Effect of low pO2 on Qo2, Na22 efflux, and contractility of muscles

1965 ◽  
Vol 208 (5) ◽  
pp. 855-860 ◽  
Author(s):  
William J. Whalen ◽  
Priscilla Bosch ◽  
Andrejs Dimants
Keyword(s):  
Lactic Acid ◽  
Membrane Potential ◽  
Gas Mixtures ◽  
Resting Membrane Potential ◽  
Minimal Level ◽  
Cellular Environment ◽  
Oxygen Tensions ◽  
Develop Tension

Previous experiments suggested that the in vivo consumption of O2 by the cell is normally limited by the pO2 in the cellular environment. We suggested that if the pO2 exceeds a certain minimal level, some or all of the energy from the "extra" respiration may be directly converted to heat. To further test the hypothesis, 39 isolated frog sartorii were placed in respirometers containing Ringer-bicarbonate solution (at 22 or 27 C) equilibrated with gas mixtures of various oxygen tensions. (All gases contained 2% CO2.) The Qo2 of muscles exposed to 98% O2 for 6–7 hr reached a stable value which was about 200% of the stable value for muscles exposed to 25% O2 for the same period of time. In other experiments the depression of the Qo2 in 25% O2 was shown to be reversible. The ability to develop tension, as judged by occasional test contractions, was not impaired in 25% O2. The amount of lactic acid liberated from the muscles was small and was independent of the pO2. In additional experiments with similar muscles exposed to either 25% O2 or 98% N2 for 5–7 hr, neither the Na22 efflux nor resting membrane potential differed significantly from the values obtained in 98% O2. The data are consistent with the hypothesis.

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.

In vivo membrane potentials of smooth muscle cells in the caudal artery of the rat

1985 ◽  
Vol 249 (1) ◽  
pp. C78-C83 ◽  
Author(s):  
H. J. Bryant ◽  
D. R. Harder ◽  
M. B. Pamnani ◽  
F. J. Haddy
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Membrane Potentials ◽  
Resting Membrane Potential ◽  
Humoral Factors ◽  
Caudal Artery ◽  
Blood Pressures

Membrane potentials measured in vivo may differ significantly from those measured in vitro in part due to humoral factors, innervation, and wall tension. These studies were initiated to determine whether it is feasible to record membrane potentials from vascular smooth muscle cells in vivo in the caudal artery of the pentobarbital-anesthetized male Wistar rat. Membrane potentials were measured using glass microelectrodes and correlated with systolic, diastolic, and mean blood pressures. For systolic blood pressures between 100 and 140 mmHg the average resting membrane potential was -38.4 +/- 0.48 mV. There was good correlation of systolic, diastolic, and mean blood pressures with membrane potential between 100 and 140 mmHg (r = 0.89, 0.75, and 0.89, respectively). Below 80 mmHg the arterial muscle cells became more depolarized than would be expected if the membrane potential were determined solely by transmural pressure. The depolarized membrane potential at low arterial pressures may be due to enhanced neural input. Spontaneous electrical activity was observed in some of the in vivo cells. When action potentials were present, they were generated at rates between 1-2/s and 6-7/min. These studies indicate that it is feasible to measure membrane potentials from arterial smooth muscle cells in vivo in the caudal artery of the rat.

scholarly journals Association of the Kv1 family of K+ channels and their functional blueprint in the properties of auditory neurons as revealed by genetic and functional analyses

2013 ◽  
Vol 110 (8) ◽  
pp. 1751-1764 ◽  
Author(s):  
Wenying Wang ◽  
Hyo Jeong Kim ◽  
Ping Lv ◽  
Bruce Tempel ◽  
Ebenezer N. Yamoah
Keyword(s):  
Membrane Potential ◽  
Developmental Plasticity ◽  
Spiral Ganglion ◽  
Membrane Properties ◽  
Resting Membrane Potential ◽  
Underlying Mechanisms ◽  
Null Mutant Mice ◽  
Ganglion Neurons

Developmental plasticity in spiral ganglion neurons (SGNs) ensues from profound alterations in the functional properties of the developing hair cell (HC). For example, prehearing HCs are spontaneously active. However, at the posthearing stage, HC membrane properties transition to graded receptor potentials. The dendrotoxin (DTX)-sensitive Kv1 channel subunits (Kv1.1, 1.2, and 1.6) shape the firing properties and membrane potential of SGNs, and the expression of the channel undergoes developmental changes. Because of the stochastic nature of Kv subunit heteromultimerization, it has been difficult to determine physiologically relevant subunit-specific interactions and their functions in the underlying mechanisms of Kv1 channel plasticity in SGNs. Using Kcna2 null mutant mice, we demonstrate a surprising paradox in changes in the membrane properties of SGNs. The resting membrane potential of Kcna2−/− SGNs was significantly hyperpolarized compared with that of age-matched wild-type (WT) SGNs. Analyses of outward currents in the mutant SGNs suggest an apparent approximately twofold increase in outward K+ currents. We show that in vivo and in vitro heteromultimerization of Kv1.2 and Kv1.4 α-subunits underlies the striking and unexpected alterations in the properties of SGNs. The results suggest that heteromeric interactions of Kv1.2 and Kv1.4 dominate the defining features of Kv1 channels in SGNs.

