scholarly journals Astrocytic Acidosis in Hyperglycemic and Complete Ischemia

1990 ◽  
Vol 10 (1) ◽  
pp. 104-114 ◽  
Author(s):  
Richard P. Kraig ◽  
Mitchell Chesler
Keyword(s):  
Cardiac Arrest ◽  
Input Resistance ◽  
Ion Permeability ◽  
Animal Group ◽  
Negative Change ◽  
Anoxic Depolarization ◽  
Concomitant Reduction ◽  
Acidic Conditions ◽  
Complete Brain Ischemia ◽  
Passive Electrical Properties

Nearly complete brain ischemia under normoglycemic conditions results in death of only selectively vulnerable neurons. With prior elevation of brain glucose, such injury is enhanced to include pancellular necrosis (i.e., infarction), perhaps because an associated, severe lactic acidosis preferentially injures astrocytes. However, no direct physiologic measurements exist to support this hypothesis. Therefore, we used microelectrodes to measure intracellular pH and passive electrical properties of cortical astrocytes as a first approach to characterizing the physiologic behavior of these cells during hyperglycemic and complete ischemia, conditions that produce infarction in reperfused brain. Anesthesized rats (n = 26) were made extremely hyperglycemic (blood glucose, 51.4 ± 2.8 m M) so as to create potentially the most extreme acidic conditions possible; then ischemia was induced by cardiac arrest. Two loci more acidic than the interstitial space (6.17–6.20 pH) were found. The more acidic locus [4.30 ± 0.19 (n = 5); range: 3.82–4.89] was occasionally seen at the onset of anoxic depolarization, 3–7 min after cardiac arrest. The less acidic locus [5.30 ± 0.07 (n = 53); range 4.46–5.93)] was seen 5–46 min after cardiac arrest. A small negative change in DC potential [8 ± 1 mV (n = 5); range –3 to –12 mV and 7 ± 2 mV (n = 53); range + 3 to –31 mV, respectively] was always seen upon impalement of acidic loci, suggesting cellular penetration. In a separate group of five animals, electrical characteristics of these cells were specifically measured (n = 17): membrane potential was –12 ± 0.2 mV (range –3 to –24 mV), input resistance was 114 ± 16 MΩ (range 25–250 MΩ), and time constant was 4.4 ± 0.4 ms (range 3.0–7.9 ms). Injection of horseradish peroxidase into cells from either animal group uniformly stained degenerating astrocytes. These findings establish previously unrecognized properties of ischemic astrocytes that may be prerequisites for infarction from nearly complete ischemia: the capacity to develop profound cellular acidosis and a concomitant reduction in cell membrane ion permeability.

scholarly journals Active and passive electrical properties of single bullfrog atrial cells.

1981 ◽  
Vol 78 (1) ◽  
pp. 19-42 ◽  
Author(s):  
J R Hume ◽  
W Giles
Keyword(s):  
Rana Catesbeiana ◽  
Single Cells ◽  
Input Resistance ◽  
Isolated Cells ◽  
Atrial Cells ◽  
Long Duration ◽  
Electrophysiological Measurements ◽  
3 Omega ◽  
Passive Electrical Properties ◽  
Atrial Cell

