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Does sodium oxybate inhibit brain dopamine release in humans? An exploratory neuroimaging study
Author(s) -
Kish Stephen J,
O'Leary Gerald,
Mamelak Mortimer,
McCluskey Tina,
Warsh Jerry J,
Shapiro Colin,
Bies Robert,
Yu Yifan,
Pollock Bruce,
Tong Junchao,
Boileau Isabelle
Publication year - 2021
Publication title -
human psychopharmacology: clinical and experimental
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.461
H-Index - 78
eISSN - 1099-1077
pISSN - 0885-6222
DOI - 10.1002/hup.2791
Subject(s) - raclopride , dopamine , binding potential , ventral striatum , psychology , striatum , dopamine receptor d2 , medicine , narcolepsy , endocrinology , neuroscience , neurology
Objective To establish in an exploratory neuroimaging study whether γ‐hydroxybutyrate (sodium oxybate [SO]), a sedative, anti‐narcoleptic drug with abuse potential, transiently inhibits striatal dopamine release in the human. Methods Ten healthy participants (30 years; 6M, 4F) and one participant with narcolepsy received a baseline positron emission tomography scan of [C‐11]raclopride, a D2/3 dopamine receptor radioligand sensitive to dopamine occupancy, followed approximately one week later by an oral sedative 3g dose of SO and two [C‐11]raclopride scans (1 h, 7 h post SO). Plasma SO levels and drowsiness duration were assessed. Results No significant changes were detected in [C‐11]raclopride binding in striatum overall 1 or 7 h after SO, but a small non‐significant increase in [C‐11]raclopride binding, implying decreased dopamine occupancy, was noted in limbic striatal subdivision at one hour (+6.5%; p uncorrected = 0.045; +13.2%, narcolepsy participant), returning to baseline at 7 h. A positive correlation was observed between drowsiness duration and percent change in [C‐11]raclopride binding in limbic striatum ( r  = 0.73; p  = 0.017). Conclusions We did not find evidence in this sample of human subjects of a robust striatal dopamine change, as was reported in non‐human primates. Our preliminary data, requiring extension, suggest that a 3g sedative SO dose might cause slight transient inhibition of dopamine release in limbic striatum.

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