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Journal articles on the topic 'Depolarization'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 July 2025

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1

Higuchi, Tomoyasu, Yoshimasa Takeda, Megumi Hashimoto, Osamu Nagano, and Masahisa Hirakawa. "Dynamic Changes in Cortical NADH Fluorescence and Direct Current Potential in Rat Focal Ischemia: Relationship between Propagation of Recurrent Depolarization and Growth of the Ischemic Core." Journal of Cerebral Blood Flow & Metabolism 22, no. 1 (2002): 71–79. http://dx.doi.org/10.1097/00004647-200201000-00009.

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Forty rats were subjected to 3 hours of focal ischemia by occluding the left middle cerebral and left common carotid arteries. The propagation of recurrent depolarization around the ischemic core was analyzed using direct-current potential and NADH (reduced nicotinamide adenine dinucleotide) fluorescence images by irradiating the parietal-temporal cortex with ultraviolet light. Based on histological evaluation at direct-current recording sites, the total time of depolarization causing 50% neuronal injury was estimated to be 18.2 minutes. The sites showing recurrent depolarizations resulted in

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2

Winkler, Maren KL, Nora Dengler, Nils Hecht, et al. "Oxygen availability and spreading depolarizations provide complementary prognostic information in neuromonitoring of aneurysmal subarachnoid hemorrhage patients." Journal of Cerebral Blood Flow & Metabolism 37, no. 5 (2016): 1841–56. http://dx.doi.org/10.1177/0271678x16641424.

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Multimodal neuromonitoring in neurocritical care increasingly includes electrocorticography to measure epileptic events and spreading depolarizations. Spreading depolarization causes spreading depression of activity (=isoelectricity) in electrically active tissue. If the depression is long-lasting, further spreading depolarizations occur in still isoelectric tissue where no activity can be suppressed. Such spreading depolarizations are termed isoelectric and are assumed to indicate energy compromise. However, experimental and clinical recordings suggest that long-lasting spreading depolarizati

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3

Lyu, R. M., L. Smith, and J. B. Smith. "Ca2+ influx via Na(+)-Ca2+ exchange in immortalized aortic myocytes. II. Feedback inhibition by [Ca2+]i." American Journal of Physiology-Cell Physiology 263, no. 3 (1992): C635—C641. http://dx.doi.org/10.1152/ajpcell.1992.263.3.c635.

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Depolarization with 50 mM K+ evoked a spike in cytosolic free Ca2+ ([Ca2+]i) and increased 45Ca2+ uptake in immortalized aortic myocytes. The following evidence indicates that the electrogenic Na(+)-Ca2+ exchanger caused the Ca2+ influx that was evoked by K+ depolarization. First, K+ depolarization had no effect on [Ca2+]i and 45Ca2+ uptake in cells with basal Na+ but strikingly increased both in Na(+)-loaded cells. Second, the [Ca2+]i increases produced by K+ depolarization depended hyperbolically on external Ca2+ (50% maximum concentration = 1.5 mM). Third, the increases in [Ca2+]i and 45Ca2

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4

Thoreson, Wallace B., and Dwight A. Burkhardt. "Effects of synaptic blocking agents on the depolarizing responses of turtle cones evoked by surround illumination." Visual Neuroscience 5, no. 6 (1990): 571–83. http://dx.doi.org/10.1017/s0952523800000730.

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AbstractThe effects of synaptic blocking agents on the antagonistic surround of the receptive field of cone photoreceptors were studied intracellular recording in the retina of hte turtle (Pseudemys scripta elegans) Illumination of a cone's receptive-field surround typically evoked a hybriid depolarizing response composed of two componests: (1) the graded synaptic feedback depolarization and (2) the prolonged depolarization a distinctive, intrinsic response of the cone. The locus of action of synaptic blocking agents was analyzed by comparing their effects on the light-evoked response of horiz

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5

HILL, ROBERT B. "Correlation of Electrical and Mechanical Activity of Holothurian Muscle." Journal of Experimental Biology 130, no. 1 (1987): 331–39. http://dx.doi.org/10.1242/jeb.130.1.331.

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1. Spontaneous contractions of segments of an isolated longitudinal muscle of Holothuna cinerascens are not propagated across a sucrose gap. Asynchronous spiking and spontaneous depolarizations leading to contraction can be recorded independently on each side of the gap. 2. Caffeine-induced contractures are not the result of depolarization. 3. Depolarization with KCl temporarily restores contractility lost in a series of caffeine-induced contractures. 4. Acetylcholine causes a depolarization which induces contraction. 5. Individual muscle units may spike quite independently as depolarization p

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6

Oka, Fumiaki, Ulrike Hoffmann, Jeong Hyun Lee, et al. "Requisite ischemia for spreading depolarization occurrence after subarachnoid hemorrhage in rodents." Journal of Cerebral Blood Flow & Metabolism 37, no. 5 (2016): 1829–40. http://dx.doi.org/10.1177/0271678x16659303.

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Spontaneous spreading depolarizations are frequent after various forms of human brain injury such as ischemic or hemorrhagic stroke and trauma, and worsen the outcome. We have recently shown that supply-demand mismatch transients trigger spreading depolarizations in ischemic stroke. Here, we examined the mechanisms triggering recurrent spreading depolarization events for many days after subarachnoid hemorrhage. Despite large volumes of subarachnoid hemorrhage induced by cisternal injection of fresh arterial blood in rodents, electrophysiological recordings did not detect a single spreading dep

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7

Richter, Frank, Annett Eitner, Johannes Leuchtweis, Reinhard Bauer, Alfred Lehmenkühler, and Hans-Georg Schaible. "Effects of interleukin-1ß on cortical spreading depolarization and cerebral vasculature." Journal of Cerebral Blood Flow & Metabolism 37, no. 5 (2016): 1791–802. http://dx.doi.org/10.1177/0271678x16641127.

