GABAA receptor impairment in the genetic absence epilepsy rats from Strasbourg (GAERS)

an immunocytochemical and receptor binding autoradiographic study

R. Spreafico, T. Mennini, L. Danober, A. Cagnotto, M. C. Regondi, A. Miari, A. De Blas, M. Vergnes, G. Avanzini

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

Some aspects of the GABA and cholinergic systems have been investigated in the cortex and thalamus of GAERS Wistar rats, a model of petit-mal epilepsy, and in a non-epileptic control strain. GABA and its synthetic enzyme, glutamic acid decarboxylase (GAD), were located by immunocytochemistry; the GABAA receptors were evaluated by autoradiography of GABA-enhanced 3H-flunitrazepam binding and by immunocytochemistry using specific antibodies against the β23 subunits of GABAPA receptor protein. GABA and GAD immunocytochemistry did not show up any difference in density or distribution of immunoreactive elements (fibers, terminals and neurons) between epileptic and control animals, but autoradiographic and immunocytochemical studies showed a decreased enhancement of 3H-flunitrazepam binding and of β23 subunits of GABAA receptor in the sensorimotor cortex and anterior thalamic areas of the epileptic strain. No differences were found in benzodiazepine receptors in the two strains. GABAB receptors were measured as 3H-baclofen binding in a crude synaptic membrane preparation and there was no difference between epileptic and control animals. Choline acetyltransferase, the synthetic enzyme for acetylcholine, and muscarinic receptor subtypes (M1 and M2), visualized respectively by an immunocytochemical procedure and binding autoradiography, did not differ in epileptic and normal rats. The data suggest an impairment of the 'GABAA system' in restricted brain regions of epileptic rats, due to a reduction of receptor β23 subunits and coupling to benzodiazepine receptors despite the normal synthesis and location of the neurotransmitter.

Original languageEnglish
Pages (from-to)229-238
Number of pages10
JournalEpilepsy Research
Volume15
Issue number3
DOIs
Publication statusPublished - 1993

Fingerprint

Absence Epilepsy
GABA-A Receptors
gamma-Aminobutyric Acid
Flunitrazepam
Glutamate Decarboxylase
Immunohistochemistry
Autoradiography
Muscarinic M2 Receptors
Muscarinic M1 Receptors
Synaptic Membranes
Baclofen
Choline O-Acetyltransferase
Enzymes
Thalamus
Cholinergic Agents
Acetylcholine
Neurotransmitter Agents
Wistar Rats
Neurons
Antibodies

Keywords

  • Absence epilepsy
  • Cortex
  • GABAA receptor
  • Immunocytochemistry
  • Rats
  • Receptor binding

ASJC Scopus subject areas

  • Clinical Neurology
  • Pediatrics, Perinatology, and Child Health
  • Neurology

Cite this

GABAA receptor impairment in the genetic absence epilepsy rats from Strasbourg (GAERS) : an immunocytochemical and receptor binding autoradiographic study. / Spreafico, R.; Mennini, T.; Danober, L.; Cagnotto, A.; Regondi, M. C.; Miari, A.; De Blas, A.; Vergnes, M.; Avanzini, G.

In: Epilepsy Research, Vol. 15, No. 3, 1993, p. 229-238.

Research output: Contribution to journalArticle

Spreafico, R. ; Mennini, T. ; Danober, L. ; Cagnotto, A. ; Regondi, M. C. ; Miari, A. ; De Blas, A. ; Vergnes, M. ; Avanzini, G. / GABAA receptor impairment in the genetic absence epilepsy rats from Strasbourg (GAERS) : an immunocytochemical and receptor binding autoradiographic study. In: Epilepsy Research. 1993 ; Vol. 15, No. 3. pp. 229-238.
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