Abstract
High affinity, gamma-aminobutyric acid (GABA) plasma membrane transporters (GATs) influence the availability of GABA, the main inhibitory neurotransmitter in the brain. Recent studies suggest a crucial role for GATs in maintaining levels of synaptic GABA in normal as well as abnormal (i.e., epileptic) adult brain. However, the role of GATs during development and specifically changes in their expression in response to developmental seizures are unknown. The present study examined GAT-1-immunolabeling in infant rats with two types of developmental seizures, one induced by corticotropin-releasing hormone (CRH) lasting about 2 h and the other by hyperthermia (a model of febrile seizures) lasting only 20 min. The number of GAT-1-immunoreactive (ir) neurons was increased in several forebrain regions 24 h after induction of seizures by CRH as compared to the control group. Increased numbers of detectable GAT-1-ir cell bodies were found in the hippocampal formation including the dentate gyrus and CA1, and in the neocortex, piriform cortex and amygdala. In contrast, hyperthermia-induced seizures did not cause significant changes in the number of detectable GAT-1-ir somata. The increase in GAT-1-ir somata in the CRH model and not in the hyperthermia model may reflect the difference in the duration of seizures. The brain regions where this increase occurs correlate with the occurrence of argyrophyllic neurons in the CRH model.
Highlights
The majority of seizures occurring in the developing human are not spontaneous; i.e., they areS
The results of this study indicate that GAT-1ir is altered by corticotropin-releasing hormone (CRH)-induced seizures but not by hyperthermia or hyperthermia-induced seizures
Our data showed significant increases in the number of detectable GAT-1-ir neuronal somata in specific forebrain areas in the 24 h CRH group as compared to the control group
Summary
The majority of seizures occurring in the developing human are not spontaneous; i.e., they areS. Repeated administration of CRH doses (150 × 10−12 mole), which results in status epilepticus, leads to enhanced excitability of the limbic circuit (Baram and Hatalski, 1998) and to excitotoxic injury in select hippocampal and amygdala neurons in the infant rat (Baram and Ribak, 1995; Ribak and Baram, 1996). This information suggests that some stressors (i.e., hypoxia and hyperthermia) may provoke seizures early in life by increasing the levels of CRH in limbic structures. This may be partially due to high levels of the CRH receptor in limbic regions at this time (Avishai-Eliner et al, 1996)
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