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During brain damage and ischemia, the cytokine interleukin-1ß is rapidly upregulated due to activation of inflammasomes. We studied whether interleukin-1ß influences cortical spreading depolarization, and whether lipopolysaccharide, often used for microglial stimulation, influences cortical spreading depolarizations. In anaesthetized rats, cortical spreading depolarizations were elicited by microinjection of KCl. Interleukin-1ß, the IL-1 receptor 1 antagonist, the GABAA receptor blocker bicuculline, and lipopolysaccharide were administered either alone or combined (interleukin-1ß + IL-1 recept

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8

Dreier, Jens P., Martin Fabricius, Cenk Ayata, et al. "Recording, analysis, and interpretation of spreading depolarizations in neurointensive care: Review and recommendations of the COSBID research group." Journal of Cerebral Blood Flow & Metabolism 37, no. 5 (2016): 1595–625. http://dx.doi.org/10.1177/0271678x16654496.

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Spreading depolarizations (SD) are waves of abrupt, near-complete breakdown of neuronal transmembrane ion gradients, are the largest possible pathophysiologic disruption of viable cerebral gray matter, and are a crucial mechanism of lesion development. Spreading depolarizations are increasingly recorded during multimodal neuromonitoring in neurocritical care as a causal biomarker providing a diagnostic summary measure of metabolic failure and excitotoxic injury. Focal ischemia causes spreading depolarization within minutes. Further spreading depolarizations arise for hours to days due to energ

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9

Hertelendy, Péter, Ákos Menyhárt, Péter Makra, et al. "Advancing age and ischemia elevate the electric threshold to elicit spreading depolarization in the cerebral cortex of young adult rats." Journal of Cerebral Blood Flow & Metabolism 37, no. 5 (2016): 1763–75. http://dx.doi.org/10.1177/0271678x16643735.

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Spreading depolarizations of long cumulative duration have been implicated in lesion development and progression in patients with stroke and traumatic brain injury. Spreading depolarizations evolve less likely in the aged brain, but it remains to be determined at what age the susceptibility to spreading depolarizations starts to decline, especially in ischemia. Spreading depolarizations were triggered by epidural electric stimulation prior and after ischemia induction in the cortex of 7–30 weeks old anesthetized rats ( n = 38). Cerebral ischemia was achieved by occlusion of both common carotid

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10

Hartings, Jed A., C. William Shuttleworth, Sergei A. Kirov, et al. "The continuum of spreading depolarizations in acute cortical lesion development: Examining Leão’s legacy." Journal of Cerebral Blood Flow & Metabolism 37, no. 5 (2016): 1571–94. http://dx.doi.org/10.1177/0271678x16654495.

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A modern understanding of how cerebral cortical lesions develop after acute brain injury is based on Aristides Leão’s historic discoveries of spreading depression and asphyxial/anoxic depolarization. Treated as separate entities for decades, we now appreciate that these events define a continuum of spreading mass depolarizations, a concept that is central to understanding their pathologic effects. Within minutes of acute severe ischemia, the onset of persistent depolarization triggers the breakdown of ion homeostasis and development of cytotoxic edema. These persistent changes are diagnosed as

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11

Ong, Boon-Hooi, Gordon F. Tomaselli, and Jeffrey R. Balser. "A Structural Rearrangement in the Sodium Channel Pore Linked to Slow Inactivation and Use Dependence." Journal of General Physiology 116, no. 5 (2000): 653–62. http://dx.doi.org/10.1085/jgp.116.5.653.

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Voltage-gated sodium (Na+) channels are a fundamental target for modulating excitability in neuronal and muscle cells. When depolarized, Na+ channels may gradually enter long-lived, slow-inactivated conformational states, causing a cumulative loss of function. Although the structural motifs that underlie transient, depolarization-induced Na+ channel conformational states are increasingly recognized, the conformational changes responsible for more sustained forms of inactivation are unresolved. Recent studies have shown that slow inactivation components exhibiting a range of kinetic behavior (f

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12

Daniel, E. E., J. Jury, R. Serio, and L. P. Jager. "K+-channel blockers do not decrease acetylcholine depolarizations in canine trachealis." Canadian Journal of Physiology and Pharmacology 70, no. 1 (1992): 43–52. http://dx.doi.org/10.1139/y92-007.

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Using the double sucrose gap, we have examined the role of K+ channels in the cholinergic depolarizations in response to field stimulation and acetylcholine (Ach) in canine trachealis. Acetylcholine-like depolarization per se decreased electrotonic potentials from hyperpolarizing currents. The net effect of acetylcholine (10−6 M) depolarization on membrane conductance was a small increase after the depolarization was compensated by current clamp. Reversal potentials for acetylcholine depolarization and for the excitatory junction potential (EJP) were determined by extrapolation to be 20–30 mV

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13

Saito, Yasuhiko, and Tadashi Isa. "Organization of Interlaminar Interactions in the Rat Superior Colliculus." Journal of Neurophysiology 93, no. 5 (2005): 2898–907. http://dx.doi.org/10.1152/jn.01051.2004.

