Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Site Tools

  • AAAS
  • Subscribe
  • Feedback

Site Search

Search Advanced

Science 13 July 1979:
Vol. 205. no. 4402, pp. 211 - 214
DOI: 10.1126/science.109922

Articles

Science, Vol 205, Issue 4402, 211-214
Copyright © 1979 by American Association for the Advancement of Science


articles

Inhibitory, GABAergic nerve terminals decrease at sites of focal epilepsy

CE Ribak, AB Harris, JE Vaughn, and E Roberts

Using an immunocytochemical method for the localization of the gamma-aminobutyric acid (GABA) synthesizing enzyme, glutamic acid decarboxylase (GAD), we have observed GABAergic nerve terminals distributed throughout all layers of normal monkey sensorimotor cortex. These terminals displayed ultrastructural characteristics that suggested that they arose from aspinous and sparsely spinous stellate neurons. In monkeys (Macaca mulatta and M. fascicularis) made epileptic by cortical application of alumina gel, a highly significant numerical decrease of GAD-positive nerve terminals occurred at sites of seizure foci indicating a functional loss of GABAergic inhibitory synapses. A loss of such inhibition at seizure foci could lead to epileptic activity of cortical pyramidal neurons.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Enhanced excitatory synaptic connectivity in layer v pyramidal neurons of chronically injured epileptogenic neocortex in rats..
X. Jin, D. A. Prince, and J. R. Huguenard (2006)
J. Neurosci. 26, 4891-4900
   Abstract »    Full Text »    PDF »
Effects of focal injection of kainic acid into the mouse hippocampus in vitro and ex vivo.
C. Le Duigou, L. Wittner, L. Danglot, and R. Miles (2005)
J. Physiol. 569, 833-847
   Abstract »    Full Text »    PDF »
Transient Depression of Excitatory Synapses on Interneurons Contributes to Epileptiform Bursts During Gamma Oscillations in the Mouse Hippocampal Slice.
R. D. Traub, I. Pais, A. Bibbig, F. E.N. LeBeau, E. H. Buhl, H. Garner, H. Monyer, and M. A. Whittington (2005)
J Neurophysiol 94, 1225-1235
   Abstract »    Full Text »    PDF »
Compromised generation of GABAergic interneurons in the brains of Vax1-/- mice.
P. Taglialatela, J. M. Soria, V. Caironi, A. Moiana, and S. Bertuzzi (2004)
Development 131, 4239-4249
   Abstract »    Full Text »    PDF »
Increased Pyramidal Excitability and NMDA Conductance Can Explain Posttraumatic Epileptogenesis Without Disinhibition: A Model.
P. C. Bush, D. A. Prince, and K. D. Miller (1999)
J Neurophysiol 82, 1748-1758
   Abstract »    Full Text »    PDF »
Changes in Membrane and Synaptic Properties of Thalamocortical Circuitry Caused by Hydrogen Peroxide.
M. V. Frantseva, J. L. P. Velazquez, and P. L. Carlen (1998)
J Neurophysiol 80, 1317-1326
   Abstract »    Full Text »    PDF »
Cellular mechanisms of epilepsy: a status report.
M. Dichter and G. Ayala (1987)
Science 237, 157-164
   Abstract »    PDF »
Functional coupling of gamma-aminobutyric acid receptors to chloride channels in brain membranes.
R. Harris and A. Allan (1985)
Science 228, 1108-1110
   Abstract »    PDF »
Focal cortical seizures cause distant thalamic lesions.
R. Collins and J. Olney (1982)
Science 218, 177-179
   Abstract »    PDF »
Clinical Implications of Enzyme-Mediated Alterations of {gamma}-Aminobutyric Acid Content in Human CSF.
T. A. Hare, J. H. Wood, and B. V. Manyam (1981)
Arch Neurol 38, 491-494
   Abstract »    PDF »



To Advertise     Find Products


Science. ISSN 0036-8075 (print), 1095-9203 (online)