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Tetanus Toxin Enhances Protein Kinase C Activity Translocation and Increases Polyphosphoinositide Hydrolysis in Rat Cerebral Cortex Preparations by Carles Gil; Marisol Ruiz-Meana; María Álava; Ephraim Yavin; José Aguilera is a Neuroscience article available to read on EtoBox.

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Abstract: Tetanus toxin (TeTx) has been recently demonstrated to be a Zn^2+^‐dependent endopeptidase that cleaves synaptobrevin, a protein in part responsible for neurotransmitter release. Nevertheless, certain aspects of TeTx action, for example, the causal relationship between TeTx and protein kinase C (PKC; EC 2.7.1.37) activity cannot be explained by this cleavage alone. In the present study, primary neurons from fetal rat brain, synaptosomes, and whole slices have been used to examine this issue. Low doses of TeTx (≤ 10^−8^__M__) caused PKC activity translocation in a manner similar to that produced by 12‐__O__‐tetradecanoylphorbol 13‐acetate (TPA). TPA (≤ 10^−7^__M__) caused sustained PKC activity translocation, whereas TeTx produced translocation followed by relocation, depending on the dose and time of exposure. Immunoidentification with a monoclonal antibody recognizing both α and β isoforms revealed that TeTx induced moderate losses of PKC in the cytosolic fraction, without a comparable increase in the particulate fraction. Although moderate losses of activity were also noticed in the cytosolic fraction, the inconsistency with respect to activity translocation may be expl

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Author

Carles Gil; Marisol Ruiz-Meana; María Álava; Ephraim Yavin; José Aguilera

Publisher

John Wiley and Sons; Wiley (Blackwell Publishing); Blackwell Publishing Inc.; Wiley (ISSN 0022-3042)

Published

1998

Language

EN

Field

Neuroscience (Life Sciences)