Single cells from the bullfrog (Rana catesbeiana) atrium have been prepared by using a modification of the enzymatic dispersion procedure described by Bagby et al. (1971. Nature [Long.]. 234:351--352) and Fay and Delise (1973. Proc. Natl. Acad. Sci. U.S.A. 70:641--645). Visualization of relaxed cells via phase-contrast or Nomarski optics (magnification, 400--600) indicates that cells range between 150 and 350 micrometers in length and 4 and 7 micrometers in diameter. The mean sarcomere length in relaxed, quiescent atrial cells in 2.05 micrometer. Conventional electrophysiological measurements have been made. In normal Ringer's solution (2.5 mM K+, 2.5 mM Ca++) acceptable cells have stable resting potentials of about -88 mV, and large (125 mV) long-duration (approximately 720 ms) action potentials can be elicited. The Vm vs. log[K+]0 relation obtained from isolated cells is similar to that of the intact atrium. The depolarizing phase of the action potential of isolated atrial myocytes exhibits two pharmacologically separable components: tetrodotoxin (10(-6) g/ml) markedly suppresses the initial regenerative depolarization, whereas verapamil (3 x 10(-6) M) inhibits the secondary depolarization and reduce the plateau height. A bridge circuit was used to estimate the input resistance (220 +/- 7 M omega) and time constant 20 +/- 7 ms) of these cells. Two-microelectrode experiments have revealed small differences in the electrotonic potentials recorded simultaneously at two different sites within a single cell. The equations for a linear, short cable were used to calculate the electrical constants of relaxed, single atrial cells: lambda = 921.3 +/- 29.5 micrometers; Ri = 118.1 +/- 24.5 omega cm; Rm = 7.9 +/- 1.2 x 10(3) omega cm2; Cm = 2.2 +/- 0.3 mu Fcm-2. These results and the atrial cell morphology suggest that this preparation may be particularly suitable for voltage-clamp studies.

Passive Properties of Swimmeret Motor Neurons

1997 ◽  
Vol 78 (1) ◽  
pp. 92-102 ◽  
Author(s):  
Carolyn M. Sherff ◽  
Brian Mulloney
Keyword(s):  
Motor Neurons ◽  
Continuous Production ◽  
Motor Pattern ◽  
Input Resistance ◽  
Membrane Potentials ◽  
Power Stroke ◽  
Return Stroke ◽  
Time Constants ◽  
Large Motor ◽  
Passive Electrical Properties

Sherff, Carolyn M. and Brian Mulloney. Passive properties of swimmeret motor neurons. J. Neurophysiol. 78: 92–102, 1997. Four different functional types of motor neurons innervate each swimmeret: return-stroke excitors (RSEs), power-stroke excitors (PSEs), return-stroke inhibitors (RSIs), and power-stroke inhibitors (PSIs). We studied the structures and passive electrical properties of these neurons, and tested the hypothesis that different types of motor neurons would have different passive properties that influenced generation of the swimmeret motor pattern. Cell bodies of neurons innervating one swimmeret were clustered in two anatomic groups in the same ganglion. The shapes of motor neurons in both groups were similar, despite the differences in locations of their cell bodies and in their functions. Diameters of their axons in the swimmeret nerve ranged from <2 to ∼35 μm. Resting membrane potentials, input resistances, and membrane time constants were recorded with microelectrodes in the processes of swimmeret motor neurons in isolated abdominal nerve cord preparations. Membrane potentials had a median of −59 mV, with 25th and 75th percentiles of −66.0 and −53 mV. The median input resistance was 6.4 MΩ, with 25th and 75th percentiles of 3.4 and 13.7 MΩ. Membrane time constants had a median of 9.3 ms, with 25th and 75th percentiles of 5.7 and 15.0 ms. Excitatory and inhibitory motor neurons had similar passive properties. RSE motor neurons were typically more depolarized than the other types, but the passive properties of RSE, PSE, RSI, and PSI neurons were not significantly different. Membrane time constants measured from cell bodies were briefer than those measured from neuropil processes, but membrane potentials and input resistances were not significantly different. The relative sizes of different motor neurons were measured from the sizes of their impulses recorded extracellularly from the swimmeret nerve. Smaller motor neurons had lower membrane potentials and were more likely to be active in the motor pattern than were large motor neurons. Motor neurons of different sizes had similar input resistances and membrane time constants. Motor neurons that were either oscillating or oscillating and firing in phase with the swimmeret motor pattern had lower average membrane potentials and longer time constants than those that were not oscillating. When the state of the swimmeret system changed from quiescence to continuous production of the motor pattern, the resting potentials, input resistances, and membrane time constants of individual swimmeret motor neurons changed only slightly. On average, both input resistance and membrane time constant increased. These similarities are considered in light of the functional task each motor neuron performs, and a hypothesis is developed that links the brief time constants of these neurons and graded synaptic transmission by premotor interneurons to control of the swimmeret muscles and the performance of the swimmeret system.

