STUDIES ON Na<sup>+</sup>‐K<sup>+</sup>‐STIMULATED ATPase OF HUMAN BRAIN*

Samaha, Frederick J.

doi:10.1111/j.1471-4159.1967.tb09530.x

Cited by 29 publications

(6 citation statements)

References 29 publications

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“…Quinidine also had no significant effect on its integral (from −62.4 ± 7.2 to −50.4 ± 9.1 mV s; p = .33; n = 5 cells, 5 slices, 4 rats; Figure Dc). Thus, despite the small observed effect that may be due to quinidine itself reducing NKA activity (Samaha, ), these data do not support a role for Na + ‐gated K + channels in generating the Ca 2+ ‐independent sAHP.…”

Section: Resultsmentioning

confidence: 67%

Differential contributions of Ca²⁺‐activated K⁺ channels and Na⁺/K⁺‐ATPases to the generation of the slow afterhyperpolarization in CA1 pyramidal cells

Tiwari¹,

Mohan²,

Biala³

et al. 2018

Hippocampus

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In many types of CNS neurons, repetitive spiking produces a slow afterhyperpolarization (sAHP), providing sustained, intrinsically generated negative feedback to neuronal excitation. Changes in the sAHP have been implicated in learning behaviors, in cognitive decline in aging, and in epileptogenesis. Despite its importance in brain function, the mechanisms generating the sAHP are still controversial. Here we have addressed the roles of M‐type K+ current (I M), Ca2+‐gated K+ currents (I Ca(K)'s) and Na+/K+‐ATPases (NKAs) current to sAHP generation in adult rat CA1 pyramidal cells maintained at near‐physiological temperature (35 °C). No evidence for I M contribution to the sAHP was found in these neurons. Both I Ca(K)'s and NKA current contributed to sAHP generation, the latter being the predominant generator of the sAHP, particularly when evoked with short trains of spikes. Of the different NKA isoenzymes, α1‐NKA played the key role, endowing the sAHP a steep voltage‐dependence. Thus normal and pathological changes in α1‐NKA expression or function may affect cognitive processes by modulating the inhibitory efficacy of the sAHP.

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Section: Resultsmentioning

confidence: 67%

Differential contributions of Ca²⁺‐activated K⁺ channels and Na⁺/K⁺‐ATPases to the generation of the slow afterhyperpolarization in CA1 pyramidal cells

Tiwari¹,

Mohan²,

Biala³

et al. 2018

Hippocampus

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“…Our fits of post‐stimulus recovery of [K + ] o from longer duration stimuli were performed over a longer time frame so the measurements of τ slow from these longer stimuli may more accurately reflect the true time constant of the axonal pumps. These points, and the fact that increasing stimulus duration increases the size of pH o transients (Ransom et al 1986), a parameter that modulates pump activity (Samaha, 1967), complicates evaluation of the effects of stimulus duration on τ slow .…”

Section: Discussionmentioning

confidence: 99%

Activity‐dependent extracellular K⁺ accumulation in rat optic nerve: the role of glial and axonal Na⁺ pumps

Ransom

Sontheimer

2000

The Journal of Physiology

184

199

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We measured activity‐dependent changes in [K+]o with K+‐selective microelectrodes in adult rat optic nerve, a CNS white matter tract, to investigate the factors responsible for post‐stimulus recovery of [K+]o. Post‐stimulus recovery of [K+]o followed a double‐exponential time course with an initial, fast time constant, τfast, of 0.9 ± 0.2 s (mean ±s.d.) and a later, slow time constant, τslow, of 4.2 ± 1 s following a 1 s, 100 Hz stimulus. τfast, but not τslow, decreased with increasing activity‐dependent rises in [K+]o. τslow, but not τfast, increased with increasing stimulus duration. Post‐stimulus recovery of [K+]o was temperature sensitive. The apparent temperature coefficients (Q10, 27–37°C) for the fast and slow components following a 1 s, 100 Hz stimulus were 1.7 and 2.6, respectively. Post‐stimulus recovery of [K+]o was sensitive to Na+ pump inhibition with 50 μM strophanthidin. Following a 1 s, 100 Hz stimulus, 50 μM strophanthidin increased τfast and τslow by 81 and 464%, respectively. Strophanthidin reduced the temperature sensitivity of post‐stimulus recovery of [K+]o. Post‐stimulus recovery of [K+]o was minimally affected by the K+ channel blocker Ba2+ (0.2 mm). Following a 10 s, 100 Hz stimulus, 0.2 mm Ba2+ increased τfast and τslow by 24 and 18%, respectively. Stimulated increases in [K+]o were followed by undershoots of [K+]o. Post‐stimulus undershoot amplitude increased with stimulus duration but was independent of the peak preceding [K+]o increase. These observations imply that two distinct processes contribute to post‐stimulus recovery of [K+]o in central white matter. The results are compatible with a model of K+ removal that attributes the fast, initial phase of K+ removal to K+ uptake by glial Na+ pumps and the slower, sustained decline to K+ uptake via axonal Na+ pumps.

