transmission and interaction studies were carried out with rocuronium, finding no conclusive interaction between roCuronium and zidvudine.

Cocaine and Mefloquine-induced Acute Effects in Ventral Tegmental Area Dopamine and GABA Neurons

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The findings suggest cocaine reduces activity-dependent GABA release on DA neurons in the VTA, and that cocaine’s usedependent blockade of VTA GABA neuron voltage-sensitive sodium channels (VSSCs) may synergize with its DAT inhibiting properties to enhance mesolimbic DA transmission implicated in cocaine reinforcement.

Effects of Constitutive and Acute Connexin 36 Deficiency on Brain-Wide Susceptibility to PTZ-Induced Neuronal Hyperactivity

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