Activity-related extracellular potassium transients in the neonatal rat spinal cord: an in vitro study.
Transient increases and decreases in extracellular potassium (delta[K+]o) were recorded from the gray matter of hemisected, neonatal rat spinal cords isolated from 3, 4, 9- and 10-day-old pups. delta[K+]o were evoked in both the ventral and dorsal regions of the gray matter by electrical stimulation. In the ventral horn, repetitive stimulation of the ventral root was required to elicit detectable delta[K+]o. By contrast, single dorsal root stimuli evoked clear delta[K+]o. In the dorsal horn, single orthodromic stimuli elicited delta[K+]o as large as 4-5 mM from a baseline of 4.5 mM. With repetitive stimulation the [K+]o reached, but never exceeded, a ceiling of 10-11 mM. Undershoots were seen only after repetitive stimulation. Spontaneous delta[K+]o were observed in the ventral horn and were well correlated with ventral root activity. Spontaneous delta[K+]o were rare in the dorsal cord, but were recorded after bath application of apamin or tetraethylammonium. The magnitude and distribution of evoked K+ transients and postsynaptic components of the evoked field potential were well correlated in both the dorsal and the ventral gray matter. delta[K+]o were reversibly blocked by 1 mM CdCl2 in the bath and diminished by 1 mM BaCl2. Bath application of mephenesin, apamin or tetraethylammonium diminished evoked delta[K+]o in a stimulus-dependent manner. In apamin and tetraethylammonium, decreases from control responses were largest with high intensity stimulation, the opposite was the case with mephenesin. These results are interpreted in terms of the spinal circuits activated by high- and low-intensity electrical stimulation. We conclude that activity-related delta[K+]o in neonatal spinal cord are large enough to modulate neuronal electrical activity and the [K+]o is well regulated compared to other immature CNS regions studied. Thus, local increases in [K+]o may, by modulating neuronal activity, play a role in neonatal spinal cord developmental processes.
Walton
K D
KD
Department of Physiology and Biophysics, New York University Medical Center, NY 10016.
Chesler
M
M
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D000831:Animals, Newborn / Q000502:physiology; D001030:Apamin / Q000494:pharmacology; D002104:Cadmium / Q000494:pharmacology; D019256:Cadmium Chloride; D004558:Electric Stimulation; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology*; D009046:Motor Neurons / Q000187:drug effects / Q000502:physiology; D011188:Potassium / Q000502:physiology*; D051381:Rats; D013116:Spinal Cord / Q000187:drug effects / Q000502:physiology*; D013757:Tetraethylammonium Compounds / Q000494:pharmacology
D007473:Ion Channels; D013757:Tetraethylammonium Compounds; D002104:Cadmium; D001030:Apamin; D019256:Cadmium Chloride; D011188:Potassium