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Our previous studies have shown that when slices of the rat superior colliculus (SC) are exposed to a solution containing 10 μM bicuculline and a low concentration of Mg2+ (0.1 mM), most neurons in the intermediate gray layer (stratum griseum intermediale; SGI), wide-field vertical (WFV) cells in the optic layer (stratum opticum; SO), and a minor population of neurons in the superficial gray layer (stratum griseum superficiale; SGS) exhibit spontaneous depolarization and burst firing, which are synchronous among adjacent neurons. These spontaneous and synchronous depolarizations were thought t

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14

Carlson, Andrew P., C. William Shuttleworth, Sebastian Major, Coline L. Lemale, Jens P. Dreier, and Jed A. Hartings. "Terminal spreading depolarizations causing electrocortical silencing prior to clinical brain death: case report." Journal of Neurosurgery 131, no. 6 (2019): 1773–79. http://dx.doi.org/10.3171/2018.7.jns181478.

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The authors report on a 57-year-old woman in whom progression to brain death occurred on day 9 after aneurysmal subarachnoid hemorrhage without evidence of significant brain edema or vasospasm. Neuromonitoring demonstrated that brain death was preceded by a series of cortical spreading depolarizations that occurred in association with progressive hypoxic episodes. The depolarizations induced final electrical silence in the cortex and ended with a terminal depolarization that persisted > 7 hours. To the authors’ knowledge, this is the first report of terminal spreading depolarization in the

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15

Ullah, Aman, Minh Tuan Hoang-Trong, William Jonathan Lederer, Raimond L. Winslow, and Mohsin Saleet Jafri. "Critical Requirements for the Initiation of a Cardiac Arrhythmia in Rat Ventricle: How Many Myocytes?" Cells 11, no. 12 (2022): 1878. http://dx.doi.org/10.3390/cells11121878.

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Cardiovascular disease is the leading cause of death worldwide due in a large part to arrhythmia. In order to understand how calcium dynamics play a role in arrhythmogenesis, normal and dysfunctional Ca2+ signaling in a subcellular, cellular, and tissued level is examined using cardiac ventricular myocytes at a high temporal and spatial resolution using multiscale computational modeling. Ca2+ sparks underlie normal excitation–contraction coupling. However, under pathological conditions, Ca2+ sparks can combine to form Ca2+ waves. These propagating elevations of (Ca2+)i can activate an inward N

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16

Urbach, Anja, Eileen Baum, Falko Braun, and Otto W. Witte. "Cortical spreading depolarization increases adult neurogenesis, and alters behavior and hippocampus-dependent memory in mice." Journal of Cerebral Blood Flow & Metabolism 37, no. 5 (2016): 1776–90. http://dx.doi.org/10.1177/0271678x16643736.

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Cortical spreading depolarizations are an epiphenomenon of human brain pathologies and associated with extensive but transient changes in ion homeostasis, metabolism, and blood flow. Previously, we have shown that cortical spreading depolarization have long-lasting consequences on the brains transcriptome and structure. In particular, we found that cortical spreading depolarization stimulate hippocampal cell proliferation resulting in a sustained increase in adult neurogenesis. Since the hippocampus is responsible for explicit memory and adult-born dentate granule neurons contribute to this fu

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17

Nordin, C. "Response of Ca(2+)-loaded, depolarized guinea pig myocytes to critically timed premature stimulations." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 2 (1996): H447—H465. http://dx.doi.org/10.1152/ajpheart.1996.270.2.h447.

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Single premature stimulations during trains of nondriven action potentials induced by depolarization normally cause a transient hyperpolarization of diastolic membrane potential before the subsequent spontaneous upstroke. However, rare, marked transient depolarizations have also been reported. This paper presents experimental data and computer simulations that characterize transient depolarization following premature stimulations and investigate the role of intracellular [Ca2+] in generating this unusual response. In isolated guinea pig myocytes, transient depolarizations (range 4-58 mV) consi

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18

Reyes, Fredy D., and Edgar T. Walters. "Long-Lasting Synaptic Potentiation Induced by Depolarization Under Conditions That Eliminate Detectable Ca2+ Signals." Journal of Neurophysiology 103, no. 3 (2010): 1283–94. http://dx.doi.org/10.1152/jn.00704.2009.

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Activity-dependent alterations of synaptic transmission important for learning and memory are often induced by Ca2+ signals generated by depolarization. While it is widely assumed that Ca2+ is the essential transducer of depolarization into cellular plasticity, little effort has been made to test whether Ca2+-independent responses to depolarization might also induce memory-like alterations. It was recently discovered that peripheral axons of nociceptive sensory neurons in Aplysia display long-lasting hyperexcitability triggered by conditioning depolarization in the absence of Ca2+ entry (using

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19

Rogers, Michelle L., Chi Leng Leong, Sally AN Gowers, et al. "Simultaneous monitoring of potassium, glucose and lactate during spreading depolarization in the injured human brain – Proof of principle of a novel real-time neurochemical analysis system, continuous online microdialysis." Journal of Cerebral Blood Flow & Metabolism 37, no. 5 (2016): 1883–95. http://dx.doi.org/10.1177/0271678x16674486.

