Effects of anoxia and metabolic arrest on turtle and rat cortical neurons

• Published in: The American journal of physiology Vol. 260; no. 4 Pt 2; pp. R747 - R755
• Main Authors: Doll, C J, Hochachka, P W, Reiner, P B
• Format: Journal Article
• Language: English
• Published: United States 01-04-1991
• Subjects: Action Potentials; Animals; Cell Survival; Cerebral Cortex - cytology; Cerebral Cortex - physiology; Male; Membrane Potentials; Neurons - physiology; Ouabain - pharmacology; Oxygen - administration & dosage; Rats; Rats, Inbred Strains; Sodium-Potassium-Exchanging ATPase - metabolism; Temperature; Turtles - physiology
• ISSN: 0002-9513
• DOI: 10.1152/ajpregu.1991.260.4.R747

The responses of turtle and rat cortical pyramidal neurons to various pharmacological treatments were measured using intracellular recordings. Turtle neurons survived both anoxia and pharmacological anoxia for 180 min with no noticeable effect. Rat pyramidal neurons responded with a loss in membrane resistance, followed by a transient hyperpolarization, and a subsequent depolarization to a zero membrane potential (41.3 +/- 6.5 min, anoxia; 25.8 +/- 12.6 min, pharmacological anoxia). Metabolic arrest caused a rapid loss in membrane resistance, transient hyperpolarization, and a rapid depolarization in both turtle (4.6 +/- 1.1 min) and rat (3.1 +/- 0.5 min) neurons. Iodoacetate alone had a similar effect on the rat as metabolic arrest (6.5 +/- 0.8 min), but the turtle exhibited more prolonged survival (53.5 +/- 4.6 min). Ouabain caused a rapid depolarization in the rat cortical neuron (8.6 +/- 1.1 min), but no initial loss in membrane resistance or a hyperpolarization. These results demonstrate that the turtle neuron, which survives anoxia, is no better at surviving total metabolic inhibition than the rat neuron. In addition, anoxia takes 13 times longer to depolarize a rat cortical neuron than metabolic arrest, and neither of these treatments is totally mimicked by ouabain alone.