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Ventral Midbrain NMDA Receptor Blockade: From Enhanced Reward and Dopamine Inactivation.

Author(s): Hernandez G, Cossette MP, Shizgal P, Rompré PP

Front Behav Neurosci. 2016;10:161 Authors: Hernandez G, Cossette MP, Shizgal P, Rompré PP

Article GUID: 27616984
Endocannabinoids promote cocaine-induced impulsivity and its rapid dopaminergic correlates.

Author(s): Hernandez G, Oleson EB, Gentry RN, Abbas Z, Bernstein DL, Arvanitogiannis A, Cheer JF

Biol Psychiatry. 2014 Mar 15;75(6):487-98 Authors: Hernandez G, Oleson EB, Gentry RN, Abbas Z, Bernstein DL, Arvanitogiannis A, Cheer JF

Article GUID: 24138924
Adolescent Exposure to Methylphenidate Increases Impulsive Choice Later in Life.

Author(s): Abbas Z, Sweet A, Hernandez G, Arvanitogiannis A

Front Behav Neurosci. 2017;11:214 Authors: Abbas Z, Sweet A, Hernandez G, Arvanitogiannis A

Article GUID: 29163086
Title:Ventral Midbrain NMDA Receptor Blockade: From Enhanced Reward and Dopamine Inactivation.
Authors:Hernandez G,  Cossette MP,  Shizgal P,  Rompré PP
Link:https://www.ncbi.nlm.nih.gov/pubmed/27616984?dopt=Abstract
DOI:10.3389/fnbeh.2016.00161
Category:Front Behav Neurosci
PMID:27616984
Dept Affiliation: PSYCHOLOGY
1 Département de Neurosciences, Université de Montréal Montréal, QC, Canada.
2 FRQ-S Research Group in Behavioral Neurobiology, Department of Psychology, Concordia University Montréal, QC, Canada.
3 Département de Neurosciences, Université de MontréalMontréal, QC, Canada; FRQ-S Research Group in Behavioral Neurobiology, Department of Psychology, Concordia UniversityMontréal, QC, Canada.

Description:

Ventral Midbrain NMDA Receptor Blockade: From Enhanced Reward and Dopamine Inactivation.

Front Behav Neurosci. 2016;10:161

Authors: Hernandez G, Cossette MP, Shizgal P, Rompré PP

Abstract

Glutamate stimulates ventral midbrain (VM) N-Methyl-D-Aspartate receptors (NMDAR) to initiate dopamine (DA) burst firing activity, a mode of discharge associated with enhanced DA release and reward. Blockade of VM NMDAR, however, enhances brain stimulation reward (BSR), the results can be explained by a reduction in the inhibitory drive on DA neurons that is also under the control of glutamate. In this study, we used fast-scan cyclic voltammetry (FSCV) in anesthetized animals to determine whether this enhancement is associated with a change in phasic DA release in the nucleus accumbens. Rats were implanted with a stimulation electrode in the dorsal-raphe (DR) and bilateral cannulae above the VM and trained to self-administer trains of electrical stimulation. The curve-shift method was used to evaluate the effect of a single dose (0.825 nmol/0.5 µl/side) of the NMDAR antagonist, (2R,4S)-4-(3-Phosphopropyl)-2-piperidinecarboxylic acid (PPPA), on reward. These animals were then anesthetized and DA release was measured during delivery of electrical stimulation before and after VM microinjection of the vehicle followed by PPPA. As expected, phasic DA release and operant responding depended similarly on the frequency of rewarding electrical stimulation. As anticipated, PPPA produced a significant reward enhancement. Unexpectedly, PPPA produced a decrease in the magnitude of DA transients at all tested frequencies. To test whether this decrease resulted from excessive activation of DA neurons, we injected apomorphine 20 min after PPPA microinjection. At a dose (100 µg s.c.) sufficient to reduce DA firing under control conditions, apomorphine restored electrical stimulation-induced DA transients. These findings show that combined electrical stimulation and VM NMDARs blockade induce DA inactivation, an effect that indirectly demonstrates that VM NMDARs blockade enhances reward by potentiating stimulation-induced excitation in the mesoaccumbens DA pathway.

PMID: 27616984 [PubMed]