Extracellular potassium ion activity and electrophysiology in the hippocampal slice

paradoxical recovery of synaptic transmission during anoxia

Thomas Sick, Emily L. Solow, Eugene L Roberts

Research output: Contribution to journalArticle

69 Citations (Scopus)

Abstract

The relationship between extracellular potassium ion activity and neuronal excitability during anoxia was investigated in hippocampal slices in vitro. Extracellular field potentials and K+ activity were measured with double-barreled ion-selective microelectrodes placed either in the stratum pyramidale or stratum radiatum of field CA1. Orthodromic spike ctivity of CA1 pyramidal cells and field excitatory postsynaptic potentials (f-EPSPs) failed rapidly after anoxia with little change in potassium ion activity and without failure of the Schaffer collateral prevolley or antidromic responses of pyramidal cells. As [K+]0 approached 8-10 mM, f-EPSPs and orthodromic spike activity recovered spontaneously. Continued anoxia resulted in massive release of K+ into extracellular space and complete electrical silence. Presynaptic activity and antidromically elicited spike activity recovered promptly upon reoxygenation after anoxia, but synaptic transmission remained blocked for many minutes. Spontaneous recovery of f-EPSPs and spike activity suggests that a simple mechanism involving depolarization of hyperpolarization of neuronal elements cannot account for failure of synaptic transmission observed during anoxia. However, continued elevation of [K+]0 and the associated loss of pre- and postsynaptic excitability with more prolonged anoxia indicated that depolarization was responsible for the eventual electrical silence as anoxia progressed.

Original languageEnglish
Pages (from-to)227-234
Number of pages8
JournalBrain Research
Volume418
Issue number2
DOIs
StatePublished - Aug 25 1987

Fingerprint

Electrophysiology
Synaptic Transmission
Potassium
Ions
Excitatory Postsynaptic Potentials
Pyramidal Cells
Hippocampal CA1 Region
Extracellular Space
Microelectrodes
Hypoxia
Hippocampus

Keywords

  • Anoxia
  • Electrophysiology
  • Hippocampal slice
  • Potassium ion

ASJC Scopus subject areas

  • Developmental Biology
  • Molecular Biology
  • Clinical Neurology
  • Neuroscience(all)

Cite this

Extracellular potassium ion activity and electrophysiology in the hippocampal slice : paradoxical recovery of synaptic transmission during anoxia. / Sick, Thomas; Solow, Emily L.; Roberts, Eugene L.

In: Brain Research, Vol. 418, No. 2, 25.08.1987, p. 227-234.

Research output: Contribution to journalArticle

@article{5ebe52a0d610404abe0ab07e75e4d71b,
title = "Extracellular potassium ion activity and electrophysiology in the hippocampal slice: paradoxical recovery of synaptic transmission during anoxia",
abstract = "The relationship between extracellular potassium ion activity and neuronal excitability during anoxia was investigated in hippocampal slices in vitro. Extracellular field potentials and K+ activity were measured with double-barreled ion-selective microelectrodes placed either in the stratum pyramidale or stratum radiatum of field CA1. Orthodromic spike ctivity of CA1 pyramidal cells and field excitatory postsynaptic potentials (f-EPSPs) failed rapidly after anoxia with little change in potassium ion activity and without failure of the Schaffer collateral prevolley or antidromic responses of pyramidal cells. As [K+]0 approached 8-10 mM, f-EPSPs and orthodromic spike activity recovered spontaneously. Continued anoxia resulted in massive release of K+ into extracellular space and complete electrical silence. Presynaptic activity and antidromically elicited spike activity recovered promptly upon reoxygenation after anoxia, but synaptic transmission remained blocked for many minutes. Spontaneous recovery of f-EPSPs and spike activity suggests that a simple mechanism involving depolarization of hyperpolarization of neuronal elements cannot account for failure of synaptic transmission observed during anoxia. However, continued elevation of [K+]0 and the associated loss of pre- and postsynaptic excitability with more prolonged anoxia indicated that depolarization was responsible for the eventual electrical silence as anoxia progressed.",
keywords = "Anoxia, Electrophysiology, Hippocampal slice, Potassium ion",
author = "Thomas Sick and Solow, {Emily L.} and Roberts, {Eugene L}",
year = "1987",
month = "8",
day = "25",
doi = "10.1016/0006-8993(87)90090-4",
language = "English",
volume = "418",
pages = "227--234",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "2",

}

TY - JOUR

T1 - Extracellular potassium ion activity and electrophysiology in the hippocampal slice

T2 - paradoxical recovery of synaptic transmission during anoxia

AU - Sick, Thomas

AU - Solow, Emily L.

AU - Roberts, Eugene L

PY - 1987/8/25

Y1 - 1987/8/25

N2 - The relationship between extracellular potassium ion activity and neuronal excitability during anoxia was investigated in hippocampal slices in vitro. Extracellular field potentials and K+ activity were measured with double-barreled ion-selective microelectrodes placed either in the stratum pyramidale or stratum radiatum of field CA1. Orthodromic spike ctivity of CA1 pyramidal cells and field excitatory postsynaptic potentials (f-EPSPs) failed rapidly after anoxia with little change in potassium ion activity and without failure of the Schaffer collateral prevolley or antidromic responses of pyramidal cells. As [K+]0 approached 8-10 mM, f-EPSPs and orthodromic spike activity recovered spontaneously. Continued anoxia resulted in massive release of K+ into extracellular space and complete electrical silence. Presynaptic activity and antidromically elicited spike activity recovered promptly upon reoxygenation after anoxia, but synaptic transmission remained blocked for many minutes. Spontaneous recovery of f-EPSPs and spike activity suggests that a simple mechanism involving depolarization of hyperpolarization of neuronal elements cannot account for failure of synaptic transmission observed during anoxia. However, continued elevation of [K+]0 and the associated loss of pre- and postsynaptic excitability with more prolonged anoxia indicated that depolarization was responsible for the eventual electrical silence as anoxia progressed.

AB - The relationship between extracellular potassium ion activity and neuronal excitability during anoxia was investigated in hippocampal slices in vitro. Extracellular field potentials and K+ activity were measured with double-barreled ion-selective microelectrodes placed either in the stratum pyramidale or stratum radiatum of field CA1. Orthodromic spike ctivity of CA1 pyramidal cells and field excitatory postsynaptic potentials (f-EPSPs) failed rapidly after anoxia with little change in potassium ion activity and without failure of the Schaffer collateral prevolley or antidromic responses of pyramidal cells. As [K+]0 approached 8-10 mM, f-EPSPs and orthodromic spike activity recovered spontaneously. Continued anoxia resulted in massive release of K+ into extracellular space and complete electrical silence. Presynaptic activity and antidromically elicited spike activity recovered promptly upon reoxygenation after anoxia, but synaptic transmission remained blocked for many minutes. Spontaneous recovery of f-EPSPs and spike activity suggests that a simple mechanism involving depolarization of hyperpolarization of neuronal elements cannot account for failure of synaptic transmission observed during anoxia. However, continued elevation of [K+]0 and the associated loss of pre- and postsynaptic excitability with more prolonged anoxia indicated that depolarization was responsible for the eventual electrical silence as anoxia progressed.

KW - Anoxia

KW - Electrophysiology

KW - Hippocampal slice

KW - Potassium ion

UR - http://www.scopus.com/inward/record.url?scp=0023203155&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0023203155&partnerID=8YFLogxK

U2 - 10.1016/0006-8993(87)90090-4

DO - 10.1016/0006-8993(87)90090-4

M3 - Article

VL - 418

SP - 227

EP - 234

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 2

ER -