Enhancement of learning and memory after activation of cerebral Rho GTPases
| Autor: | Massimo Pieri, Sara Travaglione, Giovanni Diana, Alessia Fabbri, Carla Fiorentini, Stefania Meschini, Loredana Falzano, Cristina Zona, Giovanni Valentini |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2007 |
| Předmět: |
Male
rho GTP-Binding Proteins RHOA Dendritic spine Bacterial toxins CDC42 Inbred C57BL Hippocampus Synaptic Transmission Dendritic spines Conditioning (Psychology) memory Mice PAK1 conditioning Conditioning Psychological Cytotoxic necrotizing factor 1 neurotransmission cysteine Bacteria (microorganisms) Cells Cultured Neurons Multidisciplinary learning Cultured biology Cytotoxins Escherichia coli Proteins Mus article Brain Fear Biological Sciences Cell biology Rac1 protein priority journal nerve cell network Drug therapy RhoA guanine nucleotide binding protein actin amino acid substitution Cells animal experiment Spatial Behavior RAC1 Settore BIO/09 animal tissue dendrite serine Escherichia coli Animals controlled study protein Cdc42 Actin mouse nonhuman enzyme activation nerve cell plasticity Dendrites Actin cytoskeleton Actins Mice Inbred C57BL biology.protein recombinant cytotoxic necrotizing factor 1 MDia1 Rho guanine nucleotide binding protein cytotoxic necrotizing factor 1 recombinant protein Bacterial Toxins Enzyme Activation Learning Memory |
| Popis: | The mechanism whereby the morphology and connectivity of the dendritic tree is regulated depends on an actin dynamics that, in turn, is controlled by Rho GTPases, a family of small GTP-binding proteins encompassing Rho, Rac, and Cdc42 subfamilies. Cytotoxic necrotizing factor 1 (CNF1), a protein toxin from Escherichia coli , constitutively activates Rho GTPases, thus leading to remodeling of the actin cytoskeleton in intact cells. Here, we show that the modulation of cerebral RhoA and Rac1 activity induced by CNF1 in mice leads to ( i ) rearrangement of cerebral actin cytoskeleton, ( ii ) enhanced neurotransmission and synaptic plasticity, and ( iii ) improved learning and memory in various behavioral tasks. The effects persist for weeks and are not observed in mice treated with a recombinant CNF1, in which the enzymatic activity was abolished by substituting serine to cysteine at position 866. The results suggest that learning ability can be improved through pharmacological manipulation of neural connectivity. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|