Premium
Imaging the neuroimmune response to alcohol exposure in adolescent baboons: a TSPO PET study using 18 F‐DPA‐714
Author(s) -
Saba Wadad,
Goutal Sébastien,
Auvity Sylvain,
Kuhnast Bertrand,
Coulon Christine,
Kouyoumdjian Virginie,
Buvat Irène,
Leroy Claire,
Tournier Nicolas
Publication year - 2018
Publication title -
addiction biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.445
H-Index - 78
eISSN - 1369-1600
pISSN - 1355-6215
DOI - 10.1111/adb.12548
Subject(s) - alcohol , ethanol , translocator protein , binge drinking , alcohol dependence , central nervous system , medicine , immune system , endocrinology , physiology , microglia , chemistry , immunology , biochemistry , alcohol consumption , inflammation
The effects of acute alcohol exposure to the central nervous system are hypothesized to involve the innate immune system. The neuroimmune response to an initial and acute alcohol exposure was investigated using translocator protein 18 kDa (TSPO) PET imaging, a non‐invasive marker of glial activation, in adolescent baboons. Three different alcohol‐naive adolescent baboons (3–4 years old, 9 to 14 kg) underwent 18 F‐DPA‐714 PET experiments before, during and 7–12 months after this initial alcohol exposure (0.7–1.0 g/l). The brain distribution of 18 F‐DPA‐714 ( V T ; in ml/cm 3 ) was estimated in several brain regions using the Logan plot analysis and the metabolite‐corrected arterial input function. Compared with alcohol‐naive animals ( V Tbrain = 3.7 ± 0.7 ml/cm 3 ), the regional V T s of 18 F‐DPA‐714 were significantly increased during alcohol exposure ( V Tbrain = 7.2 ± 0.4 ml/cm 3 ; p < 0.001). Regional V T s estimated several months after alcohol exposure ( V Tbrain = 5.7 ± 1.4 ml/cm 3 ) were lower ( p < 0.001) than those measured during alcohol exposure, but remained significantly higher ( p < 0.001) than in alcohol‐naive animals. The acute and long‐term effects of ethanol exposure were observed globally across all brain regions. Acute alcohol exposure increased the binding of 18 F‐DPA‐714 to the brain in a non‐human primate model of alcohol exposure that reflects the ‘binge drinking’ situation in adolescent individuals. The effect persisted for several months, suggesting a ‘priming’ of glial cell function after initial alcohol exposure.