AustralieFrV1, Main, Merge, bibRecord, 003531

Selective Augmentation of Striatal Functional Connectivity Following NMDA Receptor Antagonism: Implications for Psychosis

Identifieur interne : 003531 ( Main/Merge ); précédent : 003530; suivant : 003532

Selective Augmentation of Striatal Functional Connectivity Following NMDA Receptor Antagonism: Implications for Psychosis

Auteurs : Orwa Dandash [Australie] ; Ben J. Harrison [Australie] ; Ram Adapa [Royaume-Uni] ; Raphael Gaillard [France] ; Francesco Giorlando [Australie] ; Stephen J. Wood [Australie, Royaume-Uni] ; Paul C. Fletcher [Royaume-Uni] ; Alex Fornito [Australie]

Source :

Neuropsychopharmacology [ 0893-133X ] ; 2014.

RBID : PMC:4246009

Descripteurs français

KwdFr :
- Adulte, Corps strié (), Corps strié (physiologie), Cortex préfrontal (), Femelle, Humains, Imagerie par résonance magnétique, Jeune adulte, Kétamine (pharmacologie), Lobe frontal (), Lobe frontal (physiologie), Mâle, Mésencéphale (), Mésencéphale (physiologie), Méthode en double aveugle, Neuroimagerie fonctionnelle, Noyau accumbens (), Noyau accumbens (physiologie), Psychoses toxiques (physiopathologie), Récepteurs du N-méthyl-D-aspartate (antagonistes et inhibiteurs), Thalamus (), Thalamus (physiologie), Voies nerveuses (), Voies nerveuses (physiologie).
MESH :
- antagonistes et inhibiteurs : Récepteurs du N-méthyl-D-aspartate.
- pharmacologie : Kétamine.
- physiologie : Corps strié, Lobe frontal, Mésencéphale, Noyau accumbens, Thalamus, Voies nerveuses.
- physiopathologie : Psychoses toxiques.
- Adulte, Corps strié, Cortex préfrontal, Femelle, Humains, Imagerie par résonance magnétique, Jeune adulte, Lobe frontal, Mâle, Mésencéphale, Méthode en double aveugle, Neuroimagerie fonctionnelle, Noyau accumbens, Thalamus, Voies nerveuses.

English descriptors

KwdEn :
- Adult, Corpus Striatum (drug effects), Corpus Striatum (physiology), Double-Blind Method, Female, Frontal Lobe (drug effects), Frontal Lobe (physiology), Functional Neuroimaging, Humans, Ketamine (pharmacology), Magnetic Resonance Imaging, Male, Mesencephalon (drug effects), Mesencephalon (physiology), Neural Pathways (drug effects), Neural Pathways (physiology), Nucleus Accumbens (drug effects), Nucleus Accumbens (physiology), Prefrontal Cortex (drug effects), Psychoses, Substance-Induced (physiopathology), Receptors, N-Methyl-D-Aspartate (antagonists & inhibitors), Thalamus (drug effects), Thalamus (physiology), Young Adult.
MESH :
- chemical , antagonists & inhibitors : Receptors, N-Methyl-D-Aspartate.
- chemical , pharmacology : Ketamine.
- drug effects : Corpus Striatum, Frontal Lobe, Mesencephalon, Neural Pathways, Nucleus Accumbens, Prefrontal Cortex, Thalamus.
- physiology : Corpus Striatum, Frontal Lobe, Mesencephalon, Neural Pathways, Nucleus Accumbens, Thalamus.
- physiopathology : Psychoses, Substance-Induced.
- Adult, Double-Blind Method, Female, Functional Neuroimaging, Humans, Magnetic Resonance Imaging, Male, Young Adult.

Abstract

The psychotomimetic effect of the N-methyl-D-aspartate receptor (NMDAR) antagonist ketamine is thought to arise from a functional modulation of the brain's fronto-striato-thalamic (FST) circuits. Animal models suggest a pronounced effect on ventral ‘limbic' FST systems, although recent work in patients with psychosis and high-risk individuals suggests specific alterations of dorsal ‘associative' FST circuits. Here, we used functional magnetic resonance imaging to investigate the effects of a subanesthetic dose of ketamine on measures of functional connectivity as indexed by the temporal coherence of spontaneous neural activity in both dorsal and ventral FST circuits, as well as their symptom correlates. We adopted a placebo-controlled, double-blind, randomized, repeated-measures design in which 19 healthy participants received either an intravenous saline infusion or a racemic mixture of ketamine (100 ng/ml) separated by at least 1 week. Compared with placebo, ketamine increased functional connectivity between the dorsal caudate and both the thalamus and midbrain bilaterally. Ketamine additionally increased functional connectivity of the ventral striatum/nucleus accumbens and ventromedial prefrontal cortex. Both connectivity increases significantly correlated with the psychosis-like and dissociative symptoms under ketamine. Importantly, dorsal caudate connectivity with the ventrolateral thalamus and subthalamic nucleus showed inverse correlation with ketamine-induced symptomatology, pointing to a possible resilience role to disturbances in FST circuits. Although consistent with the role of FST in mediating psychosis, these findings contrast with previous research in clinical samples by suggesting that acute NMDAR antagonism may lead to psychosis-like experiences via a mechanism that is distinct from that implicated in frank psychotic illness.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4246009

DOI: 10.1038/npp.2014.210
PubMed: 25141922
PubMed Central: 4246009

Links to Exploration step

PMC:4246009

Le document en format XML

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<front><div type="abstract" xml:lang="en"><p>The psychotomimetic effect of the <italic>N</italic>
-methyl-<sc>D</sc>
-aspartate receptor (NMDAR) antagonist ketamine is thought to arise from a functional modulation of the brain's fronto-striato-thalamic (FST) circuits. Animal models suggest a pronounced effect on ventral ‘limbic' FST systems, although recent work in patients with psychosis and high-risk individuals suggests specific alterations of dorsal ‘associative' FST circuits. Here, we used functional magnetic resonance imaging to investigate the effects of a subanesthetic dose of ketamine on measures of functional connectivity as indexed by the temporal coherence of spontaneous neural activity in both dorsal and ventral FST circuits, as well as their symptom correlates. We adopted a placebo-controlled, double-blind, randomized, repeated-measures design in which 19 healthy participants received either an intravenous saline infusion or a racemic mixture of ketamine (100 ng/ml) separated by at least 1 week. Compared with placebo, ketamine increased functional connectivity between the dorsal caudate and both the thalamus and midbrain bilaterally. Ketamine additionally increased functional connectivity of the ventral striatum/nucleus accumbens and ventromedial prefrontal cortex. Both connectivity increases significantly correlated with the psychosis-like and dissociative symptoms under ketamine. Importantly, dorsal caudate connectivity with the ventrolateral thalamus and subthalamic nucleus showed inverse correlation with ketamine-induced symptomatology, pointing to a possible resilience role to disturbances in FST circuits. Although consistent with the role of FST in mediating psychosis, these findings contrast with previous research in clinical samples by suggesting that acute NMDAR antagonism may lead to psychosis-like experiences via a mechanism that is distinct from that implicated in frank psychotic illness.</p>
</div>
</front>
</TEI>
</record>

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Selective Augmentation of Striatal Functional Connectivity Following NMDA Receptor Antagonism: Implications for Psychosis

Selective Augmentation of Striatal Functional Connectivity Following NMDA Receptor Antagonism: Implications for Psychosis

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