Nitrous Oxide and Xenon Prevent Amphetamine-Induced Carrier-Mediated Dopamine Release in a Memantine-Like Fashion and Protect Against Behavioral Sensitization

  title={Nitrous Oxide and Xenon Prevent Amphetamine-Induced Carrier-Mediated Dopamine Release in a Memantine-Like Fashion and Protect Against Behavioral Sensitization},
  author={H{\'e}l{\`e}ne N. David and Marc Ansseau and Marc Lemaire and Jacques H Abraini},
  journal={Biological Psychiatry},

Argon blocks the expression of locomotor sensitization to amphetamine through antagonism at the vesicular monoamine transporter-2 and mu-opioid receptor in the nucleus accumbens

We investigated the effects of the noble gas argon on the expression of locomotor sensitization to amphetamine and amphetamine-induced changes in dopamine release and mu-opioid neurotransmission in

Argon prevents the development of locomotor sensitization to amphetamine and amphetamine-induced changes in mu opioid receptor in the nucleus accumbens

It is indicated that argon inhibits the development of both locomotor sensitization and mu opioid receptor activation induced by repeated administration of amphetamine.

Short‐term development of behavioral sensitization to amphetamine requires N‐methyl‐D‐aspartate‐ and nicotinic‐dependent mechanisms in the nucleus accumbens

It is reported that the concomitant blockade of glutamatergic and nicotinic ionotropic receptors in the core of the nucleus accumbens blocks the development of behavioral sensitization to amphetamine and further abolishes the increase in extracellular dopamine release induced by amphetamine in the nucleus Accumbens.

The effect of sertindole on behavioural sensitisation to methamphetamine in mice

The present study assessed whether memantine would influence behavioural sensitisation to the stimulatory effects of methampheta- mine on mouse locomotion.

Mechanism of block and behavioral effects of the N-methyl-D-aspartate receptor antagonists memantine and ketamine

The research shows NMDA receptors possess a second binding site at which memantine, but not ketamine, can inhibit activity, and the dramatic effect physiological concentrations of magnesium has on the ability of these drugs to inhibit NMDA receptor activity.

In vivo evidence for functional NMDA receptor blockade by memantine in rat hippocampal neurons

Therapeutic doses of memantine are able to antagonize NMDA receptor-mediated activity in the principal cells of the hippocampus in vivo, i.e. in the presence of physiological concentrations of Mg2+.

Implication of NMDA receptors in behavioural sensitization to psychostimulants: a short review.



MK-801 prevents alterations in the mesoaccumbens dopamine system associated with behavioral sensitization to amphetamine

  • Menas WolfFJ WhiteX.-T. Hu
  • Biology, Psychology
    The Journal of neuroscience : the official journal of the Society for Neuroscience
  • 1994
Coadministration of the noncompetitive NMDA antagonist MK-801 with amphetamine was examined to suggest NMDA receptor stimulation is required for the development of both autoreceptor subsensitivity in the VTA and postsynaptic D1 receptor supers sensitivity in the NAc during repeated amphetamine treatment, and a dissociation can be demonstrated between the intensity of Amphetamine-stimulated behavioral responses and amphetamine- Stimulated DA release in theNAc.

Amphetamine and Other Weak Bases Act to Promote Reverse Transport of Dopamine in Ventral Midbrain Neurons

The weak base mechanism of amphetamine action, in which amphetamine reduces vesicular pH gradients resulting in increased cytoplasmic dopamine that promotes reverse transport, is extended.

Amphetamine Distorts Stimulation-Dependent Dopamine Overflow: Effects on D2 Autoreceptors, Transporters, and Synaptic Vesicle Stores

Amphetamine (AMPH) is known to raise extracellular dopamine (DA) levels by inducing stimulation-independent DA efflux via reverse transport through the DA transporter and by inhibiting DA re-uptake.

Amphetamine: evaluation of d- and l-isomers as releasing agents and uptake inhibitors for 3H-dopamine and 3H-norepinephrine in slices of rat neostriatum and cerebral cortex.

It is concluded that in the cortex, d-amphetamine can act both to release and to block uptake of 3H-norepinephrine, and in the neostriatum, there is releasing action of 2H-dopamine by d- methamphetamine, but the apparent blockade of "uptake" is of questionable significance and appears to result from the release of previously accumulated3H- dopamine.

Previous Exposure to Amphetamine Enhances the Subsequent Locomotor Response to a D1 Dopamine Receptor Agonist When Glutamate Reuptake Is Inhibited

In the NAcc, increased GLU neurotransmission and activation of D(1) DA receptors, neither of which is by itself sufficient, together contribute to the expression of locomotor sensitization by AMPH are suggested.

Amphetamine attenuates the stimulated release of dopamine in vivo.

In isolated striatal synaptic vesicles, amphetamine is found to block dopamine uptake and induce its release and in vitro evidence provides a possible mechanism for the observed in vivo actions of amphetamine.

Mechanisms of Amphetamine Action Revealed in Mice Lacking the Dopamine Transporter

Findings suggest that in the absence of pharmacological manipulation, such as the use of amphetamine, endogenous cytoplasmic DA normally does not reach sufficient concentrations to reverse the DAT.