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Start Over Author "Sarò, G" Topic rac1 gtp-binding protein
2 results on '"Sarò, G"'

1. Disruption of ArhGAP15 results in hyperactive Rac1, affects the architecture and function of hippocampal inhibitory neurons and causes cognitive deficits.

Author

Zamboni V, Armentano M, Sarò G, Ciraolo E, Ghigo A, Germena G, Umbach A, Valnegri P, Passafaro M, Carabelli V, Gavello D, Bianchi V, D'Adamo P, de Curtis I, El-Assawi N, Mauro A, Priano L, Ferri N, Hirsch E, and Merlo GR

Subjects
Animals, Behavior, Animal physiology, Cell Movement genetics, Cells, Cultured, Cognition Disorders etiology, Female, GTPase-Activating Proteins genetics, Gene Expression Regulation, Developmental, Hippocampus pathology, Interneurons pathology, Male, Memory, Short-Term physiology, Mice, Mutant Strains, Neurons pathology, Neuropeptides genetics, Rats, rac GTP-Binding Proteins genetics, rac GTP-Binding Proteins metabolism, rac1 GTP-Binding Protein genetics, Cognition Disorders genetics, GTPase-Activating Proteins metabolism, Hippocampus physiopathology, Neurons physiology, Neuropeptides metabolism, rac1 GTP-Binding Protein metabolism
Abstract

During brain development, the small GTPases Rac1/Rac3 play key roles in neuronal migration, neuritogenesis, synaptic formation and plasticity, via control of actin cytoskeleton dynamic. Their activity is positively and negatively regulated by GEFs and GAPs molecules, respectively. However their in vivo roles are poorly known. The ArhGAP15 gene, coding for a Rac-specific GAP protein, is expressed in both excitatory and inhibitory neurons of the adult hippocampus, and its loss results in the hyperactivation of Rac1/Rac3. In the CA3 and dentate gyrus (DG) regions of the ArhGAP15 mutant hippocampus the CR+, PV+ and SST+ inhibitory neurons are reduced in number, due to reduced efficiency and directionality of their migration, while pyramidal neurons are unaffected. Loss of ArhGAP15 alters neuritogenesis and the balance between excitatory and inhibitory synapses, with a net functional result consisting in increased spike frequency and bursts, accompanied by poor synchronization. Thus, the loss of ArhGAP15 mainly impacts on interneuron-dependent inhibition. Adult ArhGAP15 -/- mice showed defective hippocampus-dependent functions such as working and associative memories. These findings indicate that a normal architecture and function of hippocampal inhibitory neurons is essential for higher hippocampal functions, and is exquisitely sensitive to ArhGAP15-dependent modulation of Rac1/Rac3.

Published
2016
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2. Disruption of ArhGAP15 results in hyperactive Rac1, affects the architecture and function of hippocampal inhibitory neurons and causes cognitive deficits

Author

Giorgio R. Merlo, Nicola Ferri, Ivanmatteo De Curtis, Valentina Zamboni, Alessandro Umbach, Giulia Germena, Maria Armentano, Elisa Ciraolo, Lorenzo Priano, Nadia El-Assawi, Pamela Valnegri, Patrizia D'Adamo, Gabriella Saró, Alessandra Ghigo, Daniela Gavello, Maria Passafaro, Emilio Hirsch, Valentina Carabelli, Veronica Bianchi, Alessandro Mauro, Zamboni, V, Armentano, M, Sarò, G, Ciraolo, E, Ghigo, A, Germena, G, Umbach, A, Valnegri, P, Passafaro, M, Carabelli, V, Gavello, D, Bianchi, V, D'Adamo, P, DE CURTIS, Ivanmatteo, El Assawi, N, Mauro, A, Priano, L, Ferri, N, Hirsch, E, and Merlo, Gr

Subjects
Male, rac1 GTP-Binding Protein, 0301 basic medicine, Hippocampus, RAC1, Hippocampal formation, Inhibitory postsynaptic potential, Article, 03 medical and health sciences, 0302 clinical medicine, Cell Movement, Interneurons, Animals, Cells, Cultured, Neurons, Regulation of gene expression, Multidisciplinary, Behavior, Animal, Chemistry, Dentate gyrus, GTPase-Activating Proteins, Neuropeptides, Gene Expression Regulation, Developmental, Actin cytoskeleton, Mice, Mutant Strains, Rats, rac GTP-Binding Proteins, Memory, Short-Term, 030104 developmental biology, nervous system, Excitatory postsynaptic potential, Female, Cognition Disorders, Neuroscience, 030217 neurology & neurosurgery
Abstract

During brain development, the small GTPases Rac1/Rac3 play key roles in neuronal migration, neuritogenesis, synaptic formation and plasticity, via control of actin cytoskeleton dynamic. Their activity is positively and negatively regulated by GEFs and GAPs molecules, respectively. However their in vivo roles are poorly known. The ArhGAP15 gene, coding for a Rac-specific GAP protein, is expressed in both excitatory and inhibitory neurons of the adult hippocampus, and its loss results in the hyperactivation of Rac1/Rac3. In the CA3 and dentate gyrus (DG) regions of the ArhGAP15 mutant hippocampus the CR+, PV+ and SST+ inhibitory neurons are reduced in number, due to reduced efficiency and directionality of their migration, while pyramidal neurons are unaffected. Loss of ArhGAP15 alters neuritogenesis and the balance between excitatory and inhibitory synapses, with a net functional result consisting in increased spike frequency and bursts, accompanied by poor synchronization. Thus, the loss of ArhGAP15 mainly impacts on interneuron-dependent inhibition. Adult ArhGAP15−/− mice showed defective hippocampus-dependent functions such as working and associative memories. These findings indicate that a normal architecture and function of hippocampal inhibitory neurons is essential for higher hippocampal functions, and is exquisitely sensitive to ArhGAP15-dependent modulation of Rac1/Rac3.

Published
2016
Full Text
View/download PDF

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