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Spreading depolarizations occur spontaneously and frequently in injured human brain. They propagate slowly through injured tissue often cycling around a local area of damage. Tissue recovery after an spreading depolarization requires greatly augmented energy utilisation to normalise ionic gradients from a virtually complete loss of membrane potential. In the injured brain, this is difficult because local blood flow is often low and unreactive. In this study, we use a new variant of microdialysis, continuous on-line microdialysis, to observe the effects of spreading depolarizations on brain met

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20

Schneider, David A., and James J. Galligan. "Presynaptic nicotinic acetylcholine receptors in the myenteric plexus of guinea pig intestine." American Journal of Physiology-Gastrointestinal and Liver Physiology 279, no. 3 (2000): G528—G535. http://dx.doi.org/10.1152/ajpgi.2000.279.3.g528.

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Presynaptic nicotinic acetylcholine receptors (nAChRs) were studied in myenteric plexus preparations from guinea pig ileum using intracellular electrophysiological methods. Microapplication of nicotine (1 mM) caused a biphasic depolarization in all AH neurons ( n = 30) and in 36 of 49 S neurons. Cytisine (1 mM) caused fast depolarizations in S neurons and no response in AH neurons. Mecamylamine (10 μM) blocked all responses caused by nicotine and cytisine. TTX (0.3 μM) blocked slow excitatory synaptic potentials in S and AH neurons but had no effect on fast depolarizations caused by nicotine.

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21

Renzetti, L. M., M. B. Wang, and J. P. Ryan. "Modulation of cat antral slow waves by ion substitution, Ca2+ and K+ channel blockade, and ACh stimulation." American Journal of Physiology-Gastrointestinal and Liver Physiology 263, no. 6 (1992): G880—G886. http://dx.doi.org/10.1152/ajpgi.1992.263.6.g880.

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Two distinct slow waves can be recorded from smooth muscle cells on the submucosal border (submucosal cells) and the myenteric border (myenteric cells) in the circular layer of the cat antrum. The present studies examined the effects of decreasing extracellular Na+ ([Na+]o) or Ca2+ concentration ([Ca2+]o), Ca2+ and K+ channel blockade, and acetylcholine (ACh) stimulation on "submucosal" and "myenteric" slow waves using intracellular recording techniques. Decreasing [Na+]o (30 mM) reduced the upstroke depolarization of slow waves from submucosal cells but had no effect on the upstroke depolariz

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22

Peet, M. J., K. Curry, D. S. Magnuson, and H. McLennan. "Ca2+-dependent depolarization and burst firing of rat CA1 pyramidal neurones induced by N-methyl-D-aspartic acid and quinolinic acid: antagonism by 2-amino-5-phosphonovaleric and kynurenic acids." Canadian Journal of Physiology and Pharmacology 64, no. 2 (1986): 163–68. http://dx.doi.org/10.1139/y86-024.

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The excitatory effects of microiontophoretically applied quisqualic (QUIS), N-methyl-D-aspartic (NMDA), and quinolinic (QUIN) acids were investigated using intracellular recording from CA1 pyramidal neurones in slices of rat hippocampus. QUIS evoked only simple action potentials superimposed upon a depolarization which attained a clear plateau. When this level had been reached, increased ejecting currents did not produce further depolarization. By contrast, with low currents NMD A and QUIN elicited small membrane depolarizations which triggered bursts of action potentials superimposed upon rhy

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23

Barnes, S., and M. C. Deschenes. "Contribution of Ca and Ca-activated Cl channels to regenerative depolarization and membrane bistability of cone photoreceptors." Journal of Neurophysiology 68, no. 3 (1992): 745–55. http://dx.doi.org/10.1152/jn.1992.68.3.745.

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1. Cone photoreceptors in several vertebrate species generate Ca-dependent regenerative depolarizations (e.g., Ca spikes lasting up to 2 s) in response to current injection or surround illumination and may remain in a state of prolonged depolarization (e.g., a permanent plateau near 0 mV) after these stimuli. This paper, while confirming the role of Ca channels in the regenerative depolarization, demonstrates that Ca-activated Cl channels either enhance or hinder prolonged depolarization, depending on the value of the chloride equilibrium potential (ECl). 2. Current- and voltage-clamp recordin

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Sorimachi, Takatoshi, Hiroshi Abe, Shigekazu Takeuchi, and Ryuichi Tanaka. "Ischemic depolarization monitoring: evaluation of protein synthesis in the hippocampal CA1 after brief unilateral ischemia in a gerbil model." Journal of Neurosurgery 97, no. 1 (2002): 104–11. http://dx.doi.org/10.3171/jns.2002.97.1.0104.

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Object. The authors investigate whether depolarization monitoring is an accurate index of ischemic damage in a gerbil model of unilateral ischemia and assess the effects of brief cerebral ischemia on protein synthesis in this model. Methods. The authors evaluate the relationship between the duration of ischemic depolarization caused by unilateral carotid artery occlusion and ischemia-induced neuronal damage in the CA1 subregion 7 days after ischemia. When the depolarization period exceeded 210 seconds, some neuronal damage was detected, and almost complete neuronal damage was observed when the

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25

Yamane, T., T. Furukawa, and M. Hiraoka. "4-Aminopyridine block of the noninactivating cloned K+ channel Kv1.5 expressed in Xenopus oocytes." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 2 (1995): H556—H564. http://dx.doi.org/10.1152/ajpheart.1995.269.2.h556.

