Cortical malformations from altered development are common causes of human epilepsy. The cellular mechanisms responsible for the epileptic state of cortex remain unclear and a significant portion of these cases do not respond to treatment. Previous electrophysiological recordings in the Jacobs lab in a rat polymicrogyria model indicated an increased response to group I metabotropic glutamate receptor agonists in the region adjacent to the malformation (PMZ). In addition there was a novel response in low threshold spiking (LTS) interneurons via mGluR5 activation. To determine whether cell specific expression of these receptors was altered in malformed cortex immunohistochemical stains were performed for group I mGluRs along with non-overlapping interneuron subtype specific markers, a neuronal marker and general inhibitory cell marker. There was no altered mGluR5 expression seen in the PMZ. There was an altered expression seen in PMZ mGluR1α labeled cells and cells in other cortical regions.
","abstract_html":"<p>Cortical malformations from altered development are common causes of human epilepsy. The cellular mechanisms responsible for the epileptic state of cortex remain unclear and a significant portion of these cases do not respond to treatment. Previous electrophysiological recordings in the Jacobs lab in a rat polymicrogyria model indicated an increased response to group I metabotropic glutamate receptor agonists in the region adjacent to the malformation (PMZ). In addition there was a novel response in low threshold spiking (LTS) interneurons via mGluR5 activation. To determine whether cell specific expression of these receptors was altered in malformed cortex immunohistochemical stains were performed for group I mGluRs along with non-overlapping interneuron subtype specific markers, a neuronal marker and general inhibitory cell marker. There was no altered mGluR5 expression seen in the PMZ. There was an altered expression seen in PMZ mGluR1α labeled cells and cells in other cortical regions.</p>","abstract_has_math":false,"creators":["Bruch, William"],"institution":null,"degree_name":"Master of Science","degree_level":"Thesis","degree_discipline":"Anatomy & Neurobiology","degree_department":null,"school":null,"contributors":["Kimberle Jacobs"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2012,"date_issued":"2012-01-01T08:00:00Z","date_published":"2012-01-01T08:00:00Z","updated_at":"2026-07-24T05:53:56Z","subjects":["mGluR1","mGluR5","Polymicrogyria","Epilepsy","Anatomy","Medicine and Health Sciences","Nervous System"],"languages":[],"rights":["© The Author"],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["https://scholarscompass.vcu.edu/etd/378"],"render_values":[{"text":"https://scholarscompass.vcu.edu/etd/378","href":"https://scholarscompass.vcu.edu/etd/378","code":true}]}]},"links":{"outbound_url":"https://doi.org/10.25772/6HNS-Y919","outbound_label":"DOI","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Kimberle Jacobs"]},{"key":"dc:creator","label":"Author","values":["Bruch, William"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date.available","label":"Dc Date Available","values":["2017-07-26T07:00:00Z"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Anatomy & Neurobiology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Thesis"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Master of Science"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["mGluR1","mGluR5","Polymicrogyria","Epilepsy","Anatomy","Medicine and Health Sciences","Nervous System"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:rights","label":"Dc Rights","values":["© The Author"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://doi.org/10.25772/6HNS-Y919","https://scholarscompass.vcu.edu/etd/378"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Cortical malformations from altered development are common causes of human epilepsy. The cellular mechanisms responsible for the epileptic state of cortex remain unclear and a significant portion of these cases do not respond to treatment. Previous electrophysiological recordings in the Jacobs lab in a rat polymicrogyria model indicated an increased response to group I metabotropic glutamate receptor agonists in the region adjacent to the malformation (PMZ). In addition there was a novel response in low threshold spiking (LTS) interneurons via mGluR5 activation. To determine whether cell specific expression of these receptors was altered in malformed cortex immunohistochemical stains were performed for group I mGluRs along with non-overlapping interneuron subtype specific markers, a neuronal marker and general inhibitory cell marker. There was no altered mGluR5 expression seen in the PMZ. There was an altered expression seen in PMZ mGluR1α labeled cells and cells in other cortical regions.
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