Neural and hormonal control of membrane conductance in the pig pancreatic acinar cell

1984 ◽  
Vol 247 (5) ◽  
pp. G520-G526 ◽  
Author(s):  
G. T. Pearson ◽  
P. M. Flanagan ◽  
O. H. Petersen
Keyword(s):  
Acinar Cell ◽  
Membrane Conductance ◽  
Input Resistance ◽  
Electrical Field Stimulation ◽  
Mean Value ◽  
Pancreatic Acinar Cell ◽  
Hormonal Control ◽  
Hormonal Stimulation ◽  
Membrane Hyperpolarization ◽  
Concomitant Reduction

Intracellular microelectrode recordings from superfused segments of pig pancreas have shown the resting acinar cell membrane potentials to range widely, with a mean value of -30.5 +/- 1.3 mV. Electrical field stimulation (FS) of the intrinsic pancreatic nerves induced frequency-dependent membrane hyperpolarization (10-15 mV) accompanied by a concomitant reduction in input resistance. Similar effects could be evoked by the superfusion or electroionophoresis of acetylcholine, amphibian or mammalian bombesin [gastrin-releasing peptide (GRP)], and pentagastrin. In normal Ca2+-containing solutions sustained secretagogue superfusion resulted in sustained hyperpolarization. In the absence of external Ca2+, similar stimulation caused only a transient hyperpolarizing response, with subsequent periods of secretagogue application having no effect. Atropine completely abolished the FS-evoked hyperpolarizations but had no effect on the responses evoked by bombesin, GRP, and pentagastrin. The present findings support the contention that neural and hormonal stimulation of the pig pancreas evokes Ca2+-dependent acinar cell hyperpolarization by causing a selective increase in membrane K+ permeability. A hypothesis is proposed that cellular K+ release through the opened conductance pathway promotes a K+-Na+-Cl- cotransport into the cell that serves a key function in the generation of acinar salt secretion.

White noise approach for estimating the passive electrical properties of neurons

1996 ◽  
Vol 76 (5) ◽  
pp. 3442-3450 ◽  
Author(s):  
W. N. Wright ◽  
B. L. Bardakjian ◽  
T. A. Valiante ◽  
J. L. Perez-Velazquez ◽  
P. L. Carlen
Keyword(s):  
Electrical Properties ◽  
White Noise ◽  
Input Impedance ◽  
Granule Cells ◽  
Short Pulse ◽  
Input Resistance ◽  
Membrane Resistance ◽  
Somatic Membrane ◽  
Dendritic Membrane ◽  
Passive Electrical Properties

1. The passive electrical properties of whole cell patched dentate granule cells were studied with the use of zero-mean Gaussian white noise current stimuli. Transmembrane voltage responses were used to compute the first-order Wiener kernels describing the current-voltage relationship at the soma for six cells. Frequency domain optimization techniques using a gradient method for function minimization were then employed to identify the optimal electrical parameter values. Low-power white noise stimuli are presented as a favorable alternative to the use of short-pulse current inputs for investigating neuronal passive electrical properties. 2. The optimization results demonstrated that the lumped resistive and capacitive properties of the recording electrode must be included in the analytic input impedance expression to optimally fit the measured cellular responses. The addition of the electrode resistance (Re) and capacitance (Ce) to the original parameters (somatic conductance, somatic capacitance, axial resistance, dendritic conductance, and dendritic capacitance) results in a seven-parameter model. The mean Ce value from the six cells was 5.4 +/- 0.3 (SE) pF, whereas Re following formation of the patch was found to be 20 +/- 2 M omega. 3. The six dentate granule cells were found to have an input resistance of 600 +/- 20 M omega and a dendritic to somatic conductance ratio of 6.3 +/- 1.1. The electronic length of the equivalent dendritic cylinder was found to be 0.42 +/- 0.03. The membrane time constant in the soma was found to be 13 +/- 3 ms, whereas the membrane time constant of the dendrites was 58 +/- 5 ms. Incorporation of morphological estimations led to the following distributed electrical parameters: somatic membrane resistance = 25 +/- 4 k omega cm2, somatic membrane capacitance = 0.48 +/- 0.05 microF/cm2, Ri (input resistance) = 72 +/- 5 omega cm, dendritic membrane resistance = 59 +/- 4 k omega cm2, and dendritic membrane capacitance = 0.97 +/- 0.06 microF/cm2. On the basis of capacitive measurements, the ratio of dendritic surface area to somatic surface area was found to be 34 +/- 2. 4. For comparative purposes, hyperpolarizing short pulses were also injected into each cell. The short-pulse input impedance measurements were found to underestimate the input resistance of the cell and to overestimate both the somatic conductance and the membrane time constants relative to the white noise input impedance measurements.