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The blocking action of 4-aminopyridine (4-AP) on the cloned K+ channel Kv1.5 expressed in Xenopus oocytes was studied using the two-microelectrode voltage-clamp method. Application of 4-AP to the bath solution reversibly suppressed the expressed current in a voltage- and concentration-dependent manner decreasing with membrane depolarization and with a half-maximal inhibitory concentration of 0.14 mM (at +40 mV). Both block and unblock occurred mainly during a depolarization when channels were activated. With successive depolarizations, 4-AP decreased not only the peak amplitudes of the current

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26

Balança, Baptiste, Anne Meiller, Laurent Bezin, Jens P. Dreier, Stéphane Marinesco, and Thomas Lieutaud. "Altered hypermetabolic response to cortical spreading depolarizations after traumatic brain injury in rats." Journal of Cerebral Blood Flow & Metabolism 37, no. 5 (2016): 1670–86. http://dx.doi.org/10.1177/0271678x16657571.

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Spreading depolarizations are waves of near-complete breakdown of neuronal transmembrane ion gradients, free energy starving, and mass depolarization. Spreading depolarizations in electrically inactive tissue are associated with poor outcome in patients with traumatic brain injury. Here, we studied changes in regional cerebral blood flow and brain oxygen (PbtO2), glucose ([Glc]b), and lactate ([Lac]b) concentrations in rats, using minimally invasive real-time sensors. Rats underwent either spreading depolarizations chemically triggered by KCl in naïve cortex in absence of traumatic brain injur

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Chen, Qun, Michael Chopp, Gordon Bodzin, and Hua Chen. "Temperature Modulation of Cerebral Depolarization during Focal Cerebral Ischemia in Rats: Correlation with Ischemic Injury." Journal of Cerebral Blood Flow & Metabolism 13, no. 3 (1993): 389–94. http://dx.doi.org/10.1038/jcbfm.1993.52.

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The role of cerebral depolarizations in focal cerebral ischemia is unknown. We therefore measured the direct current (DC) electrical activity in the cortex of Wistar rats subjected to transient occlusion of the middle cerebral artery (MCA). Focal ischemia was induced for 90 min by insertion of an intraluminal filament to occlude the MCA. To modulate cell damage, we subjected the rats to hypothermic (30°C, n = 4), normothermic (37°C, n = 4), and hyperthermic (40°C, n = 6) ischemia. Controlled temperatures were also maintained during 1 h of reperfusion. Continuous cortical DC potential changes w

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Nicolet, M., M. Schnaiter, and O. Stetzer. "Circular depolarization ratios of single water droplets and finite ice circular cylinders: a modeling study." Atmospheric Chemistry and Physics 12, no. 9 (2012): 4207–14. http://dx.doi.org/10.5194/acp-12-4207-2012.

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Abstract. Computations of the phase matrix elements for single water droplets and ice crystals in fixed orientations are presented to determine if circular depolarization δC is more accurate than linear depolarization for phase discrimination. T-matrix simulations were performed to calculate right-handed and left-handed circular depolarization ratios δ+C, respectively δ−C and to compare them with linear ones. Ice crystals are assumed to have a circular cylindrical shape where their surface-equivalent diameters range up to 5 μm. The circular depolarization ratios of ice particles were generally

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Ferragamo, Michael J., and Donata Oertel. "Octopus Cells of the Mammalian Ventral Cochlear Nucleus Sense the Rate of Depolarization." Journal of Neurophysiology 87, no. 5 (2002): 2262–70. http://dx.doi.org/10.1152/jn.00587.2001.

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Whole cell patch recordings in slices show that the probability of firing of action potentials in octopus cells of the ventral cochlear nucleus depends on the dynamic properties of depolarization. Octopus cells fired only when the rate of rise of a depolarization exceeded a threshold value that varied between 5 and 15 mV/ms among cells. The threshold rate of rise was independent of whether depolarizations were evoked synaptically or by the intracellular injection of current. Previous work showed that octopus cells are contacted by many auditory nerve fibers, each providing less than 1-mV depol

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Szczupak, L., J. Edgar, ML Peralta, and WB Kristan. "Long-lasting depolarization of leech neurons mediated by receptors with a nicotinic binding site." Journal of Experimental Biology 201, no. 12 (1998): 1895–906. http://dx.doi.org/10.1242/jeb.201.12.1895.

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The serotonergic Retzius neurons of the leech midbody ganglia respond in a complex manner to pressure pulses of acetylcholine (ACh) applied onto their soma with a fast depolarization followed by a slower hyperpolarization and an additional delayed long-lasting depolarization. The delayed depolarization is the subject of the present study. The delayed depolarization could be elicited by long (&gt;1 s) ACh pressure pulses or by short pulses (10 ms) of carbachol, nicotine and DMPP, but not by muscarinic agonists. It was inhibited by bath application of nicotine (10-100 micromol l-1), strychni

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Schwindt, Peter, and Wayne Crill. "Mechanisms Underlying Burst and Regular Spiking Evoked by Dendritic Depolarization in Layer 5 Cortical Pyramidal Neurons." Journal of Neurophysiology 81, no. 3 (1999): 1341–54. http://dx.doi.org/10.1152/jn.1999.81.3.1341.

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Mechanisms underlying burst and regular spiking evoked by dendritic depolarization in layer 5 cortical pyramidal neurons. Apical dendrites of layer 5 pyramidal cells in a slice preparation of rat sensorimotor cortex were depolarized focally by long-lasting glutamate iontophoresis while recording intracellularly from their soma. In most cells the firing pattern evoked by the smallest dendritic depolarization that evoked spikes consisted of repetitive bursts of action potentials. During larger dendritic depolarizations initial burst firing was followed by regular spiking. As dendritic depolariza

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Lin, Jen-Wei, Feiyuan Yu, Wolfgang S. Müller, Gösta Ehnholm, and Yoshio Okada. "Focused ultrasound transiently increases membrane conductance in isolated crayfish axon." Journal of Neurophysiology 121, no. 2 (2019): 480–89. http://dx.doi.org/10.1152/jn.00541.2018.

