Abstract
Previous studies have shown significantly greater GABA levels and numbers of GABAergic neurons in the central nucleus of the inferior colliculus (ICCN) of genetically epilepsy-prone rats (GEPR-9s). In the present study, in situ hybridization and emulsion autoradiographic techniques were used to determine whether there are also evated numbers of ICCN cells that contain the 67-kD form of mRNA for the GABA synthesizing enzyme, glutamate decarboxylase (GAD), in GEPR-9s as compared to normal Sprague-Dawley (SD) rats. Hybridization with a 35S-labeled RNA probe complementary to a span of monkey GAD mRNA labeled cells throughout the brain including the ICCN. Labeled cells in the ICCN appeared to be of different sizes that corresponded with previous descriptions of GABAergic neurons from immunocytochemical studies. In the GEPR-9s, a larger number of GAD 67 cRNA labeled neurons was observed in the ICCN as compared to SD rats. The external nucleus of the inferior colliculus was also found to contain significantly greater numbers of GAD 67 cRNA labeled neurons whereas in the frontal cortex, a region of the brain that is not required for audiogenic seizure activity in GEPR-9s, there were no significant differences in hybridization between GEPR-9s and SD rats. Interestingly, within the superficial layers of the superior colliculus there was a higher density of hybridization in GEPR-9s than in SD rats indicating higher levels of GAD expression. The data on hybridization within the inferior colliculus are consistent with previous results that showed elevated numbers of GABAergic neurons in the central and external nuclei of GEPR-9s and provide further support for an abnormality of the GABAergic system in this model of genetic epilepsy.
Highlights
Previous studies have shown that 7-aminobutyric acid (GABA) is a major inhibitory neurotransmitter in the inferior colliculus (IC) and plays a role in seizure initiation following auditory stimulation in both normal Sprague-Dawley (SD) rats and genetically epilepsy-prone rats (GEPR-9s) 1'7'1°
The objective of this study was to use in situ hybridization to determine whether abnormalities in the numbers and distributions of neurons containing GAD67 mRNA exist in the inferior coliiculus of GEPR-9s
We examined the autoradiographic localization of hybridization of a 35S-labeled RNA probe, complementary to the 67-kD form of glutamate decarboxylase (GAD) mRNA, in tissue sections through the three major nuclei of the IC of both GEPR-9s and SD rats
Summary
Previous studies have shown that 7-aminobutyric acid (GABA) is a major inhibitory neurotransmitter in the inferior colliculus (IC) and plays a role in seizure initiation following auditory stimulation in both normal Sprague-Dawley (SD) rats and genetically epilepsy-prone rats (GEPR-9s) 1'7'1°. Morphological studies using immunocytochemistry with an antiserum to glutamate decarboxylase (GAD) have shown greater numbers of GABAergic and total neurons in the IC of GEPR-9s as compared to non-epileptic SD rats 1~'tt'. There appears to be an abnormality of the GABAergic system in the IC of GEPR-9s, and it may play a vital role in their seizure susceptibility. The objective of this study was to use in situ hybridization to determine whether abnormalities in the numbers and distributions of neurons containing GAD67 mRNA exist in the inferior coliiculus of GEPR-9s
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