Abstract
The numbers of GABAergic neurons as determined by GAD immunocytochemistry and total neurons as determined from Nissl preparations were counted and classified at the light microscopic level in the inferior colliculus (IC) of the genetically epilepsy-prone rat (GEPR) and the non-epileptic Sprague-Dawley (SD) strain of rat. GAD-positive neurons are abundant in the IC in all 3 subdivisions. Several sizes of multipolar neurons as well as medium-sized bipolar or fusiform neurons are GAD-positive. GAD-positive punctate structures that were interpreted to be axon terminals and transversely-sectioned dendrites and preterminal axons are abundant in the IC of both the GEPR and SD. A dramatic increase in the number of GAD-positive neurons occur in the GEPR as compared to the SD. This increase is most evident in the middle of the rostrocaudal extent of the IC. Although the increase is statistically significant in all subdivisions of the IC, it is most pronounced in the central nucleus, especially the ventral lateral portion. Within the central nucleus, the increase in the number of GAD-positive neurons is due to a selective increase in the small (200%) and medium (90%) cell body size populations (10–15 μm and 15–25 μm in diameter, respectively). Concomitant with this increase in the number of GAD-positive neurons, an increase in total numbers of neurons occurs as determined from Nissl preparations. A 100% increase in the number of small neurons and a 30% increase in the number of medium-sized neurons occur in the GEPR as compared to the SD rat. The proportion of GAD-positive neurons to total neurons is also increased in the GEPR. Approximately 25% of the neurons in the IC in SD rat are GAD-positive, while about 35% of the neurons in the GEPR are GAD-positive. These data demonstrate an anatomical difference in the IC of the GEPR as compared to the SD which appears to be preferential for the GABAergic system.
Highlights
The genetically epilepsy-prone rat (GEPR) exhibits severe generalized motor seizures in response to intense auditory stimuli
Distribution of glutamic acid decarboxylase (GAD)-positive structures in the inferior colliculus (IC) of the Sprague-Dawley rat Numerous GAD-positive neuronal somata were found in the IC in all 3 of its subdivisions, the central nucleus (ICCN), the pericentral nucleus (PCN) and the external nucleus (EN)
These data as well as qualitative findings from other brain regions suggest that the increase in neuronal density is not a whole brain phenomena but is possibly restricted to the IC. While this does not rule out the possibility that other brain regions may be similarily affected, it suggests that the change observed in the IC may be preferential. These results indicate a change in the GABAergic system in the IC of the GEPR
Summary
The genetically epilepsy-prone rat (GEPR) exhibits severe generalized motor seizures in response to intense auditory stimuli. Lesion studies indicate that the primary neuronal pathways involved in the manifestation of audiogenic seizures are subcortical because ablation of auditory cortex does not prevent seizures1,2,13.14. Lesions of the inferior colliculus (IC) prevent seizures and other data support the notion that the IC is involved with audiogenic seizures. Pharmacological studies indicate that GABA and benzodiazepine binding is abnormal in the IC 5. An increase in after discharge-like responses similar to that observed in other types of seizures has been observed in the IC of the G E P R 4. These studies indicate several abnormalities within the IC of the GEPR, including a possible loss of GABA-mediated inhibition
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