Effect of insulin on membrane potential and potassium content of rat muscle

1959 ◽  
Vol 197 (3) ◽  
pp. 515-523 ◽  
Author(s):  
Kenneth L. Zierler
Keyword(s):  
Membrane Potential ◽  
Extensor Digitorum Longus ◽  
Extensor Digitorum ◽  
Potassium Content ◽  
Resting Membrane Potential ◽  
Extracellular Potassium ◽  
Conventional Theory ◽  
Rat Muscle

Insulin increased resting membrane potential of excised rat muscle, extensor digitorum longus, by about 5 mv in less than 1 hour. In 1 hour insulin caused no increase in the ratio of intra- to extracellular potassium, but in 2–3 hours intracellular K increased by about 10%. It is concluded that the increase in intracellular K is probably too small and too late to account for the hyperpolarization on the basis of conventional theory and it is suggested that the hyperpolarization produced by insulin is the cause of the potassium shift.

scholarly journals Resting membrane potential and Na+,K+-ATPase of rat fast and slow muscles during modeling of hypogravity

2009 ◽  
pp. 599-603 ◽  
Author(s):  
O Tyapkina ◽  
E Volkov ◽  
L Nurullin ◽  
B Shenkman ◽  
I Kozlovskaya ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Membrane Potential ◽  
Extensor Digitorum Longus ◽  
Extensor Digitorum ◽  
The Other ◽  
Hindlimb Suspension ◽  
Resting Membrane Potential ◽  
Sodium Permeability ◽  
Fast And Slow Muscles ◽  
Edl Muscle

Antiorthostatic hindlimb suspension (unloading) decreased the resting membrane potential (RMP) of skeletal muscle fibers in fast extensor digitorum longus (EDL) and slow soleus (SOL) muscle of the rat by about 10 % within 7 days and more. Inactivation of the membrane Na+, K+-pump by ouabain brought about similar depolarization as unloading. The increased sodium permeability of the membrane was excluded as the major cause of this depolarization by experiments in which TRIS was substituted for Na+ in the medium. On the other hand, the decrease in the electrogenic participation of the Na+,K+-pump is apparently one of the causes of RMP decrease during hypogravity, in EDL muscle in particular.

Hyperpolarization of muscle by insulin in a glucose-free environment

1959 ◽  
Vol 197 (3) ◽  
pp. 524-526 ◽  
Author(s):  
Kenneth L. Zierler
Keyword(s):  
Membrane Potential ◽  
Glucose Uptake ◽  
Extensor Digitorum Longus ◽  
Potassium Concentration ◽  
Extensor Digitorum ◽  
Muscle Membrane ◽  
Resting Membrane Potential ◽  
Free Solution ◽  
Longus Muscle ◽  
Free Environment

In a glucose-free solution, insulin increased resting membrane potential of rat extensor digitorum longus muscle by as much as it had in the presence of glucose. Even in the absence of glucose there was probably net accumulation of potassium by muscle, but the increase in muscle potassium concentration was too small to have been the cause of the observed hyperpolarization. It is concluded that insulin hyperpolarizes muscle membrane, as a result of which potassium moves into muscle, and that the eventual effect of insulin on potassium movement can be independent of any effect insulin may also have on glucose uptake.

Disorders of potassium homeostasis

2010 ◽  
pp. 3831-3845 ◽  
Author(s):  
J Firth
Keyword(s):  
Membrane Potential ◽  
Potassium Concentration ◽  
Resting Membrane Potential ◽  
Extracellular Potassium ◽  
Normal Range ◽  
Critical Determinant ◽  
Potassium Homeostasis ◽  
Extracellular Potassium Concentration

The normal range of potassium concentration in serum is 3.5 to 5.0 mmol/litre and within cells it is 150 to 160 mmol/litre, the ratio of intracellular to extracellular potassium concentration being a critical determinant of cellular resting membrane potential and thereby of the function of excitable tissues....

Conductance changes underlying a late synaptic hyperpolarization in hippocampal CA3 neurons

1987 ◽  
Vol 58 (1) ◽  
pp. 160-179 ◽  
Author(s):  
J. J. Hablitz ◽  
R. H. Thalmann
Keyword(s):  
Membrane Potential ◽  
Voltage Clamp ◽  
Time Course ◽  
Membrane Potentials ◽  
Resting Membrane Potential ◽  
Extracellular Potassium ◽  
Voltage Sensitivity ◽  
Base Line ◽  
Membrane Hyperpolarization ◽  
Ca3 Neurons