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We report a novel phenomenon produced by focused ultrasound (US) that may be important for understanding its effects on cell membranes. When a US burst (2.1 MHz, 1-mm focal diameter, 0.1–1 MPa) was focused on a motor axon of the crayfish neuromuscular junction, it consistently produced a fast hyperpolarization, which was followed or superseded by subthreshold depolarizations or action potentials in a stochastic manner. The depolarization persisted in the presence of voltage-gated channel blockers [1 µM TTX ( INa), 50 µM ZD7288 ( Ih), and 200 µM 4-aminopyridine ( IK)] and typically started shor

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Klink, Ruby, and Angel Alonso. "Ionic Mechanisms of Muscarinic Depolarization in Entorhinal Cortex Layer II Neurons." Journal of Neurophysiology 77, no. 4 (1997): 1829–43. http://dx.doi.org/10.1152/jn.1997.77.4.1829.

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Klink, Ruby and Angel Alonso. Ionic mechanisms of muscarinic depolarization in entorhinal cortex layer II neurons. J. Neurophysiol. 77: 1829–1843, 1997. The mechanisms underlying direct muscarinic depolarizing responses in the stellate cells (SCs) and non-SCs of medial entorhinal cortex layer II were investigated in tissue slices by intracellular recording and pressure-pulse applications of carbachol (CCh). Subthreshold CCh depolarizations were largely potentiated in amplitude and duration when paired with a short DC depolarization that triggered cell firing. During Na+ conductance block, CCh

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Sackin, H. "Electrophysiology of salamander proximal tubule. I. Effects of rapid cooling." American Journal of Physiology-Renal Physiology 251, no. 2 (1986): F319—F333. http://dx.doi.org/10.1152/ajprenal.1986.251.2.f319.

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The response of the amphibian proximal tubule to a rapid decrease in temperature was studied in isolated perfused tubules of Ambystoma tigrinum. Cooling from 23 to 4 degrees C increased paracellular and cellular electrical resistances by factors of 1.7 and 3.6, respectively, but had virtually no effect on the ionic selectivity of the paracellular pathway. When lumen and bath solutions were maintained identical by rapid tubule perfusion, decreasing bath temperature from 22 to 0 degree C in 400 ms depolarized the transepithelial potential (Vte) from -3.7 +/- 0.3 to -1.1 +/- 0.2 mV and depolarize

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Olcese, Riccardo, Ramón Latorre, Ligia Toro, Francisco Bezanilla, and Enrico Stefani. "Correlation between Charge Movement and Ionic Current during Slow Inactivation in Shaker K+ Channels." Journal of General Physiology 110, no. 5 (1997): 579–89. http://dx.doi.org/10.1085/jgp.110.5.579.

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Prolonged depolarization induces a slow inactivation process in some K+ channels. We have studied ionic and gating currents during long depolarizations in the mutant Shaker H4-Δ(6–46) K+ channel and in the nonconducting mutant (Shaker H4-Δ(6–46)-W434F). These channels lack the amino terminus that confers the fast (N-type) inactivation (Hoshi, T., W.N. Zagotta, and R.W. Aldrich. 1991. Neuron. 7:547–556). Channels were expressed in oocytes and currents were measured with the cut-open-oocyte and patch-clamp techniques. In both clones, the curves describing the voltage dependence of the charge mov

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Coburn, R. F. "Stretch-induced membrane depolarization in ferret trachealis smooth muscle cells." Journal of Applied Physiology 62, no. 6 (1987): 2320–25. http://dx.doi.org/10.1152/jappl.1987.62.6.2320.

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We determined the effects of increasing the length of the ferret trachealis muscle on smooth muscle membrane potentials recorded on successive impalements by microelectrodes. The preparation included the paratracheal ganglion nerve plexus as well as trachealis muscle. With sustained increases in muscle length over the range 0.5–0.8 to 1.2 maximal length (Lmax), depolarization occurred, which was related to the amplitude of the length increase. Membrane depolarizations were also evoked after stretching to lengths approximately 1.1 Lmax and returning to the control length. Stretch-induced membra

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Gossard, J. P., J. M. Cabelguen, and S. Rossignol. "Intra-axonal recordings of cutaneous primary afferents during fictive locomotion in the cat." Journal of Neurophysiology 62, no. 5 (1989): 1177–88. http://dx.doi.org/10.1152/jn.1989.62.5.1177.

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1. Cutaneous primary afferents were recorded intracellularly during fictive locomotion in decorticated cats with the goal of improving our understanding of how locomotor networks might centrally control the transmission in cutaneous pathways at a presynaptic level. 2. Identified cutaneous axons from superficialis peroneal nerve (SP) or tibialis posterior nerve (TP) were recorded intracellularly together with the electroneurograms (ENGs) of representative flexor and extensor muscle nerves of the hindlimb as well as dorsal root potential from L6 or L7 (DRP). Fictive locomotion occurred spontaneo

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Nagao, Tetsuhiko, and Paul M. Vanhoutte. "Electrical and Mechanical Changes during Anoxic Contractions of the Isolated Canine Basilar Artery." Journal of Cerebral Blood Flow & Metabolism 13, no. 3 (1993): 498–502. http://dx.doi.org/10.1038/jcbfm.1993.64.

