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A neurophysiological analysis of the effect of kainic acid on nerve fibres and terminals in the cat spinal cord.
Author(s) -
Curtis D R,
Malik R
Publication year - 1985
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1985.sp015848
Subject(s) - antidromic , kainic acid , orthodromic , spinal cord , chemistry , bicuculline , neuroscience , anatomy , cats , afferent , biophysics , electrophysiology , receptor , medicine , gabaa receptor , biology , biochemistry , glutamate receptor
Kainic acid was administered micro‐electrophoretically in relatively small amounts (approx. 0.15 nmol) near gastrocnemius motoneurones in the spinal cord of cats anaesthetized with sodium pentobarbitone. After initial excitation, extracellularly recorded orthodromic and antidromic field potentials were reduced. Such neurophysiological evidence for motoneuronal damage or death persisted for 5 h, the longest period of observation. At the site of administration, the terminations of gastrocnemius group Ia afferent fibres were electrically inexcitable for approximately 1 h. Subsequently, the number and excitability of these terminations appeared to be normal, as were the depolarizing actions at bicuculline‐sensitive receptors of micro‐electrophoretic piperidine‐4‐sulphonic acid and of gamma‐aminobutyric acid (GABA) released at axoaxonic synapses on these terminations. Central myelinated and non‐myelinated fibres and terminals of muscle group Ia afferent fibres, and the synaptic release of GABA on these terminals at axo‐axonic synapses formed by certain spinal interneurones, thus appear to be relatively insensitive to kainic acid administered in amounts which damage or destroy motoneurones.