Open AccessGlutamatergic and GABAergic reactivity and cognition in 22q11.2 deletion syndrome and healthy volunteers: A randomized double-blind 7-Tesla pharmacological MRS study
Author(s) -
Claudia Vingerhoets,
Desmond H. Y. Tse,
Mathilde van Oudenaren,
Dennis Hernaus,
Esther van Duin,
Janneke Zinkstok,
Johannes G. Ramaekers,
Jacobus F.A. Jansen,
Gráinne McAlonan,
Thérèse van Amelsvoort
Publication year - 2020
Publication title -
journal of psychopharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.333
H-Index - 114
eISSN - 1461-7285
pISSN - 0269-8811
DOI - 10.1177/0269881120922977
Subject(s) - riluzole , glutamate receptor , glutamatergic , glutamine , gabaergic , pharmacology , metabolite , neuroscience , placebo , psychology , nmda receptor , medicine , anesthesia , chemistry , inhibitory postsynaptic potential , biochemistry , amino acid , receptor , alternative medicine , pathology
22q11.2 deletion syndrome (22q11.2DS) is associated with impaired cognitive functioning. Glutamatergic pathways have been linked with cognition and are hypothesized to be disrupted in 22q11.2DS patients, possibly 'shifting' the excitatory (glutamate)/inhibitory (GABA) balance. Hence, the glutamate/GABA balance may constitute a target for pharmacological treatment. We aimed to examine alterations of glutamate/GABA metabolites in 22q11.2DS in vivo using riluzole, a compound with glutamate/GABA-modulating action, as pharmacological challenge.