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Isometric tension and membrane potential were measured to determine the electrophysiological events occurring during anoxia in the isolated canine basilar artery. Anoxia induced transient contractions which were inhibited by the Ca2+-channel inhibitor, diltiazem, and were abolished in Ca2+-free solution. Anoxic contractions were accompanied by membrane depolarizations, which were resistant to diltiazem. When matched contractions were obtained with anoxia and high K+, the level of membrane depolarization was smaller during anoxic contractions. These results support the importance of voltage-dep

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Kruse, Martin, Susy C. Kohout, and Bertil Hille. "Reinterpretation of the substrate specificity of the voltage-sensing phosphatase during dimerization." Journal of General Physiology 151, no. 2 (2019): 258–63. http://dx.doi.org/10.1085/jgp.201812260.

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Voltage-sensing phosphatases (VSPs) cleave both 3- and 5-phosphates from inositol phospholipids in response to membrane depolarization. When low concentrations of Ciona intestinalis VSP are expressed in Xenopus laevis oocytes, the 5-phosphatase reaction can be observed during large membrane depolarizations. When higher concentrations are expressed, the 5-phosphatase activity is observed with smaller depolarizations, and the 3-phosphatase activity is revealed with strong depolarization. Here we ask whether this apparent induction of 3-phosphatase activity is attributable to the dimerization tha

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Hillsley, Kirk, and Gary M. Mawe. "5-HT is present in nerves of guinea pig sphincter of Oddi and depolarizes sphincter of Oddi neurons." American Journal of Physiology-Gastrointestinal and Liver Physiology 275, no. 5 (1998): G1018—G1027. http://dx.doi.org/10.1152/ajpgi.1998.275.5.g1018.

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This study involved immunohistochemistry and intracellular electrophysiology to investigate serotonergic neurotransmission in the sphincter of Oddi (SO). 5-Hydroxytryptamine (HT)-positive neurons (14 cells/preparation) and nerve fibers were observed in the ganglionated plexus. Serotonergic nerve fibers, which persisted under 2- to 6-day organ culture, were densely distributed, with varicose endings encircling some SO neurons. When 5-HT was applied to SO neurons, it elicited three different responses: 1) a fast depolarization to 5-HT in 31 of 62 cells was mimicked by 2-methyl-5-HT and blocked b

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PEARSON, K. G., and J. M. RAMIREZ. "Influence of input from the Forewing Stretch Receptors on Motoneurones in Flying Locusts." Journal of Experimental Biology 151, no. 1 (1990): 317–40. http://dx.doi.org/10.1242/jeb.151.1.317.

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1. Previous studies on the forewing stretch receptors (FSRs) of locusts have suggested that feedback from these receptors during flight contributes to the excitation of depressor motoneurones and reduces the duration of depolarizations in elevator motoneurones. We have investigated these proposals by measuring the timing of FSR activity relative to depressor activity and by examining the effects of stimulating the FSRs on the membrane potential oscillations in flight motoneurones. 2. Activity in the FSRs was recorded in tethered intact animals flying in a windstream and in preparations that al

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Gokin, A. P., K. Hillsley, and G. M. Mawe. "Cholecystokinin depolarizes guinea pig sphincter of Oddi neurons by activating CCK-A receptors." American Journal of Physiology-Gastrointestinal and Liver Physiology 272, no. 6 (1997): G1365—G1371. http://dx.doi.org/10.1152/ajpgi.1997.272.6.g1365.

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Motility studies indicate that cholecystokinin (CCK) acts through a neural mechanism in the sphincter of Oddi (SO) after meals. To evaluate its actions in SO ganglia, CCK was applied by microejection (0.1 mM) or superfusion (0.1 to 300 nM) while recording was carried out intracellularly from intact SO neurons. In tonic cells, microejection and superfusion of CCK caused a prolonged depolarization accompanied by action potentials. In phasic cells, microejection of CCK caused brief and/or prolonged depolarizations, but superfusion caused only prolonged depolarizations. In afterhyperpolarized cell

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van den Bergh, Walter M., J. Karel Zuur, Niels A. Kamerling, et al. "Role of magnesium in the reduction of ischemic depolarization and lesion volume after experimental subarachnoid hemorrhage." Journal of Neurosurgery 97, no. 2 (2002): 416–22. http://dx.doi.org/10.3171/jns.2002.97.2.0416.

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Object. Ischemia-induced tissue depolarizations probably play an important role in the pathophysiology of cerebral ischemia caused by parent vessel occlusion. Their role in ischemia caused by subarachnoid hemorrhage (SAH) remains to be investigated. The authors determined whether ischemic depolarizations (IDs) or cortical spreading depressions (CSDs) occur after SAH, and how these relate to the extent of tissue injury measured on magnetic resonance (MR) images. In addition, they assessed whether administration of MgSO4 reduces depolarization time and lesion volume. Methods. By means of the end

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Jobling, P. "Electrophysiological events during neuroeffector transmission in the spleen of guinea‐pigs and rats." Journal of Physiology 476, no. 1 (1994): 153–65. http://dx.doi.org/10.1113/jphysiol.1994.sp020119.

