Presentation Title

An Investigation of the Relationship Between Ethanol Exposure and Epilepsy in the Developing Brain

Faculty Mentor

Kerry Thompson

Start Date

23-11-2019 8:00 AM

End Date

23-11-2019 8:45 AM

Location

93

Session

poster 1

Type of Presentation

Poster

Subject Area

biological_agricultural_sciences

Abstract

Alcohol consumption during pregnancy can result in Fetal Alcohol Spectrum Disorder (FASD), which consist of a range of deficits from decreased brain mass to disturbances in learning, memory, and behavior (Wozniak et al. 2004). Ethanol exposure during critical periods in neurodevelopment can lead to detrimental consequences, including robust, widespread cell death. Early alcohol exposure has been linked to induction of widespread apoptosis using basic models (Ikonomidou et al. 2000), and clinically, in utero exposure is correlated with seizures and epilepsy (Bell et al. 2010). Ethanol is an inhibitory drug that induces apoptosis during periods of synaptogenesis by blocking N-methyl-D-aspartate (NMDA) glutamate receptors and inducing excessive activation of GABAA receptors. NMDA and GABAA are responsible for excitation and inhibition respectively. GABAergic interneurons in the hippocampus of immature brains have been identified as a vulnerable population of cells (Saito et al. 2019). Loss of inhibition in the hippocampus would be expected to lead to unregulated excitation that could lead to cell synchrony and seizures. We hypothesize that a single episode of ethanol exposure during development may damage key areas of the brain involved in seizure susceptibility. In our study, we utilize an established model of FASD. We injected saline (S) or ethanol (E) at postnatal day 10 in rats and returned them to their homecages. When the animals were approximately two months of age, we surgically implanted a stimulating/recording electrode into the right amygdala and tested afterdischarge [electrical seizure] threshold (ADT) and afterdischarge duration (ADD) using the kindling model of epilepsy. After establishing these measures over three trials (ADT: Saline=83μA +- 16, Ethanol=153μA +- 32 and ADD: Saline=27s +- 7, Ethanol=25s +- 2), we then stimulated the animals above threshold once daily, to evaluate the rate of behavioral seizure development (Saline=11.25 +- 1.49, Ethanol=9.17 +- 1.17). Histological evaluations designed to compare the number of hippocampal GABAergic interneurons is in progress. Research in this area is needed to better understand the effects of ethanol on the developing brain and its consequences related to seizure susceptibility.

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Nov 23rd, 8:00 AM Nov 23rd, 8:45 AM

An Investigation of the Relationship Between Ethanol Exposure and Epilepsy in the Developing Brain

93

Alcohol consumption during pregnancy can result in Fetal Alcohol Spectrum Disorder (FASD), which consist of a range of deficits from decreased brain mass to disturbances in learning, memory, and behavior (Wozniak et al. 2004). Ethanol exposure during critical periods in neurodevelopment can lead to detrimental consequences, including robust, widespread cell death. Early alcohol exposure has been linked to induction of widespread apoptosis using basic models (Ikonomidou et al. 2000), and clinically, in utero exposure is correlated with seizures and epilepsy (Bell et al. 2010). Ethanol is an inhibitory drug that induces apoptosis during periods of synaptogenesis by blocking N-methyl-D-aspartate (NMDA) glutamate receptors and inducing excessive activation of GABAA receptors. NMDA and GABAA are responsible for excitation and inhibition respectively. GABAergic interneurons in the hippocampus of immature brains have been identified as a vulnerable population of cells (Saito et al. 2019). Loss of inhibition in the hippocampus would be expected to lead to unregulated excitation that could lead to cell synchrony and seizures. We hypothesize that a single episode of ethanol exposure during development may damage key areas of the brain involved in seizure susceptibility. In our study, we utilize an established model of FASD. We injected saline (S) or ethanol (E) at postnatal day 10 in rats and returned them to their homecages. When the animals were approximately two months of age, we surgically implanted a stimulating/recording electrode into the right amygdala and tested afterdischarge [electrical seizure] threshold (ADT) and afterdischarge duration (ADD) using the kindling model of epilepsy. After establishing these measures over three trials (ADT: Saline=83μA +- 16, Ethanol=153μA +- 32 and ADD: Saline=27s +- 7, Ethanol=25s +- 2), we then stimulated the animals above threshold once daily, to evaluate the rate of behavioral seizure development (Saline=11.25 +- 1.49, Ethanol=9.17 +- 1.17). Histological evaluations designed to compare the number of hippocampal GABAergic interneurons is in progress. Research in this area is needed to better understand the effects of ethanol on the developing brain and its consequences related to seizure susceptibility.