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Regulation of Parvalbumin Interactome in the Perilesional Cortex after Experimental Traumatic Brain Injury.
Hiltunen, Johanna; Ndode-Ekane, Xavier Ekolle; Lipponen, Anssi; Drexel, Meinrad; Sperk, Günther; Puhakka, Noora; Pitkänen, Asla.
Afiliación
  • Hiltunen J; A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, PO Box 1627, 70211 Kuopio, Finland.
  • Ndode-Ekane XE; A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, PO Box 1627, 70211 Kuopio, Finland.
  • Lipponen A; A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, PO Box 1627, 70211 Kuopio, Finland.
  • Drexel M; Institute of Molecular and Cellular Pharmacology, Medical University Innsbruck, Peter-Mayr-Str. 1, 6020 Innsbruck, Austria.
  • Sperk G; Department of Pharmacology, Medical University Innsbruck, Peter-Mayr-Str. 1a, 6020 Innsbruck, Austria.
  • Puhakka N; A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, PO Box 1627, 70211 Kuopio, Finland.
  • Pitkänen A; A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, PO Box 1627, 70211 Kuopio, Finland. Electronic address: asla.pitkanen@uef.fi.
Neuroscience ; 475: 52-72, 2021 11 01.
Article en En | MEDLINE | ID: mdl-34455012
Traumatic brain injury (TBI) causes 10-20% of structural epilepsy, with seizures typically originating in the cortex. Alterations in the neuronal microcircuits in the cortical epileptogenic zone, however, are poorly understood. Here, we assessed TBI-induced changes in perisomatic gamma aminobutyric acid (GABA)-ergic innervation in the perilesional cortex. We hypothesized that TBI will damage parvalbumin (PV)-immunoreactive inhibitory neurons and induce regulation of the associated GABAergic molecular interactome. TBI was induced in adult male Sprague-Dawley rats by lateral fluid-percussion injury. At 1-month post-TBI, the number of PV-positive somata was plotted on unfolded cortical maps and the distribution and density of immunopositive terminals analyzed. Qualitative analysis revealed either patchy microlesions of several hundred micrometers in diameter or diffuse neuronal loss. Quantitative analysis demonstrated a reduction in the number of PV-positive interneurons in patches down to 0% of that in sham-operated controls in the perilesional cortex. In the majority of patches, the cell numbers ranged from 71% to 90% that of the controls. The loss of PV-positive somata was accompanied by decreased axonal labeling. In situ hybridization revealed downregulated PV mRNA expression in the perilesional cortex. Gene Set Enrichment Analysis indicated a robustly downregulated expression profile of PV-related genes, which was confirmed by quantitative reverse transcriptase polymerase chain reaction. Specifically, we found that genes encoding postsynaptic GABA-A receptor genes, Gabrg2 and Gabrd, were downregulated in TBI animals compared with controls. Our data suggests that patchy reduction in PV-positive perisomatic inhibitory innervation contributes to the development of focal cortical inhibitory deficit after TBI.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Epilepsia / Lesiones Traumáticas del Encéfalo Tipo de estudio: Qualitative_research Límite: Animals Idioma: En Revista: Neuroscience Año: 2021 Tipo del documento: Article País de afiliación: Finlandia Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Epilepsia / Lesiones Traumáticas del Encéfalo Tipo de estudio: Qualitative_research Límite: Animals Idioma: En Revista: Neuroscience Año: 2021 Tipo del documento: Article País de afiliación: Finlandia Pais de publicación: Estados Unidos