1. Single-electrode current- and voltage-clamp techniques were employed to study properties of the conductance underlying an orthodromically evoked late synaptic hyperpolarization or late inhibitory postsynaptic potential (IPSP) in CA3 pyramidal neurons in the rat hippocampal slice preparation. 2. Late IPSPs could occur without preceding excitatory postsynaptic potentials at the resting membrane potential and were graded according to the strength of the orthodromic stimulus. The membrane hyperpolarization associated with the late IPSP peaked within 140-200 ms after orthodromic stimulation of mossy fiber afferents. The late IPSP returned to base line with a half-decay time of approximately 200 ms. 3. As determined from constant-amplitude hyperpolarizing-current pulses, the membrane conductance increase during the late IPSP, and the time course of its decay, were similar whether measurements were made near the resting membrane potential or when the cell was hyperpolarized by approximately 35 mV. 4. When 1 mM cesium was added to the extracellular medium to reduce inward rectification, late IPSPs could be examined over a range of membrane potentials from -60 to -140 mV. For any given neuron, the late IPSP amplitude-membrane potential relationship was linear over the same range of membrane potentials for which the slope input resistance was constant. The late IPSP reversed symmetrically near -95 mV. 5. Intracellular injection of ethyleneglycol-bis-(beta-aminoethylether)-N,N'-tetraacetic acid or extracellular application of forskolin, procedures known to reduce or block certain calcium-dependent potassium conductances in CA3 neurons, had no significant effect on the late IPSP. 6. Single-electrode voltage-clamp techniques were used to analyze the time course and voltage sensitivity of the current underlying the late IPSP. This current [the late inhibitory postsynaptic current (IPSC)] began as early as 25 ms after orthodromic stimulation and reached a peak 120-150 ms following stimulation. 7. The late IPSC decayed with a single exponential time course (tau = 185 ms). 8. A clear reversal of the late IPSC at approximately -99 mV was observed in a physiological concentration of extracellular potassium (3.5 mM).(ABSTRACT TRUNCATED AT 400 WORDS)

Effect of insulin on potassium efflux from rat muscle in the presence and absence of glucose

1960 ◽  
Vol 198 (5) ◽  
pp. 1066-1070 ◽  
Author(s):  
Kenneth L. Zierler
Keyword(s):  
Rate Constant ◽  
Extensor Digitorum Longus ◽  
Extensor Digitorum ◽  
Muscle Membrane ◽  
Bathing Solution ◽  
Free Solution ◽  
Potassium Efflux ◽  
Rat Muscle ◽  
Longus Muscle ◽  
Driving Potential

Potassium efflux from rat extensor digitorum longus muscle was measured by counting the decrease in K42 in muscle bathed in K42-free solution. The rate constant for K efflux was 0.27 hr.–1 at 37°C and 0.16 hr.–1 at 26°C. Insulin decreased the rate constant for K efflux to 0.22 hr.–1 at 37°C and to 0.09 hr.–1 at 26°C. The effect of insulin on efflux was quantitatively the same when glucose was removed from the bathing solution. From measurement of net change in intracellular K and from measurement of changes in the driving potential for K it is concluded that insulin probably also decreases K influx, but to a lesser degree. However, when half the chloride is removed from the bathing solution, efflux and influx are decreased equally. The data can be interpreted by the hypothesis that insulin increases the positive fixed charge within the muscle membrane.

Comparative responses of brain stem and hippocampal neurons to O2 deprivation: in vitro intracellular studies

1992 ◽  
Vol 262 (5) ◽  
pp. L549-L554 ◽  
Author(s):  
D. F. Donnelly ◽  
C. Jiang ◽  
G. G. Haddad
Keyword(s):  
Membrane Potential ◽  
Brain Stem ◽  
Cortical Neurons ◽  
Oxygen Deprivation ◽  
Oxygen Availability ◽  
Hypoxic Exposure ◽  
Hypoglossal Nucleus ◽  
Resting Membrane Potential ◽  
Extracellular Potassium ◽  
Motor Nucleus

Most mammalian neurons are known to be sensitive to oxygen availability, but the nature of the sensitivity is not well understood. Previous results have suggested that brain stem neurons may respond differently than cortical neurons during oxygen deprivation. We pursued this hypothesis by examining the time course of change in membrane potential (Vm) and input resistance (Rn) during periods of reduced oxygen availability in a tissue slice preparation. Since extracellular potassium is an important factor determining resting membrane potential, extracellular K+ activity, (K+o), was also measured. Adult rat neurons from three regions were recorded: hippocampal CA1 region, hypoglossal nucleus (XII), and dorsal vagal motor nucleus (DMNX). At the end of a 5-min hypoxic exposure, all neurons depolarized and this depolarization was greatest in XII (28.8 +/- 3.2 mV) compared with DMNX (17.8 +/- 3.7 mV) and CA1 (6.7 +/- 4.4 mV). K+o increased in all regions and was larger in DMNX (7.1 +/- 2.6 mM) and XII (5.3 +/- 2.1 mM) compared with CA1 (2.2 +/- 1.4 mM). During more severe oxygen deprivation (anoxia), neurons also depolarized at different rates with XII greater than DMNX greater than CA1. K+o increased markedly (28–36 mM) by 5 min into anoxia, and no statistical difference was observed between regions. From these results we conclude that 1) all cells tested were depolarized after 5 min of hypoxia; however, regional variability exists in the sensitivity to hypoxia; brain stem neurons depolarize faster than cortical neurons; 2) during anoxia, all brain stem and cortical neurons show a major depolarization, and 3) these differences in membrane potential cannot be solely attributed to changes in extracellular K+.

scholarly journals Differential impact of Kv8.2 loss on rod and cone signaling and degeneration.

