Extracellular alkaline-acid-alkaline transients in the rat spinal cord evoked by peripheral stimulation

doi:10.1016/0006-8993(90)90625-L

Brain Research

Volume 512, Issue 2, 2 April 1990, Pages 181-189

https://doi.org/10.1016/0006-8993(90)90625-L Get rights and content

Abstract

Regional differences in extracellular pH (pH_e) were found in unstimulated rat spinal cord using double-barrel pH-sensitive microelectrodes. The pH_e in the lower dorsal horn (laminae III–VII) was about 7.15, i.e. by about 0.2 pH units lower than the measured in the cerebrospinal fluid. Transient acid shifts in pH_e by 0.01–0.05 pH units were found when acute nociceptive stimuli (pinch, press, heat) were applied to the hind paw. Chemical or thermal injury evoked by subcutaneous injection of turpentine or by application of 1–3 ml of hot oil onto the hindpaw produced a long-term decrease in pH_e base line in the lower dorsal horn by about 0.05–0.1 pH units. The decrease in pH_e began 2–10 min after injury and persisted for more than 2 h. Electrical nerve stimulation (10–100 Hz, 20–60 s) elicited biphasic (acid-alkaline) or triphasic (alkaline-acid-alkaline) changes in pH_e which have a similar depth profile as the concomitantly recorded increase in [K⁺]_e. An initial alkaline shift by about 0.005 pH units was found to be significantly decreased by La³⁺, an H⁺ channel blocker. The dominating acid shift by about 0.1–0.2 pH units was accelerated and increased by acetazolamide (carbonic anhydrase inhibitor) showing that the high buffering capacity of the extracellular fluid may hamper the resolution of acid perturbations. Stimulation-evoked acid shifts were blocked by amiloride, SITS, DIDS and La³⁺ and therefore have a complex mechanism which includes Na⁺/H⁺ exchange, Cl⁻/HCO₃⁻ cotransport and/or Na⁺/Cl⁻/H⁺/HCO₃⁻ antiport and H⁺ efflux through voltage-sensitive H⁺ channels. The poststimulation alkaline shift (alkaline undershoot) was blocked by ouabain and reflects coupled clearance of K⁺ and H⁺ by active transport processes.

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Activation of the Ca2+/H+ ATPase leads to a decrease in the concentration of extracellular H+ due to the outward transport of intracellular Ca2+ in exchange for extracellular H+ (Schwiening et al., 1993). In some CNS regions, e.g. in the optic nerve (Davis et al., 1987), in the spinal cord (Sykova and Svoboda, 1990), and in the cortex (Siesjö et al., 1985; Chesler and Kraig, 1987), neuronal activity induces an early acid shift. Activity-induced alkaline transients are also often followed by a slow, persistent acid shift.
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Extracellular alkaline-acid-alkaline transients in the rat spinal cord evoked by peripheral stimulation

Abstract

Neurosci. Lett.

Neuroscience

Brain Research

Neurosci. Lett.

Brain Research

Neuroscience

Brain Research

Brain Research

Brain Research

Prog. Biophys. Mol. Biol.

Neurosci. Lett.

Neurosci. Lett.

Neuroscience

Neutral carrier based hydrogen ion selective microelectrode for extra- and intracellular studies

Anal. Chem.

Electrogenic Na+/HCO3− cotransport in neuroglia

Glia

Concentration of carbon dioxide, interstitial pH and synaptic transmission in hippocampal formation of the rat

J. Physiol. (Lond.)

Intracellular pH of astrocytes increased rapidly with cortical stimulation

Am. J. Physiol.

Stimulation-evoked changes in extracellular pH, calcium and potassium activity in the frog spinal cord

Physiol. Bohemoslov.

The pH of brain extracellular fluid in the cat

J. Physiol. (Lond.)

The regulation of intracellular pH by identified glial cells and neurones in the central nervous system of the leech

J. Physiol. (Lond.)

Diffusion of weak acids across lipid bilayer membranes: effects of chemical reactions in the unstirred layers

Science

Extracellular pH, potassium, and calcium activities in progressive ischemia of rat cortex

J. Cereb. Blood Flow Metab.

Effects of the external pH on Ca channels: experimental studies and theoretical considerations using a two-site, two-ion model

Postsynaptic fall in intracellular pH induced by GABA-activated bicarbonate conductance

Nature (Lond.)

Electrogenic Na⁺/HCO₃⁻ cotransport in neuroglia