Examining protection from anoxic depolarization by the drugs dibucaine and carbetapentane using whole cell recording from CA1 neurons

2012 ◽  
Vol 107 (8) ◽  
pp. 2083-2095 ◽  
Author(s):  
Sean H. White ◽  
C. Devin Brisson ◽  
R. David Andrew
Keyword(s):  
Pyramidal Neurons ◽  
Cortical Excitability ◽  
Neuronal Damage ◽  
Input Resistance ◽  
Stroke Onset ◽  
Light Transmittance ◽  
Resting Membrane Potential ◽  
Whole Cell ◽  
Anoxic Depolarization

As an immediate consequence of stroke onset, failure of the Na+-K+-ATPase pump evokes a propagating anoxic depolarization (AD) across gray matter. Acute neuronal swelling and dendritic beading arise within seconds in the future ischemic core, imaged as changes in light transmittance (ΔLT). AD is itself not a target for drug-based reduction of stroke injury because it is generated in the 1st min of stroke onset. Peri-infarct depolarizations (PIDs) are milder AD-like events that recur during the hours following AD and contribute to infarct expansion. Inhibiting PIDs with drugs could limit expansion. Two types of drugs, “caines” and σ1-receptor ligands, have been found to inhibit AD onset (and may also oppose PID initiation), yet their underlying actions have not been examined. Imaging ΔLT in the CA1 region simultaneously with whole cell current-clamp recording from CA1 pyramidal neurons reveal that the elevated LT front and onset of the AD are coincident. Either dibucaine or carbetapentane pretreatment significantly delays AD onset without affecting resting membrane potential or neuronal input resistance. Dibucaine decreases excitability by raising spike threshold and decreasing action potential (AP) frequency, whereas carbetapentane eliminates the fast afterhyperpolarization while accentuating the slow afterhyperpolarization to reduce AP frequency. Orthodromic and antidromic APs are eliminated by dibucaine within 15 min but not by carbetapentane. Thus both drugs reduce cortical excitability at the level of the single pyramidal neuron but through strikingly different mechanisms. In vivo, both drugs would likely inhibit recurring PIDs in the expanding penumbra and so potentially could reduce developing neuronal damage over many hours poststroke when PIDs occur.

scholarly journals Ion Channel Involvement in Anoxic Depolarization Induced by Cardiac Arrest in Rat Brain

1995 ◽  
Vol 15 (4) ◽  
pp. 587-594 ◽  
Author(s):  
Yaxia Xie ◽  
Elke Zacharias ◽  
Patricia Hoff ◽  
Frank Tegtmeier
Keyword(s):  
Cardiac Arrest ◽  
Ion Channel ◽  
Rat Brain ◽  
Ion Homeostasis ◽  
Rapid Decline ◽  
Channel Blockers ◽  
Mk 801 ◽  
Anoxic Depolarization ◽  
Ion Activity ◽  
Cellular Ca

Anoxic depolarization (AD) and failure of ion homeostasis play an important role in ischemia-induced neuronal injury. In the present study, different drugs with known ion-channel-modulating properties were examined for their ability to interfere with cardiac-arrest-elicited AD and with the changes in the extracellular ion activity in rat brain. Our results indicate that only drugs primarily blocking membrane Na+ permeability (NBQX, R56865, and flunarizine) delayed the occurrence of AD, while compounds affecting cellular Ca2+ load (MK-801 and nimodipine) did not influence the latency time. The ischemia-induced [Na+]e reduction was attenuated by R56865. Blockade of the ATP-sensitive K+ channels with glibenclamide reduced the [K+]e increase upon ischemia, indicating an involvement of the KATP channels in ischemia-induced K+ efflux. The KATP channel opener cromakalim did not affect the AD or the [K+]e concentration. The ischemia-induced rapid decline of extracellular calcium was attenuated by receptor-operated Ca2+ channel blockers MK-801 and NBQX, but not by the voltage-operated Ca2+ channel blocker nimodipine, R56865, and flunarizine.

