FASEB J.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gundlach, A. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gundlach, A. L.

The FASEB Journal, Vol 4, 2761-2766, Copyright © 1990 by The Federation of American Societies for Experimental Biology


REVIEWS

Disorder of the inhibitory glycine receptor: inherited myoclonus in Poll Hereford calves

AL Gundlach
University of Melbourne, Department of Medicine, Austin Hospital, Heidelberg, Victoria, Australia.

Inherited congenital myoclonus in Poll Hereford calves is characterized by hyperesthesia and myoclonic jerks of the skeletal musculature that occur spontaneously and in response to sensory stimuli. The symptoms of the disorder suggest a failure of spinal inhibition and are similar to those in subconvulsive strychnine poisoning. Strychnine is a high- affinity antagonist of the synaptic actions of glycine. Our recent biochemical studies revealed a specific and marked deficit in [3H]strychnine binding sites in brain stem and spinal cord membranes from myoclonic calves compared with unaffected controls, reflecting a decrease in inhibitory glycine receptors. Glycine is a major inhibitory neurotransmitter in the mammalian central nervous system, and glycinergic transmission is important for the control of both motor and sensory functions in the spinal cord. In other studies, synaptosomes prepared from affected spinal cord showed a significantly increased ability to accumulate [3H]glycine, indicating an increased capacity of the high-affinity neuronal reuptake system for glycine. In contrast, spinal cord glycine concentrations and stimulus-induced release of endogenous glycine, measured in vitro, were unaltered. The major clinical signs of this myoclonic disorder can be explained by the reported deficiency of inhibitory glycine receptors in brain stem and spinal cord, and future research will be directed toward identifying the nature of the genetic alteration responsible for this deficiency. The characteristics of this bovine receptor abnormality are similar to those described for the mutant spastic mouse.


This article has been cited by other articles:


Home page
J. Neurol. Neurosurg. PsychiatryHome page
S C Keswani, E H Kossoff, G L Krauss, and C Hagerty
Amelioration of spinal myoclonus with levetiracetam
J. Neurol. Neurosurg. Psychiatry, October 1, 2002; 73(4): 457 - 458.
[Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1990 by The Federation of American Societies for Experimental Biology.