2021 ◽  
Author(s):  
Shivangi M Inamdar ◽  
Colten K Lankford ◽  
Deepak Poria ◽  
Joseph G Laird ◽  
Eduardo Solessio ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Ex Vivo ◽  
Light Stimulus ◽  
Resting Membrane Potential ◽  
Cone Dystrophy ◽  
Extracellular Potassium ◽  
Delayed Response ◽  
Low Frequencies ◽  
Ionic Imbalance

The voltage-gated potassium channel responsible for controlling photoreceptor signaling is a heteromeric complex of Kv2.1 subunits with a regulatory Kv8.2 subunit. Kv2.1/Kv8.2 channels are localized to the photoreceptor inner segment and carry IKx, largely responsible for setting the photoreceptor resting membrane potential. Mutations in Kv8.2 result in childhood-onset Cone Dystrophy with Supernormal Rod Response (CDSRR). We generated a Kv8.2 knockout (KO) mouse and examined retinal signaling and photoreceptor degeneration to gain deeper insight into the complex phenotypes of this disease. Using electroretinograms we show that there is a tradeoff between delayed or reduced signaling from rods depending on the intensity of the light stimulus, consistent with reduced capacity for light-evoked changes in membrane potential. The delayed response was not seen ex vivo where extracellular potassium levels are the same, so we conclude the in vivo alteration is influenced by ionic imbalance. We observed mild retinal degeneration. Signaling from cones was reduced but there was no loss of cone density. Loss of Kv8.2 altered responses to flickering light with responses attenuated at high frequencies and altered in shape at low frequencies. The Kv8.2 KO line on an all-cone retina background had reduced cone signaling associated with degeneration. We conclude that Kv8.2 is required by rods and cones for responding to dynamic changes in lighting. The timing and cell type affected by degeneration is different in the mouse and human but there is a window of time in both for therapeutic intervention.

scholarly journals Differential effects of acute changes in cell Ca2+ concentration on myofibrillar and non-myofibrillar protein breakdown in the rat extensor digitorum longus muscle in vitro. Assessment by production of tyrosine and Nτ-methylhistidine

1987 ◽  
Vol 241 (1) ◽  
pp. 121-127 ◽  
Author(s):  
M N Goodman
Keyword(s):  
Extensor Digitorum Longus ◽  
Extensor Digitorum Longus Muscle ◽  
Extensor Digitorum ◽  
Ionophore A23187 ◽  
Myofibrillar Proteins ◽  
Rat Muscle ◽  
Longus Muscle ◽  
Acute Changes ◽  
Tissue Contents

The influence of Ca2+ on myofibrillar proteolysis was evaluated in the isolated extensor digitorum longus muscle incubated in vitro with agents previously shown to increase the intracellular concentration of Ca2+. Myofibrillar proteolysis was evaluated by measuring the release of N tau-methylhistidine, and total proteolysis was evaluated by measuring tyrosine release by incubated muscles after the inhibition of protein synthesis with cycloheximide. Incubated muscles released measurable quantities of N tau-methylhistidine, and muscle contents of the amino acids remained stable over 2 h of incubation. The release of N tau-methylhistidine by incubated muscles was similar to its release by perfused rat muscle in response to brief starvation, indicating the integrity of the incubated muscles. Ca2+ ionophore A23187, dibucaine, procaine, caffeine and elevated K+ concentration increased lactate release by incubated muscles and decreased tissue contents of ATP and phosphocreatine to varying degrees, indicating the metabolic effectiveness of the agents tested. Only A23187 and dibucaine increased total cell Ca2+, and they increased tyrosine release. Caffeine and elevated [K+] increased neither cell Ca2+ nor tyrosine release; however, only A23187 and dibucaine increased tyrosine release significantly. On the other hand, these agents were without effect on myofibrillar proteolysis as assessed by N tau-methylhistidine release by incubated muscles and changes in tissue contents of the amino acid. In fact, some of the agents tested tended to decrease myofibrillar proteolysis slightly. These results indicate that acute elevation of intracellular Ca2+ is associated with increased breakdown of non-myofibrillar but not myofibrillar proteins. Because of this, the role of elevated Ca2+ in muscle atrophy in certain pathological states is questioned. The data also indicate that the breakdown of myofibrillar and non-myofibrillar proteins in muscle is regulated independently and by different pathways, a conclusion reached in previous studies with perfused rat muscle.

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