The Nucleoside-Transport Inhibitor, Mioflazine, Increases Recovery of Hippocampal Synaptic Transmission and Energy-Rich Metabolites after Normothermic Global Ischemia
Adenosine reduces transmitter release1, hyperpolarizes the membrane potentials and increases the duration of afterhyperpolarizations.2 In addition to these inhibitory effects on neuronal activity adenosine also couples local metabolism to blood flow.3 Adenosine may be a candidate endogenous anti-ischemic agent since it is found extracellularly in large quantities during ischemia.4 We previously demonstrated that specific nucleoside-transport inhibitors (NTI’s), like mioflazine, increase the duration of the effects of exogenous adenosine; and have gradually developing adenosine-like actions in hippocampal tissue.5 Since the effects of the NTI were reversible by adding adenosine deaminase, this study suggested that the compounds increase endogenous adenosine levels by blocking its re-uptake.5
KeywordsDentate Gyrus Creatine Phosphate Adenosine Triphosphate Energy Metabolite Local Metabolism
Unable to display preview. Download preview PDF.
- 1.P. Schubert and H. Mitzdorf Exp. Neurol. 90: 549–557 (1985).Google Scholar
- 2.R.W. Greene and H.L. Haas J. Physiol. (Lond.) 366: 119–127 (1985).Google Scholar
- 3.T.V. Dunwiddie Int. Rev. Neurobiol. 27: 64–139 (1984).Google Scholar
- 5.D. Ashton, R. Willems, E. De Prins, H. Van Belle, and A. Wauquier Eur. J. Pharmacol. 142: 403–408 (1987).Google Scholar