Access the full text.
Sign up today, get DeepDyve free for 14 days.
(1994)
Calcium dependence of the microtubule disaggregation in dendrites of CAI stratum radiatum caused by in vitro ischemia in the rat hippocampal slice
(1988)
Mechanisms of ischaemic brain damage
W. Lust, G. Feussner, E. Barbehenn, J. Passonneau (1981)
The enzymatic measurement of adenine nucleotides and P-creatine in picomole amounts.Analytical biochemistry, 110 2
(1987)
The action of local anaesthetics on ion channels of excitable tissue
L. Lucas, C. West, B. Rigor, A. Schurr (1989)
Protection against cerebral hypoxia by local anesthetics: a study using brain slicesJournal of Neuroscience Methods, 28
M. Shokunbi, A. Gelb, Xin Wu, Daniel Miller (1990)
Continuous lidocaine infusion and focal feline cerebral ischemia.Stroke, 21 1
A. Mitani, H. Yanase, K. Sakai, Y. Wake, K. Kataoka (1993)
Origin of intracellular Ca2+ elevation induced by in vitro ischemia-like condition in hippocampal slicesBrain Research, 601
I. Kass, A. Abramowicz, J. Cottrell, G. Chambers (1992)
The barbiturate thiopental reduces ATP levels during anoxia but improves electrophysiological recovery and ionic homeostasis in the rat hippocampal sliceNeuroscience, 49
E. Roberts, T. Sick (1988)
Calcium-sensitive recovery of extracellular potassium and synaptic transmission in rat hippocampal slices exposed to brief anoxiaBrain Research, 456
A. Schurr, B. Spears, K. Reid, C. West, H. Edmonds, B. Rigor (1986)
Lidocaine depresses synaptic activity in the rat hippocampal slice.Anesthesiology, 64 4
P. Lysko, C. Webb, T. Yue, J. Gu, G. Feuerstein (1994)
Neuroprotective Effects of Tetrodotoxin as a Na+ Channel Modulator and Glutamate Release Inhibitor in Cultured Rat Cerebellar Neurons and in Gerbil Global Brain IschemiaStroke, 25
M. Kim-lee, B. Stokes, J. McDonald (1994)
Procaine, lidocaine, and hypothermia inhibit calcium paradox in glial cells.Anesthesia and analgesia, 79 4
K. Raley-Susman, P. Lipton (1990)
In vitro ischemia and protein synthesis in the rat hippocampal slice: the role of calcium and NMDA receptor activationBrain Research, 515
M. Kaneda, Y. Oyama, Y. Ikemoto, N. Akaike (1989)
Blockade of the voltage-dependent sodium current in isolated rat hippocampal neurons by tetrodotoxin and lidocaineBrain Research, 484
T. Fujitani, N. Adachi, Hirofumi Miyazaki, Keyue Liu, Yoichi Nakamura, K. Kataoka, T. Arai (1994)
Lidocaine protects hippocampal neurons against ischemic damage by preventing increase of extracellular excitatory amino acids: a microdialysis study in Mongolian gerbilsNeuroscience Letters, 179
W. Pulsinelli, J. Brierley, F. Plum (1982)
Temporal profile of neuronal damage in a model of transient forebrain ischemiaAnnals of Neurology, 11
B. Siesjô (1992)
Pathophysiology and treatment of focal cerebral ischemia. Part I: Pathophysiology.Journal of neurosurgery, 77 2
Mark Weber, C. Taylor (1994)
Damage from oxygen and glucose deprivation in hippocampal slices is prevented by tetrodotoxin, lidocaine and phenytoin without blockade of action potentialsBrain Research, 664
J. Boening, I. Kass, J. Cottrell, G. Chambers (1989)
The effect of blocking sodium influx on anoxic damage in the rat hippocampal sliceNeuroscience, 33
P. Stys, S. Waxman, B. Ransom (1992)
Ionic mechanisms of anoxic injury in mammalian CNS white matter: role of Na+ channels and Na(+)-Ca2+ exchanger, 12
(1975)
Rate and site of action of local anaesthetics in myelinated nerve fibers
A. Harreveld, Jane Crowell, S. Malhotra (1965)
A STUDY OF EXTRACELLULAR SPACE IN CENTRAL NERVOUS TISSUE BY FREEZE-SUBSTITUTIONThe Journal of Cell Biology, 25
(1994)
Release of [ 3 H ] - D - aspartate or endogenous glutamate from rat hippocampal slices during in vitro ischemia is mediated by a high affinity Na - dependent carrier
D. Choi (1990)
Cerebral hypoxia: some new approaches and unanswered questions, 10
Doug Lobnera, Peter Lipton (1993)
Intracellular calcium levels and calcium fluxes in the CA1 region of the rat hippocampal slice during in vitro ischemia: relationship to electrophysiological cell damage, 13
