Temperature dependence of extracellular ionic changes evoked by anoxia in hippocampal slices

1. Extracellular [K] and [Ca] were measured with ion-selective microelectrodes in CA1 pyramidal cell layer of rat hippocampal slices in an interface chamber. 2. Near room temperature (21-22 degrees C), brief periods of anoxia (3- to 4-min substitution of 95% N2-5% CO2 for 95% O2-5% CO2) produced very small changes in [K]o [-0.022 +/- 0.10 (SE) mM] or [Ca]o (-0.030 +/- 0.0029 mM) and were associated with only minor depression of population spikes (-22.5 +/- 11%). 3. Stratum radiatum (SR) stimulation (0.2-5 Hz) could evoke substantial increases in [K]o (by 0.2-2 mM); although variable, they were consistent in any one slice. The same stimulation regularly caused only small depressions of [Ca]o (by less than 0.1 mM, typically). 4. Also at 21-22 degrees neither stimulation nor anoxia generated more than minimal reductions in extracellular space [by 2.3 +/- 0.94%, as measured by the tetramethylammonium (TMA) method], and spreading depression (SD) occurred in only 1 out of 20 slices. 5. At 33-34 degrees C, anoxia (also for 3-4 min) consistently produced more substantial increases in [K]o (0.83 +/- 0.18 mM); but the apparent changes in [Ca]o at 33 degrees C (0.058 +/- 0.12 mM) could not with certainty be distinguished from thermoelectric artifacts. There was a severe depression of population spikes (-76 +/- 10%). 6. Although electrical stimulation evoked greater reductions in [Ca]o, increases in [K]o were 50% smaller. 7. During anoxia at 33-34 degrees C, the extracellular space was significantly reduced, by 6.1 +/- 0.9%. Moreover, in 37% of the slices, either stimulation or anoxia triggered massive increases in [K]o (greater than 10 mM) and large reductions in [Ca]o (less than 1 mM), associated with SD-like swings in focal potential. 8. It is concluded that the extracellular ionic changes evoked by brief anoxia do not contribute in a major way to the depression of synaptic transmission.

Factors Determining the Decay of K+ Potentials and Focal Potentials in the Central Nervous System

Post-tetanic undershoots in extracellular focal potential (ΔV) and K+ potential (EK) can be recorded in the cuneate nucleus and dorsal horn of Dial-anaesthetized or decerebrate cat. They are seen best at depths where the largest ΔEK and ΔV are recorded and they increase with the frequency and duration of stimulation. The very different time courses of undershoots of ΔV and ΔEK indicate two hyperpolarizing influences: first, electrogenic pumping, and later, a reduced external K+ concentration. The importance of active K+ removal in determining the amplitude and duration of ΔEK and ΔV is illustrated by their marked potentiation (as well as the disappearance of post-tetanic undershoots) induced by a lowering of blood pressure or local application of strophanthidin.

Effects of Asphyxia and Repetitive Stimulation on Intramedullary Afferent Fibers

Effects of asphyxia and of repetitive stimulation on intramedullary projections of the afferent fibers were studied in spinal cords of cats anesthetized with Nembutal. The spinal cord focal potential, elicited by dorsal root stimulation and recorded from the cord, and the antidromically conducted response of afferent fibers produced by intraspinal needle electrode stimulation and recorded from the dorsal roots, were used as indices of afferent fiber activity. The focal potential and the antidromic response from terminal presynaptic fibers disappeared with 5–6 minutes of asphyxiation. Antidromic responses from preterminal regions were less susceptible to asphyxial block. Asphyxia impaired the ability of both types of responses to follow high frequencies of stimulation. The focal potential and the antidromic responses were observed to follow similar orders of high frequency stimulation. Double pulse stimulation of intramedullary fibers demonstrated a longer refractory period of terminal regions with progressive decrease of refractoriness in more dorsally located regions. A gradient of sensitivity to asphyxia and a postresponse recovery gradient exist along the intramedullary fibers.