scholarly journals Homeostatic recovery of embryonic spinal activity initiated by compensatory changes in resting membrane potential

2019 ◽  
Author(s):  
Carlos Gonzalez-Islas ◽  
Miguel Angel Garcia-Bereguiain ◽  
Peter Wenner
Keyword(s):  
Nervous System ◽  
Membrane Potential ◽  
Homeostatic Plasticity ◽  
Network Activity ◽  
Resting Membrane Potential ◽  
Receptor Blockade ◽  
Homeostatic Mechanism ◽  
Voltage Gated ◽  
Baseline Activity

AbstractWhen baseline activity in a neuronal network is modified by external challenges, a set of mechanisms is prompted to homeostatically restore activity levels. These homeostatic mechanisms are thought to be profoundly important in the maturation of the network. We have previously shown that 2-day blockade of either excitatory GABAergic or glutamatergic transmission in the living embryo transiently blocks the movements generated by spontaneous network activity (SNA) in the spinal cord. However, by 2 hours of persistent receptor blockade embryonic movements begin to recover, and by 12 hours we observe a complete homeostatic recovery in vivo. Compensatory changes in voltage-gated conductances in motoneurons were observed by 12 hours of blockade, but not changes in synaptic strength. It was unclear whether changes in voltage-gated conductances were observed by 2 hours of blockade when the recovery actually begins. Further, compensatory changes in voltage-gated conductances were not observed following glutamatergic blockade where embryonic movements were blocked but then recovered in a similar manner to GABAergic blockade. In this study, we discover a mechanism for homeostatic recovery in these first hours of neurotransmitter receptor blockade. In the first 6 hours of GABAergic or glutamatergic blockade there was a clear depolarization of resting membrane potential in both motoneurons and interneurons. These changes reduced action potential threshold and were mainly observed in the continued presence of the antagonist. Therefore, it appears that fast changes in resting membrane potential represent a key fast homeostatic mechanism for the maintenance of network activity in the living embryonic nervous system.SignificanceHomeostatic plasticity represents a set of mechanisms that act to recover cellular or network activity following a challenge to that activity and is thought to be critical for the developmental construction of the nervous system. The chick embryo afforded us the opportunity to observe in a living developing system the timing of the homeostatic recovery of network activity following 2 distinct perturbations. Because of this advantage, we have identified a novel homeostatic mechanism that actually occurs as the network recovers and is therefore likely to contribute to nervous system homeostasis. We found that a depolarization of the resting membrane potential in the first hour of the perturbations enhances excitability and supports the recovery of embryonic spinal network activity.

Biophysical Characterization of Rat Caudal Hypothalamic Neurons: Calcium Channel Contribution to Excitability

2000 ◽  
Vol 84 (6) ◽  
pp. 2896-2903 ◽  
Author(s):  
Yi-Ping Fan ◽  
Eric M. Horn ◽  
Tony G. Waldrop
Keyword(s):  
Membrane Potential ◽  
Low Voltage ◽  
Input Resistance ◽  
Calcium Currents ◽  
Resting Membrane Potential ◽  
Calcium Dependent ◽  
Rhythmic Firing ◽  
Almost All

Neurons in the caudal hypothalamus (CH) are responsible for the modulation of various processes including respiratory and cardiovascular output. Previous results from this and other laboratories have demonstrated in vivo that these neurons have firing rhythms matched to the respiratory and cardiovascular cycles. The goal of the present study was to characterize the biophysical properties of neurons in the CH with particular emphasis in those properties responsible for rhythmic firing behavior. Whole cell, patch-clamped CH neurons displayed a resting membrane potential of −58.0 ± 1.1 mV and an input resistance of 319.3 ± 16.6 MΩ when recorded in current-clamp mode in an in vitro brain slice preparation. A large proportion of these neurons displayed postinhibitory rebound (PIR) that was dependent on the duration and magnitude of hyperpolarizing current as well as the resting membrane potential of the cell. Furthermore these neurons discharged tonically in response to a depolarizing current pulse at a depolarized resting membrane potential (more positive than −65 mV) but switched to a rapid burst of firing to the same stimulus when the resting membrane potential was lowered. The PIR observed in these neurons was calcium dependent as demonstrated by the ability to block its amplitude by perfusion of Ca2+-free bath solution or by application of Ni2+ (0.3–0.5 mM) or nifedipine (10 μM). These properties suggest that low-voltage-activated (LVA) calcium current is involved in the PIR and bursting firing of these CH neurons. In addition, high-voltage-activated calcium responses were detected after blockade of outward potassium current or in Ba2+-replacement solution. In addition, almost all of the CH neurons studied showed spike frequency adaptation that was decreased following Ca2+ removal, indicating the involvement of Ca2+-dependent K+ current ( I K,Ca) in these cells. In conclusion, CH neurons have at least two different types of calcium currents that contribute to their excitability; the dominant current is the LVA or T-type. This LVA current appears to play a significant role in the bursting characteristics that may underlie the rhythmic firing of CH neurons.