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Intracellular recordings were made from smooth muscle cells of arterioles and the capsule of the spleen of guinea‐pig and rat, and the responses to periarterial or subcapsular nerve stimulation were recorded. The innervation of the spleen was studied using fluorescence and immunohistochemical techniques. Catecholamine‐containing axons were associated with smooth muscle of the splenic capsule, trabeculae, arterioles and amongst cells of the periarteriolar lymphoid sheath. Axons immunoreactive for neuropeptide Y (NPY) and tyrosine hydroxylase were distributed in an identical manner to catecholam

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Sivilotti, L. G., S. W. Thompson, and C. J. Woolf. "Rate of rise of the cumulative depolarization evoked by repetitive stimulation of small-caliber afferents is a predictor of action potential windup in rat spinal neurons in vitro." Journal of Neurophysiology 69, no. 5 (1993): 1621–31. http://dx.doi.org/10.1152/jn.1993.69.5.1621.

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1. The summation of depolarizing postsynaptic potentials (PSPs) evoked by stimulation of primary afferent fibers in lumbar dorsal roots was studied in dorsal and ventral horn neurons in the rat hemisected spinal cord in vitro with current-clamp intracellular recording techniques. PSPs evoked by activation of A delta and/or C fibers could summate after repetitive stimulation at low frequencies: this resulted in a progressive, long-lasting change in the neuronal membrane potential (Vm) (cumulative depolarization). Cumulative depolarization was not observed after stimulation at A beta-fiber inten

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Hung, Anne Y., and Neil S. Magoski. "Activity-Dependent Initiation of a Prolonged Depolarization in Aplysia Bag Cell Neurons: Role for a Cation Channel." Journal of Neurophysiology 97, no. 3 (2007): 2465–79. http://dx.doi.org/10.1152/jn.00941.2006.

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The translation of prior activity into changes in excitability is essential for memory and the initiation of behavior. After brief synaptic input, the bag cell neurons of Aplysia californica undergo a nearly 30-min afterdischarge to release egg-laying hormone. The present study examines a prolonged depolarization in cultured bag cell neurons. A 5-Hz, 10-s action potential train elicited a depolarization of about 10 mV, which lasted ≤30 min and was reduced by calmodulin kinase inhibition. Very broad action potentials (resulting from TEA application) decreased prolonged depolarization amplitude,

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Slish, Donald F., Donald G. Welsh, and Joseph E. Brayden. "Diacylglycerol and protein kinase C activate cation channels involved in myogenic tone." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 6 (2002): H2196—H2201. http://dx.doi.org/10.1152/ajpheart.00605.2002.

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The smooth muscle cells of resistance arteries depolarize and contract when intravascular pressure is elevated. This is a central characteristic of myogenic tone, which plays an important role in regulation of blood flow in many vascular beds. Pressure-induced vascular smooth muscle depolarization depends in part on the activation of cation channels. Here, we show that activation of these smooth muscle cation channels and pressure-induced depolarization are mediated by protein kinase C in cerebral resistance arteries. Diacylglycerol, phorbol myristate acetate, and cell swelling activate a cati

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Gold, M. R., and G. R. Strichartz. "Acute effects of repetitive depolarization on sodium current in chick myocytes." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 6 (1991): H1810—H1818. http://dx.doi.org/10.1152/ajpheart.1991.260.6.h1810.

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Acute effects of repetitive depolarization on the inward Na+ current (INa) of cultured embryonic chick atrial cells were studied using the whole cell patch-clamp technique. Stimulation rates of 1 Hz or greater produced a progressive decrement of peak INa. With depolarizations to 0 mV of 150-ms duration, applied at 2 Hz from a holding potential of -100 mV, the steady-state decrement was approximately 20%. The magnitude of this effect increased with stimulation frequency and with test potential depolarization and decreased with membrane hyperpolarization. Analysis of INa kinetics revealed that r

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Santos, Edgar, Fiorella León, Humberto Silos, et al. "Incidence, hemodynamic, and electrical characteristics of spreading depolarization in a swine model are affected by local but not by intravenous application of magnesium." Journal of Cerebral Blood Flow & Metabolism 36, no. 12 (2016): 2051–57. http://dx.doi.org/10.1177/0271678x16671317.

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The aim was to characterize the effects of magnesium sulfate, using i.v. bolus and local administration, using intrinsic signal imaging, and on electrocorticographic activity during the induction and propagation of spreading depolarizations in the gyrencephalic porcine brain. Local application of magnesium sulfate led to a complete inhibition of spreading depolarizations. One hour after washing out the topical magnesium sulfate, re-incidence of the spreading depolarizations was observed in 50% of the hemispheres. Those spreading depolarizations showed attenuation in hemodynamic characteristics

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Frey, Bret W., Andreas Carl, and Nelson G. Publicover. "Charybdotoxin block of Ca2+-activated K+ channels in colonic muscle depends on membrane potential dynamics." American Journal of Physiology-Cell Physiology 274, no. 3 (1998): C673—C680. http://dx.doi.org/10.1152/ajpcell.1998.274.3.c673.

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Charybdotoxin (ChTX) is a specific blocker of Ca2+-activated K+ channels. The voltage- and time-dependent dynamics of ChTX block were investigated using canine colonic myocytes and the whole cell patch-clamp technique with step and ramp depolarization protocols. During prolonged step depolarizations, K+ current slowly increased in the continued presence of ChTX (100 nM). The rate of increase depended on membrane potential with an e-fold change for every 60 mV. During ramp depolarizations, the effectiveness of ChTX block depended significantly on the rate of the ramp (50% at 0.01 V/s to 80% at

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