Adenosine receptor activation is responsible for prolonged depression of synaptic transmission after spreading depolarization in brain slices

Highlights ► We examined suppression of synaptic potentials following spreading depolarization (SD). ► Initial inhibition was explained by a short period of action potential failure. ► Presynaptic A1 receptor activation was responsible for the majority of suppression. ► Accumulation of adenosine may...

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Bibliographic Details
Published in:	Neuroscience Vol. 223; pp. 365 - 376
Main Authors:	Lindquist, B.E, Shuttleworth, C.W
Format:	Journal Article
Language:	English
Published:	Amsterdam Elsevier Ltd 25-10-2012 Elsevier
Subjects:	A1 receptors adenosine Adenosine - metabolism Adenosine A1 Receptor Antagonists - pharmacology Animals Biological and medical sciences Biophysics Brain - cytology Brain - drug effects Brain - physiology CA1 CA1 Region, Hippocampal - drug effects CA1 Region, Hippocampal - physiology DC shift Electric Stimulation Excitatory Amino Acid Antagonists - pharmacology Excitatory Postsynaptic Potentials - drug effects Excitatory Postsynaptic Potentials - physiology Fundamental and applied biological sciences. Psychology In Vitro Techniques Mice Mice, Inbred C57BL Nerve Fibers - drug effects Nerve Fibers - physiology Neural Inhibition - drug effects Neural Inhibition - physiology Neurology Potassium Chloride - pharmacology Quinoxalines - pharmacology Receptors, Purinergic P1 - physiology spreading depression Theophylline - analogs & derivatives Theophylline - pharmacology Time Factors Vertebrates: nervous system and sense organs voltage-inactivation Xanthines - pharmacology adenosine 5′ triphosphate A1R anoxic depolarization DMSO erythro-9-(2-hydroxy-3-nonyl)adenine hydrochloride A1 receptors 8-cyclopentyl-1,3-dimethylxanthine potassium chloride oxygen-glucose deprivation 4-(-2-[7-amino-2-(2-furyl)(1,2,4)triazolo(2,3-a)(1,3,5triazin-5-yl-amino]ethyl)phenol DC shift DNQX SD CA1 dimethyl sulfoxide fEPSP PPR voltage-inactivation 6-cyclopentyl adenosine CSD KCl 8-CPT TTX cortical spreading depression DPCPX paired-pulse ratio Cornu Ammonis area 1 8-cyclopentyl-1,3-dipropylxanthine AD 6,7-dinitroquinoxaline-2,3-dione adenosine A1 receptor IOS OGD artificial cerebrospinal fluid intrinsic optical signal adenosine spreading depression direct current field excitatory postsynaptic potential CPA EHNA spreading depolarization aCSF ZM 241385 tetrodotoxin ATP DC Adenosine Central nervous system Encephalon Depolarization Synaptic transmission Synaptic depression Adenosine receptor Spreading depression Biological receptor
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Summary:	Highlights ► We examined suppression of synaptic potentials following spreading depolarization (SD). ► Initial inhibition was explained by a short period of action potential failure. ► Presynaptic A1 receptor activation was responsible for the majority of suppression. ► Accumulation of adenosine may link metabolic demand of SD with synaptic depression.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0306-4522 1873-7544
DOI:	10.1016/j.neuroscience.2012.07.053