The Vehicle, Spring 1999

Vol. 40, No. 2 Table of Contents Poetry Eve\u27s DaughterSylvia Whippopage 1 When We Wore Canoes On Our ShouldersMandy Watsonpage 2 This Is Not A Poem About GrandpaJake Tolbertpage 3 Old relationshipsBrandi Kinneypage 5 UntitledErin Winnerpage 6 BraverySylvia Whippopage 6 deep dark closetNicole Smithpage 7 Belly EarthTara Coburnpage 9 The River and FireJake Tolbertpage 10 UntitledAutumn Williamspage 12 Action PotentialKim Evanspage 13 Chimerical (a song for children)D.M. Attrapepage 14 UntitledAutumn Williamspage 16 UntitledMatthew Armstrongpage 18 Building YouSylvia Whippopage 19 RunningKim Evanspage 20 Walking Jenn to WorkJake Tolbertpage 22 Looking InKim Hunterpage 23 Void Between Me and WisconsinMandy Watsonpage 24 Artwork UntitledWendy Finchpage 4 MeditationJennifer Lundpage 8 UntitledSteve Drakepage 15 MemoriesJennifer Lundpage 21 UntitledKathryn Kolasinskipage 25 Prose FoundKim Hunterpage 26 A Day in the Life of William Baxter, DriverDaniel Fitzgeraldpage 32https://thekeep.eiu.edu/vehicle/1072/thumbnail.jp

The Vehicle, Spring 1999

Vol. 40, No. 2 Table of Contents Poetry Eve\u27s DaughterSylvia Whippopage 1 When We Wore Canoes On Our ShouldersMandy Watsonpage 2 This Is Not A Poem About GrandpaJake Tolbertpage 3 Old relationshipsBrandi Kinneypage 5 UntitledErin Winnerpage 6 BraverySylvia Whippopage 6 deep dark closetNicole Smithpage 7 Belly EarthTara Coburnpage 9 The River and FireJake Tolbertpage 10 UntitledAutumn Williamspage 12 Action PotentialKim Evanspage 13 Chimerical (a song for children)D.M. Attrapepage 14 UntitledAutumn Williamspage 16 UntitledMatthew Armstrongpage 18 Building YouSylvia Whippopage 19 RunningKim Evanspage 20 Walking Jenn to WorkJake Tolbertpage 22 Looking InKim Hunterpage 23 Void Between Me and WisconsinMandy Watsonpage 24 Artwork UntitledWendy Finchpage 4 MeditationJennifer Lundpage 8 UntitledSteve Drakepage 15 MemoriesJennifer Lundpage 21 UntitledKathryn Kolasinskipage 25 Prose FoundKim Hunterpage 26 A Day in the Life of William Baxter, DriverDaniel Fitzgeraldpage 32https://thekeep.eiu.edu/vehicle/1072/thumbnail.jp

<it>LRRK2</it> knockout mice have an intact dopaminergic system but display alterations in exploratory and motor co-ordination behaviors

Abstract Mutations in the LRRK2 gene are the most common cause of genetic Parkinson’s disease. Although the mechanisms behind the pathogenic effects of LRRK2 mutations are still not clear, data emerging from in vitro and in vivo models suggests roles in regulating neuronal polarity, neurotransmission, membrane and cytoskeletal dynamics and protein degradation. We created mice lacking exon 41 that encodes the activation hinge of the kinase domain of LRRK2. We have performed a comprehensive analysis of these mice up to 20 months of age, including evaluation of dopamine storage, release, uptake and synthesis, behavioral testing, dendritic spine and proliferation/neurogenesis analysis. Our results show that the dopaminergic system was not functionally comprised in LRRK2 knockout mice. However, LRRK2 knockout mice displayed abnormal exploratory activity in the open-field test. Moreover, LRRK2 knockout mice stayed longer than their wild type littermates on the accelerated rod during rotarod testing. Finally, we confirm that loss of LRRK2 caused degeneration in the kidney, accompanied by a progressive enhancement of autophagic activity and accumulation of autofluorescent material, but without evidence of biphasic changes.</p

LRRK2 knockout mice have an intact dopaminergic system but display alterations in exploratory and motor co-ordination behaviors.

Mutations in the LRRK2 gene are the most common cause of genetic Parkinson's disease. Although the mechanisms behind the pathogenic effects of LRRK2 mutations are still not clear, data emerging from in vitro and in vivo models suggests roles in regulating neuronal polarity, neurotransmission, membrane and cytoskeletal dynamics and protein degradation.We created mice lacking exon 41 that encodes the activation hinge of the kinase domain of LRRK2. We have performed a comprehensive analysis of these mice up to 20 months of age, including evaluation of dopamine storage, release, uptake and synthesis, behavioral testing, dendritic spine and proliferation/neurogenesis analysis.Our results show that the dopaminergic system was not functionally comprised in LRRK2 knockout mice. However, LRRK2 knockout mice displayed abnormal exploratory activity in the open-field test. Moreover, LRRK2 knockout mice stayed longer than their wild type littermates on the accelerated rod during rotarod testing. Finally, we confirm that loss of LRRK2 caused degeneration in the kidney, accompanied by a progressive enhancement of autophagic activity and accumulation of autofluorescent material, but without evidence of biphasic changes

LRRK2 knockout mice have an intact dopaminergic system but display alterations in exploratory and motor co-ordination behaviors

Mutations in the LRRK2 gene are the most common cause of genetic Parkinson’s disease. Although the mechanisms behind the pathogenic effects of LRRK2 mutations are still not clear, data emerging from in vitro and in vivo models suggests roles in regulating neuronal polarity, neurotransmission, membrane and cytoskeletal dynamics and protein degradation. We created mice lacking exon 41 that encodes the activation hinge of the kinase domain of LRRK2. We have performed a comprehensive analysis of these mice up to 20 months of age, including evaluation of dopamine storage, release, uptake and synthesis, behavioral testing, dendritic spine and proliferation/neurogenesis analysis. Our results show that the dopaminergic system was not functionally comprised in LRRK2 knockout mice. However, LRRK2 knockout mice displayed abnormal exploratory activity in the open-field test. Moreover, LRRK2 knockout mice stayed longer than their wild type littermates on the accelerated rod during rotarod testing. Finally, we confirm that loss of LRRK2 caused degeneration in the kidney, accompanied by a progressive enhancement of autophagic activity and accumulation of autofluorescent material, but without evidence of biphasic changes.Medical Genetics, Department ofMedicine, Faculty ofNon UBCReviewedFacult