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“…The activity ofNa + ,K + -ATPase in gray matter was threefold higher than that in white matter (Samaha, 1967). An autoradiographic study showed that oua bain, which binds to Na + ,K + -ATPase, had fe w or no specific binding sites in white matter (Caspers et aI., 1987).…”

Section: Changes In a Tp Bioluminescence With Timementioning

confidence: 91%

Histochemical Representation of Regional ATP in the Brain Using a Firefly Luciferase—Immobilized Membrane in a Multilayer Film Format

Kobayashi

Kikuchi

Ishikawa

et al. 1989

J Cereb Blood Flow Metab

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Summary:The enzymatic bioluminescence of firefly lu ciferase has been used in sensitive pictorial assays of ATP. We describe a method using a membrane with im mobilized luciferase in a multilayer film format for the histochemical representation of brain A TP content. The multilayer film consisted of a transparent support, a re agent layer, and a pigment layer. The reagent layer con tained all necessary reagents, including immobilized lu ciferase. The pigment layer was effective for high image resolution. An unfixed slice of frozen brain 16 f.Lm thick was placed on the film. The chemical energy of brain ATP ATP is an important end product of energy me tabolism. Its concentration is closely related to the functional capacity or viability of cells. The regional ATP content in the brain is usually evaluated by conventional biochemical analysis with tissue sam pling, but such assays are insufficient to investigate the spatial distribution of ATP in pathological con ditions. The histochemical imaging of endogenous brain ATP has been reported by Kogure and Alonso (1978) Luca, 1978) has been reported. In the present study, the reagent was applied to brain slices as an enzyme-immobilized membrane to avoid the diffu sion artifact of the A TP histochemistry.

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STUDIES ON Na⁺‐K⁺‐STIMULATED ATPase OF HUMAN BRAIN*

Cited by 29 publications

References 29 publications

Differential contributions of Ca²⁺‐activated K⁺ channels and Na⁺/K⁺‐ATPases to the generation of the slow afterhyperpolarization in CA1 pyramidal cells

Differential contributions of Ca²⁺‐activated K⁺ channels and Na⁺/K⁺‐ATPases to the generation of the slow afterhyperpolarization in CA1 pyramidal cells

Activity‐dependent extracellular K⁺ accumulation in rat optic nerve: the role of glial and axonal Na⁺ pumps

Histochemical Representation of Regional ATP in the Brain Using a Firefly Luciferase—Immobilized Membrane in a Multilayer Film Format

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STUDIES ON Na+‐K+‐STIMULATED ATPase OF HUMAN BRAIN*

Cited by 29 publications

References 29 publications

Differential contributions of Ca2+‐activated K+ channels and Na+/K+‐ATPases to the generation of the slow afterhyperpolarization in CA1 pyramidal cells

Differential contributions of Ca2+‐activated K+ channels and Na+/K+‐ATPases to the generation of the slow afterhyperpolarization in CA1 pyramidal cells

Activity‐dependent extracellular K+ accumulation in rat optic nerve: the role of glial and axonal Na+ pumps

Histochemical Representation of Regional ATP in the Brain Using a Firefly Luciferase—Immobilized Membrane in a Multilayer Film Format

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STUDIES ON Na⁺‐K⁺‐STIMULATED ATPase OF HUMAN BRAIN*

Differential contributions of Ca²⁺‐activated K⁺ channels and Na⁺/K⁺‐ATPases to the generation of the slow afterhyperpolarization in CA1 pyramidal cells

Differential contributions of Ca²⁺‐activated K⁺ channels and Na⁺/K⁺‐ATPases to the generation of the slow afterhyperpolarization in CA1 pyramidal cells

Activity‐dependent extracellular K⁺ accumulation in rat optic nerve: the role of glial and axonal Na⁺ pumps