Ischemia inhibits GABAergic neurons of the rat thalamic reticular nucleus. An immunocytochemical study

GABA-immunoreactivity in the thalamic reticular nucleus was studied in rats subjected to 10 min global cerebral ischemia, due to experimentally induced cardiac arrest. The studies were performed in different postischemic periods (10 min, 1 h and 24 h after ischemia) with postembedding immuno-gold technique for electron microscopy, applying antisera raised against protein-gamma amino butyric acid-conjugates. Transient reduction of gold particles content, indicating GABA appearance and distribution in neuronal perikarya and synaptic terminals, was noticed 10 min and 1 h after ischemia. Reduction of immunoreactivity accompanied ultrastructural abnormalities involving both neurons and synapses and taking the form of severe swelling and disorganization of organelles arrangement. Immunocytochemical abnormalities concerning neuronal perikarya appeared earlier and were more severe. At 24th h after ischemia immunoreactivity of most of the neurons and synapses was similar to this in normal control animals. Morphologically unchanged asymmetric synapses were present in all experimental groups. The presented data confirm high vulnerability of GABAergic neuronal population of the thalamic reticular nucleus to ischemia and suggest transient nature of postischemic GABAergic insufficiency.