J. Astrup, P. Skovsted, F. Gjerris, H. Sørensen (1981)
Increase in Extracellular Potassium in the Brain during Circulatory Arrest: Effects of Hypothermia, Lidocaine, and ThiopentalAnesthesiology, 55
I. Kass, A. Abramowicz, J. Cottrell, P. Amorim, G. Chambers (1994)
Anoxia reduces depolarization induced calcium uptake in the rat hippocampal sliceBrain Research, 633
I. Kass, P. Lipton (1989)
Protection of hippocampal slices from young rats against anoxic transmission damage is due to better maintenance of ATP.The Journal of Physiology, 413
Ira Kass, Peter LIPTONt (1986)
Calcium and long‐term transmission damage following anoxia in dentate gyrus and CA1 regions of the rat hippocampal slice.The Journal of Physiology, 378
Anker Hansen (1985)
Effect of anoxia on ion distribution in the brain.Physiological reviews, 65 1
I. Kass, P. Lipton (1982)
Mechanisms involved in irreversible anoxic damage to the in vitro rat hippocampal sliceThe Journal of Physiology, 332
Anker Hansen, Carl Olsen (1980)
Brain extracellular space during spreading depression and ischemia.Acta physiologica Scandinavica, 108 4
1. The effect of sodium influx on anoxic damage was investigated in rat hippocampal slices. Previous experiments demonstrated that a concentration of tetrodotoxin which blocks neuronal transmission protects against anoxic damage. In this study we examined low concentrations of lidocaine (lignocaine; which do not block neuronal transmission), for their effect on recovery of the evoked population spike recorded from the CA1 pyramidal cell layer. 2. Recovery of the population spike, measured 60 min after a 5 min anoxic period, was 4 +/‐ 2% of its preanoxic, predrug level. Lidocaine concentrations of 10, 50, and 100 microM significantly improved recovery to 56 +/‐ 12, 80 +/‐ 7 and 70 +/‐ 14%, respectively. 3. Lidocaine (10 microM) did not alter the size of the evoked response before anoxia and had no significant effect on potassium levels or calcium influx during anoxia. It did, however, reduce cellular sodium levels (146 +/‐ 7 vs. 202 +/‐ 12 nmol mg‐1) and preserve ATP levels (2.17 +/‐ 0.07 vs. 1.78 +/‐ 0.07 nmol mg‐1) during anoxia. All values were measured at the end of 5 min of anoxia except those for Ca2+ influx which were measured during 10 min of anoxia. 4. High concentrations of lidocaine (100 microM) did not improve recovery significantly over that observed with 10 microM. They also had no significantly greater effects on sodium levels than 10 microM lidocaine (137 +/‐ 12 vs. 146 +/‐ 7 nmol mg‐1); however, 100 microM lidocaine significantly improved potassium (202 +/‐ 18 vs. 145 +/‐ 6 nmol mg‐1) and ATP (2.57 +/‐ 0.06 vs. 2.17 +/‐ 0.07 nmol mg‐1) levels, while reducing calcium influx (7.76 +/‐ 0.12 vs. 9.24 +/‐ 0.39 nmol mg‐1 (10 min)‐1) when compared with 10 microM lidocaine. 5. We conclude that sodium influx and ATP depletion are of major importance in anoxic damage since 10 microM lidocaine reduced these changes during anoxia and improved recovery of the population spike. In addition, our results indicate that the properties of the sodium channel are altered during anoxia, since sodium influx is blocked by a concentration of lidocaine that does not affect the population spike in the preanoxic period.
The Journal of Physiology – Wiley
Published: Dec 1, 1995
Read and print from thousands of top scholarly journals.
Already have an account? Log in
Bookmark this article. You can see your Bookmarks on your DeepDyve Library.
To save an article, log in first, or sign up for a DeepDyve account if you don’t already have one.
Copy and paste the desired citation format or use the link below to download a file formatted for EndNote
Access the full text.
Sign up today, get DeepDyve free for 14 days.
All DeepDyve websites use cookies to improve your online experience. They were placed on your computer when you launched this website. You can change your cookie settings through your browser.