Abstract Title

Fibroblast Growth Factor 8 Hypomorphy Does Not Affect Astrocyte Arborization Complexity in the Corpus Callosum of Adult Mice

Abstract

Fibroblast growth factor 8 (FGF8) has an array of functions in relation to a developing organism. Previous studies examined the role of FGF8 and its involvement with the formation of the corpus callosum in Fgf8 hypomorphic mice. Astrocytic glial cells are critical for the interhemispheric crossing of callosal fibers, and thus the formation of the corpus callosum. Using GFAP immunohistochemistry (IHC), we showed that midline astrocyte cell number was significantly reduced in heterozygous (+/neo) and homozygous (neo/neo) Fgf8 hypomorphic as compared to wildtype (WT) mice. These results suggest FGF8 signaling is critical for late gestational astrocyte cell development, possibly by acting on the progenitor cells that are destined to become astrocytes. Recently, it was shown that FGF8 increased astrocyte arborization complexity in cell culture (Kang et al., 2014). These findings led us to ask whether FGF8 also affected GFAP immunoreactive astrocyte arborization complexities in the corpus callosum of adult WT and Fgf8+/neo mouse brains using a computerized Sholl analysis. Our results showed, that unlike astrocytes in cell culture, corpus callosal astrocytes do not differ in complexity between WT and Fgf8+/neo adult mice. Currently, we are designing experiments that are designed to elucidate the incongruence between the in vitro and in vivo data. Indeed, cell culture astrocytes are derived from late embryonic animals. Therefore, instead of studying astrocyte arborization in adult, we will use newborn Fgf8 hypomorphic mice. Furthermore, we will study whether FGF8 signaling deficits affect the development of other glial cell types, such as oligodendrocytes and microglia using the IHC markers Olig2 and IBA-1. Future studies will address if FGF8-dependent disruption of midline glial cells development have functional consequences on the ability of midline glial cells to guide extending callosal fibers.

Research Category

Biology/Ecology

Primary Author's Major

Biochemistry

Mentor #1 Information

Dr. Wilson Chung

Mentor #2 Information

Courtney Stewart

Presentation Format

Poster

Start Date

11-3-2015 1:00 PM

End Date

11-3-2015 5:00 PM

Research Area

Biology | Developmental Neuroscience | Neuroscience and Neurobiology

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Mar 11th, 1:00 PM Mar 11th, 5:00 PM

Fibroblast Growth Factor 8 Hypomorphy Does Not Affect Astrocyte Arborization Complexity in the Corpus Callosum of Adult Mice

Fibroblast growth factor 8 (FGF8) has an array of functions in relation to a developing organism. Previous studies examined the role of FGF8 and its involvement with the formation of the corpus callosum in Fgf8 hypomorphic mice. Astrocytic glial cells are critical for the interhemispheric crossing of callosal fibers, and thus the formation of the corpus callosum. Using GFAP immunohistochemistry (IHC), we showed that midline astrocyte cell number was significantly reduced in heterozygous (+/neo) and homozygous (neo/neo) Fgf8 hypomorphic as compared to wildtype (WT) mice. These results suggest FGF8 signaling is critical for late gestational astrocyte cell development, possibly by acting on the progenitor cells that are destined to become astrocytes. Recently, it was shown that FGF8 increased astrocyte arborization complexity in cell culture (Kang et al., 2014). These findings led us to ask whether FGF8 also affected GFAP immunoreactive astrocyte arborization complexities in the corpus callosum of adult WT and Fgf8+/neo mouse brains using a computerized Sholl analysis. Our results showed, that unlike astrocytes in cell culture, corpus callosal astrocytes do not differ in complexity between WT and Fgf8+/neo adult mice. Currently, we are designing experiments that are designed to elucidate the incongruence between the in vitro and in vivo data. Indeed, cell culture astrocytes are derived from late embryonic animals. Therefore, instead of studying astrocyte arborization in adult, we will use newborn Fgf8 hypomorphic mice. Furthermore, we will study whether FGF8 signaling deficits affect the development of other glial cell types, such as oligodendrocytes and microglia using the IHC markers Olig2 and IBA-1. Future studies will address if FGF8-dependent disruption of midline glial cells development have functional consequences on the ability of midline glial cells to guide extending callosal fibers.