Calcium and increase excitability promote tolerance against anoxia in hippocampal slices

• Published in: Brain research 1999-06, Vol.833 (1), p.20-26
• Main Authors: Pérez-Pinzón, Miguel A., Born, James G., Centeno, José M.
• Format: Article
• Language: English
• Subjects: Adaptation, Physiological - physiology; Adenosine; Animals; Anoxia; Biological and medical sciences; Calcium - physiology; Central nervous system; Conditioning (Psychology) - physiology; Cortical Spreading Depression - physiology; Electrophysiology; Evoked Potentials - drug effects; Evoked Potentials - physiology; Fundamental and applied biological sciences. Psychology; Hippocampus; Hippocampus - drug effects; Hippocampus - physiopathology; Hypoxia - physiopathology; In Vitro Techniques; Ischemia; Male; Potassium Chloride - pharmacology; Rats; Rats, Wistar; Tolerance; Vertebrates: nervous system and sense organs; Xanthines - pharmacology
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(99)01462-6

We have previously demonstrated that anoxic preconditioning (APC) protects against a subsequent otherwise `lethal' anoxic insult in hippocampal slices. Tested here are two hypotheses: (a) APC requires calcium to improve electrical recovery in hippocampal slices; and (b) mild excitation promotes preconditioning neuroprotection. Control hippocampal slices were given a single `test' anoxic insult followed by reoxygenation. Experimental slices were preconditioned by three short anoxic insults of 1 min separated by 10 min of reoxygenation. At 30 min after the third `conditioning' insult, slices underwent a `test' anoxic insult [1 min of anoxic depolarization (AD)], and then slices were reoxygenated. Evoked potentials (EPs) were recorded throughout the experiment. In other slices, APC was emulated by inducing spreading depression (as determined by a negative DC shift) with KCL or by inducing increased neuronal excitability with the excitatory agent 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) (an adenosine A1 receptor blocker). `Test' anoxic insults lasted 2 min of AD in these groups. To determine the role of calcium during APC, extracellular CaCl 2 was decreased to 0.5 mM but only during the APC episodes (`test' anoxia, 1 min of AD). EP amplitudes recovered significantly better after anoxia in preconditioned slices, and in KCl- and DPCPX-treated slices (147.2±33.3, n=8, ** p