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Previous studies in our laboratory have shown that nicotine exposure decreases glucose transport across the blood-brain barrier in ischemia-reperfusion conditions. We hypothesize that nicotine can also dysregulate brain parenchymal glucose utilization by altering glucose transporters with effects on sensitivity to ischemic stroke. In this study, we investigated the effects of nicotine exposure on neuronal glucose utilization using an in vitro ischemic stroke model. We also tested the effects of e-Cig vaping on ischemic brain glucose utilization using an acute brain slice technique. Primary cortical neurons and brain slices were subjected to oxygen-glucose deprivation followed by reoxygenation to mimic ischemia-reperfusion injury. We estimated brain cell glucose utilization by measuring the uptake of [ 3 H] deoxy-d-glucose. Immunofluorescence and western blotting were done to characterize glucose transporters (GLUTs) and α7 nicotinic acetylcholine receptor (nAChR) expression. Furthermore, we used a glycolytic stress test to measure the effects of nicotine exposure on neuronal glucose metabolism. We observed that short- and long-term nicotine/cotinine exposure significantly decreased neuronal glucose utilization in ischemic conditions and the non-specific nAChR antagonist, mecamylamine reversed this effect. Nicotine/cotinine exposure also decreased neuronal GLUT1 and up-regulated α7 nAChR expression and decreased glycolysis. Exposure of mice to e-Cig vapor for 7 days likewise decreases brain glucose uptake under normoxic and ischemic conditions along with down-regulation of GLUT1 and GLUT3 expressions. These data support, from a cerebrovascular perspective, that nicotine and/or e-Cig vaping induce a state of glucose deprivation at the neurovascular unit which could lead to enhanced ischemic brain injury and/or stroke risk. OPEN PRACTICES: Open Science: This manuscript was awarded with the Open Materials Badge. For more information see: https://cos.io/our-services/open-science-badges/.

Titel:	Nicotine and electronic cigarette (E-Cig) exposure decreases brain glucose utilization in ischemic stroke.
Autor/in / Beteiligte Person:	Sifat, AE ; Vaidya, B ; Kaisar, MA ; Cucullo, L ; Abbruscato, TJ
Link:	Full Text Finder (Volltext)
Zeitschrift:	Journal of neurochemistry, Jg. 147 (2018-10-01), Heft 2, S. 204-221
Veröffentlichung:	2001- : Oxford, UK : Wiley on behalf of the International Society for Neurochemistry ; <i>Original Publication</i>: New York : Raven Press, 2018
Medientyp:	academicJournal
ISSN:	1471-4159 (electronic)
DOI:	10.1111/jnc.14561
Schlagwort:	Animals Glucose deficiency Glucose Transport Proteins, Facilitative metabolism Hypoxia, Brain metabolism In Vitro Techniques Male Mice Mice, Inbred C57BL Neurons drug effects Neurons metabolism Oxygen Consumption drug effects Primary Cell Culture alpha7 Nicotinic Acetylcholine Receptor biosynthesis alpha7 Nicotinic Acetylcholine Receptor genetics Brain Ischemia metabolism Electronic Nicotine Delivery Systems Glucose metabolism Nicotine pharmacology Nicotinic Agonists pharmacology Stroke metabolism
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Research Support, N.I.H., Extramural Language: English [J Neurochem] 2018 Oct; Vol. 147 (2), pp. 204-221. <i>Date of Electronic Publication: </i>2018 Oct 18. MeSH Terms: Electronic Nicotine Delivery Systems* ; Brain Ischemia / metabolism ; Glucose / metabolism ; Nicotine / pharmacology ; Nicotinic Agonists / pharmacology ; Stroke / *metabolism ; Animals ; Glucose / deficiency ; Glucose Transport Proteins, Facilitative / metabolism ; Hypoxia, Brain / metabolism ; In Vitro Techniques ; Male ; Mice ; Mice, Inbred C57BL ; Neurons / drug effects ; Neurons / metabolism ; Oxygen Consumption / drug effects ; Primary Cell Culture ; alpha7 Nicotinic Acetylcholine Receptor / biosynthesis ; alpha7 Nicotinic Acetylcholine Receptor / genetics References: J Cereb Blood Flow Metab. 2015 Mar 31;35(4):699-705. (PMID: 25605288) ; Fluids Barriers CNS. 2015 Apr 29;12:10. 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(PMID: 11955709) Grant Information: R01 DA029121 United States DA NIDA NIH HHS; R01 NS076012 United States NS NINDS NIH HHS; R01DA8292121 United States DA NIDA NIH HHS; R01NS076012 United States NS NINDS NIH HHS Contributed Indexing: Keywords: E-cigarette; brain; glucose utilization; ischemic stroke; neuron; nicotine Substance Nomenclature: 0 (Glucose Transport Proteins, Facilitative) ; 0 (Nicotinic Agonists) ; 0 (alpha7 Nicotinic Acetylcholine Receptor) ; 6M3C89ZY6R (Nicotine) ; IY9XDZ35W2 (Glucose) Entry Date(s): Date Created: 20180801 Date Completed: 20191002 Latest Revision: 20240214 Update Code: 20240214 PubMed Central ID: PMC6394831

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Nicotine and electronic cigarette (E-Cig) exposure decreases brain glucose utilization in ischemic stroke.