The clearing of excess potassium from extracellular space in spinal cord and cerebral cortex

Cordingley, Gary E.; Somjen, George G.

doi:10.1016/0006-8993(78)90886-7

Cited by 99 publications

(58 citation statements)

References 30 publications

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“…This discrepancy may be due to efflux of cytoplasmic K+ caused by reduced Na-K pumping at low [K+]. levels (Gardner-Medwin, 1983) (Cordingley & Somjen, 1978). Since the analysis of the relation between extracellular voltage and concentration gradients given above should apply also to these results they suggest ratios of transcellular to extracellular flux of 18: 1 and 22: 1, compared to the ratio 5: 1 indicated in the present studies on rat brain.…”

Section: Discussionmentioning

confidence: 43%

A study of the mechanisms by which potassium moves through brain tissue in the rat.

Gardner-Medwin¹

1983

The Journal of Physiology

136

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Section: Discussionmentioning

confidence: 43%

A study of the mechanisms by which potassium moves through brain tissue in the rat.

Gardner-Medwin¹

1983

The Journal of Physiology

136

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“…However, some extracellular accumulation of po tassium may occur during intense stimulation, but levels will increase < 1 mmollL (Heinemann and Lux, 1977). Therefore, energy is consumed mainly by the neuronal Na, K-ATPase and for the active removal of the slightly elevated potassium from the extracellular space (Cordingley and Somjen, 1978). During spreading depression, there is also a tran- , -2 0 -6 -I.…”

Section: Discussionmentioning

confidence: 99%

Metabolic and Hemodynamic Activation of Postischemic Rat Brain by Cortical Spreading Depression

Köcher

1990

J Cereb Blood Flow Metab

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Summary: Following transient ischemia of the brain, the coupling between somatosensory activation and the he modynamic-metabolic response is abolished for a certain period despite the partial recovery of somatosensory evoked responses. To determine whether this disturbance is due to alterations of the stimulus-induced neuronal ex citation or to a breakdown of the coupling mechanisms, cortical spreading depression was used as a metabolic stimulus in rats before and after ischemia. Adult rats were subjected to 30 min of global forebrain ischemia and 3-6 h of recirculation. EEG, cortical direct current (DC) po tential, and laser-Doppler flow were continuously re corded. Local CBF (LCBF), local CMR g lc (LCMR g1 c), regional tissue contents of ATP, glucose, and lactate, and regional pH were determined by quantitative autoradiog raphy, substrate-induced bioluminescence, and fluorom etry. Amplitude and frequency of the DC shifts did not differ between groups. In control animals, spreading de pression induced a 77% rise in cortical glucose consump tion, a 66% rise in lactate content, and a drop in tissue pH of 0.3 unit. ATP and glucose contents were not depleted.If cerebral global ischemia exceeds 10 min, long lasting impairment of neurological function will re sult. In the four-vessel occlusion model in rats that allows long-term survival after an ischemic impact, disturbances of sensorimotor integration and motor performance persist for at least 2 days (Combs and D' Alecy, 1987), although the supply of energy-rich phosphates is replenished within 1 h (Pulsinelli and Duffy, 1983;Naruse et al. , 1984).It has been suggested that despite the early re covery of energy metabolism, impaired neurologi- 564During the passage of DC shifts, transient increases «2 min) in laser-Doppler flow were observed, followed by a post-spreading depression hypoperfusion. A comparable although less expressed pattern of hemodynamic and metabolic changes was observed in the postischemic rats. Although baseline LCMR g lc was depressed after isch emia, it was activated 47% during spreading depression. Lactate increased by 26%, pH decreased by 0.3 unit, and ATP and glucose remained unchanged. The extent of the transient increase in laser-Doppler flow did not differ from that of the control group, and a post-spreading de pression hypoperfusion was also found. The results dem onstrate that the postischemic brain may, although to a lesser degree, cover additional energy demands. The pre viously observed suppression of functional activation af ter ischemia is probably caused by both alterations in afferent synaptic transmission and subsequent neuronal excitation and the diminution of the metabolic response to a local stimulus as observed during spreading depres sion.

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“…, 1978) and cerebral Na+ ,K+-ATPase activity (Yoshimura, 1973;Wu and Phillis, 1975;van der Krogt and Belfroid, 1980;Swann et aI., 1981). In addition, movements of K+ in brain extracellular fluid appear to be sensitive to factors that affect the integrity of active transport systems including Na+, K+-ATPase (Krnjevic and Morris, 1975;Cordingley and Somjen, 1978;Sick and Kreisman, 1981) and oxidative metabolism (Morris, 1974;Sick and Kreisman, 1981).…”

Section: Discussionmentioning

confidence: 99%

Does Endogenous Norepinephrine Regulate Potassium Homeostasis and Metabolism in Rat Cerebral Cortex?

Sick

Hertz

LaManna

et al. 1982

J Cereb Blood Flow Metab

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Summary:The role of endogenous cerebral norepinephrine (NE) as a mod ulator of transmembrane cation transport and energy metabolism was evalu ated by monitoring extracellular potassium ion activity ([K+jo) in vivo and by measuring cortical Na+,K+-ATPase activity and oxygen consumption in vitro, Ipsilateral cortical NE was depleted by unilateral 6-hydroxydopamine (6-OHDA) lesions of the locus ceruleus (LC), The contralateral cortex was used for control measurements, NE depletion had no effect on resting levels of cortical [K "jo or on the rate of K + removal from the extracellular space fol lowing direct cortical stimulation. There was also no effect of NE depletion on Na+,K+-ATPase activity in cortical homogenates nor on oxygen consumption of cortical slices over a wide range of K+ concentrations, These results indicate that central NE depletion does not influence movements of cortical K+ either directly through an influence on Na+,K+-ATPase activity or indirectly through effects on oxidative metabolism. It is probable, therefore, that previously de scribed effects of NE on cortical oxidative metabolism are mediated through changes in cerebral perfusion and/or modification of substrate availability in l'ivo.

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The clearing of excess potassium from extracellular space in spinal cord and cerebral cortex

Cited by 99 publications

References 30 publications

A study of the mechanisms by which potassium moves through brain tissue in the rat.

A study of the mechanisms by which potassium moves through brain tissue in the rat.

Metabolic and Hemodynamic Activation of Postischemic Rat Brain by Cortical Spreading Depression

Does Endogenous Norepinephrine Regulate Potassium Homeostasis and Metabolism in Rat Cerebral Cortex?

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