In Vivo Dynamic Clamp Study of Ih in the Mouse Inferior Colliculus

2010 ◽  
Vol 104 (2) ◽  
pp. 940-948 ◽  
Author(s):  
A. P. Nagtegaal ◽  
J.G.G. Borst
Keyword(s):  
Membrane Potential ◽  
Inferior Colliculus ◽  
Single Cells ◽  
Membrane Resistance ◽  
Resting Membrane Potential ◽  
Dynamic Clamp ◽  
Small Contribution ◽  
Functional Relevance ◽  
Rebound Spiking

Approximately half of the cells in the mouse inferior colliculus have the hyperpolarization-activated mixed cation current Ih, yet little is known about its functional relevance in vivo. We therefore studied its contribution to the processing of sound information in single cells by making in vivo whole cell recordings from the inferior colliculus (IC) of young-adult anesthetized C57Bl/6 mice. Following pharmacological block of the endogenous channels, a dynamic clamp approach allowed us to study the responses to current injections or auditory stimuli in the presence and absence of Ih within the same neuron, thus avoiding network or developmental effects. The presence of Ih changed basic cellular properties, including depolarizing the resting membrane potential and decreasing resting membrane resistance. Sound-evoked excitatory postsynaptic potentials were smaller but at the same time reached a more positive membrane potential when Ih was present. With Ih, a subset of cells showed rebound spiking following hyperpolarizing current injection. Its presence also changed more complex cellular properties. It decreased temporal summation in response to both hyperpolarizing and depolarizing repetitive current stimuli, and resulted in small changes in the cycle-averaged membrane potential during sinusoidal amplitude modulated (SAM) tones. Furthermore, Ih minimally decreased the response to a tone following a depolarization, an effect that may make a small contribution to forward masking. Our results thus suggest that previously observed differences in IC cells are a mixture of direct effects of Ih and indirect effects due to the change in membrane potential or effects due to the co-expression with other channels.

scholarly journals Muscarinic Modulation of Recruitment Threshold and Firing Rate in Rat Oculomotor Nucleus Motoneurons

2009 ◽  
Vol 101 (1) ◽  
pp. 100-111 ◽  
Author(s):  
Jose Luis Nieto-Gonzalez ◽  
Livia Carrascal ◽  
Pedro Nunez-Abades ◽  
Blas Torres
Keyword(s):  
Membrane Potential ◽  
Firing Rate ◽  
Acetylcholine Receptors ◽  
Muscarinic Acetylcholine Receptors ◽  
Resting Membrane Potential ◽  
Oculomotor Nucleus ◽  
Recruitment Threshold ◽  
Bath Application ◽  
Lower Amplitude

Above recruitment threshold, ocular motoneurons (Mns) show a firing rate linearly related with eye position. Current hypothesis suggests that synaptic inputs are determinant for establishing the recruitment threshold and firing rate gain in these Mns. We investigated this proposal by studying the cholinergic modulation in oculomotor nucleus Mns by intracellular recordings in rat brain slice preparation. All recorded Mns were silent at their resting membrane potential. Bath application of carbachol (10 μm) produced a depolarization and a sustained firing that was not silenced on returning membrane potential to the precarbachol value via DC injection. In response to similar membrane depolarization or equal-current steps, carbachol-exposed Mns produced a higher firing rate and a shorter spike afterhyperpolarization phase with lower amplitude. The relationship between injected current and firing rate ( I– F) was linear in control and carbachol-exposed Mns. The slope of these relationships ( I– F gain) decreased with carbachol exposure. Bath application of agonist and antagonist of nicotinic and muscarinic acetylcholine receptors in addition to immunohistochemical studies support the notion that muscarinic receptors are primarily involved in the preceding responses. We conclude that muscarinic inputs play an important role in determining the recruitment threshold and firing rate gain observed in oculomotor Mns in vivo.

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