Inhibition of hippocampal synaptic transmission by impairment of Ral function.
Research output: Contribution to journal › Journal article › Research › peer-review
Large clostridial cytotoxins and protein overexpression were used to probe for involvement of Ras-related GTPases (guanosine triphosphate) in synaptic transmission in cultured rat hippocampal neurons. The toxins TcdA-10463 (inactivates Rho, Rac, Cdc42, Rap) and TcsL-1522 (inactivates Ral, Rac, Ras, R-Ras, Rap) both inhibited autaptic responses. In a proportion of the neurons (25%, TcdA-10463; 54%, TcsL-1522), the inhibition was associated with a shift from activity-dependent depression to facilitation, indicating that the synaptic release probability was reduced. Overexpression of a dominant negative Ral mutant, Ral A28N, caused a strong inhibition of autaptic responses, which was associated with a shift to facilitation in a majority (80%) of the neurons. These results indicate that Ral, along with at least one other non-Rab GTPase, participates in presynaptic regulation in hippocampal neurons.
Original language | English |
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Journal | NeuroReport |
Volume | 16 |
Issue number | 16 |
Pages (from-to) | 1805-8 |
Number of pages | 3 |
ISSN | 0959-4965 |
Publication status | Published - 2005 |
Bibliographical note
Keywords: Alanine; Animals; Arabidopsis Proteins; Asparagine; Bacterial Toxins; Blotting, Western; Carbon Isotopes; Cells, Cultured; Drug Interactions; Electric Stimulation; Enterotoxins; Excitatory Amino Acid Agonists; Gene Expression Regulation; Glucose; Hippocampus; Membrane Potentials; Mutation; Neural Inhibition; Neurons; Patch-Clamp Techniques; Rats; Synaptic Transmission; Toxins, Biological; Transfection; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; gamma-Aminobutyric Acid; ral GTP-Binding Proteins
ID: 5750214