Alzheimer-associated presenilin 2 gene is dysregulated in rat medial temporal lobe cortex after complete brain ischemia due to cardiac arrest

2016 ◽  
Vol 68 (1) ◽  
pp. 155-161 ◽  
Author(s):  
Ryszard Pluta ◽  
Janusz Kocki ◽  
Marzena Ułamek-Kozioł ◽  
Anna Bogucka-Kocka ◽  
Paulina Gil-Kulik ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Temporal Lobe ◽  
Brain Ischemia ◽  
Medial Temporal Lobe ◽  
Presenilin 2 ◽  
Complete Brain Ischemia

The effect of axotomy on posttetanic potentiation of group Ia synapses in the cat

1986 ◽  
Vol 56 (4) ◽  
pp. 1174-1184 ◽  
Author(s):  
B. Gustafsson ◽  
M. J. Pinter ◽  
H. Wigstrom
Keyword(s):  
Electrical Properties ◽  
High Resistance ◽  
Previous Analysis ◽  
Normal Population ◽  
Input Resistance ◽  
Posttetanic Potentiation ◽  
High Input ◽  
Synaptic Release ◽  
High Input Resistance ◽  
Passive Electrical Properties

Posttetanic potentiation (PTP) of composite Ia excitatory postsynaptic potentials (EPSPs) has been studied in normal cat alpha-motoneurons and in motoneurons axotomized 2-3 wk earlier by ventral root section. The maximal amount of PTP of EPSP amplitude (expressed relative to unpotentiated amplitude) was considerably less in the axotomized population compared with the normal population. The decrease in PTP provoked by axotomy occurs in association with a postaxotomy increase of input resistance, the net effect being that PTP in axotomized cells was much the same as that observed by others in normal motoneurons possessing similarly high input resistance. In agreement with previous results, EPSP peak amplitudes were decreased after axotomy. This decrease seemed to be largely related to an absence of the largest EPSPs, since otherwise the EPSP distributions of normal and axotomized motoneurons showed considerable overlap. It is suggested that the observed decrease in PTP after axotomy is related to a change in synaptic release properties and not secondary to changes in the electrical properties of motoneurons. A previous analysis has suggested that axotomy causes an alteration of the distribution of passive electrical properties among motoneurons such that axotomized cells resemble normal high-resistance motoneurons. The present results suggest that axotomy may affect the distribution of Ia synaptic release properties in a similar manner, since PTP in axotomized motoneurons resembles that observed in normal high-resistance motoneurons.

scholarly journals The Morphology and Passive Electrical Properties of Claw Closer Neurones in Snapping Shrimp

1982 ◽  
Vol 101 (1) ◽  
pp. 307-319
Author(s):  
JOHN A. WILSON ◽  
DEFOREST MELLON
Keyword(s):  
Body Size ◽  
Electrical Properties ◽  
Cell Body ◽  
Input Resistance ◽  
Proximal Portion ◽  
Snapping Shrimp ◽  
Length Constant ◽  
The Difference ◽  
Passive Electrical Properties ◽  
Cell Body Size

The morphology and passive electrical properties of the dimorphic pincer and snapper claw closer neurones were examined in the snapping shrimp, Alpheus heterochelis. No differences were found between homologous pincer and snapper neurones for input resistance and length constant in the proximal portion of the axons, or for the proximal axonal and dendritic anatomies using intracellular cobalt staining. To determine the effect of cell body size upon the passive electrical properties of the neurones, we modelled the neurones by computer. The difference in cell body size causes less than a 3% change in the electrical properties of the neurone at the axon root. Thus, despite the striking behavioural dissimilarities between the pincer and snapper claws, there is no electrical or morphological basis in the claw closer neurones for this difference.

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