Neurometabolic alterations in the nucleus accumbens of smokers assessed with 1 H magnetic resonance spectroscopy: The role of glutamate and neuroinflammation
Autor: | Lea M. Hulka, Anke Henning, Andreas Hock, Erich Seifritz, Colette A. Steinegger, Niklaus Zoelch, Marcus Herdener, Etna J.E. Engeli |
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Rok vydání: | 2021 |
Předmět: |
Pharmacology
medicine.medical_specialty business.industry Glutamate receptor Medicine (miscellaneous) Craving Nucleus accumbens medicine.disease 030227 psychiatry Glutamine 03 medical and health sciences Psychiatry and Mental health Glutamatergic 0302 clinical medicine Nicotine withdrawal Endocrinology Glutamate homeostasis Internal medicine medicine medicine.symptom Prefrontal cortex business 030217 neurology & neurosurgery |
Zdroj: | Addiction Biology |
ISSN: | 1369-1600 1355-6215 |
DOI: | 10.1111/adb.13027 |
Popis: | Tobacco use is one of the leading causes of premature death and morbidity worldwide. For smokers trying to quit, relapse rates are high, even after prolonged periods of abstinence. Recent findings in animal models highlight the role of alterations in glutamatergic projections from the prefrontal cortex onto the nucleus accumbens (NAc) in relapse vulnerability. Moreover, inflammatory responses in the NAc have been reported during withdrawal. A novel proton magnetic resonance spectroscopy (1H-MRS) protocol was applied in humans to measure molar concentrations for glutamate, its sum with glutamine (Glx), and myoinositol plus glycine (mI + Gly) in the NAc (19 smokers, 20 matched controls). Smokers were measured at baseline and during withdrawal and satiation. No difference between groups or smoking states was found for glutamate or Glx, but, in smokers, stronger craving and more severe nicotine dependence were associated with lower baseline glutamate and Glx levels, respectively. Interestingly, mI + Gly concentrations were higher during withdrawal than baseline and correlated negatively with nicotine dependence severity and pack years of smoking. The lack of glutamatergic changes between groups and smoking states may imply that glutamate homeostasis is not significantly altered in smokers or that changes are too small for detection by 1H-MRS. Moreover, the observed increase in mI + Gly may imply that neuroinflammatory processes occur in the NAc during nicotine withdrawal. These findings shed light on neurobiological relapse mechanisms in smokers and may provide the opportunity to develop more effective treatment options targeting the glutamate and neuroinflammation system. |
Databáze: | OpenAIRE |
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