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2. Protein kinase C activity is not responsible for the expression of long-term potentiation in hippocampus.

Author

Muller, D, Buchs, P A, Dunant, Y, and Lynch, G

Subjects
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine, Animals, Hippocampus: enzymology, Isoquinolines: pharmacology, Membrane Potentials: drug effects, Neuronal Plasticity: physiology, Phorbol Esters: pharmacology, Piperazines: pharmacology, Protein Kinase C: antagonists & inhibitors, physiology, Rats, Receptors, N-Methyl-D-Aspartate, Receptors, Neurotransmitter: physiology, Synaptic Transmission: drug effects, physiology, Time Factors
Abstract

Long-term potentiation (LTP) in hippocampus has been proposed to result from a tonic activation of protein kinase C. This hypothesis predicts that stimulation of the kinase would produce a smaller change in response size on potentiated versus control pathways and, conversely, that inhibition of the kinase would reduce potentiated inputs to a greater degree than control responses. We tested these predictions using phorbol esters to activate and using the antagonist H-7 to inhibit protein kinase C; we found that the actions of these drugs on synaptic transmission were not affected by prior induction of LTP. Both compounds, however, significantly decreased the contribution of N-methyl-D-aspartate receptors to synaptic potentials, a result that accounts for the suppressive effects of these compounds on LTP formation. Thus protein kinase C is probably not involved in the expression of LTP but may play a role in the receptor-mediated events participating in its induction.

Published
1990

28. The lectin-like domain of tumor necrosis factor-alpha increases membrane conductance in microvascular endothelial cells and peritoneal macrophages

Author

Hribar, M., Bloc, A., van der Goot, F. G., Fransen, L., De Baetselier, P., Grau, G. E., Bluethmann, H., Matthay, M. A., Dunant, Y., Pugin, J., Lucas, R., Cellular and Molecular Immunology, and Vrije Universiteit Brussel

Subjects
Male, Patch-Clamp Techniques, Macrophages, Electric Conductivity, Inbred CBA, Vascular/cytology/immunology/*physiology, Membrane Potentials/immunology, Peritoneal/immunology/*physiology, Inbred C57BL, Mutant Strains, Mice, Animals, Lung/*blood supply/immunology/metabolism, Endothelium, Lectins/immunology/*physiology, Microcirculation/cytology/immunology, Tumor Necrosis Factor-alpha/*physiology, Peptide Fragments/immunology/*physiology, Capillary Permeability/immunology
Abstract

Herein, we show that TNF exerts a pH-dependent increase in membrane conductance in primary lung microvascular endothelial cells and peritoneal macrophages. This effect was TNF receptor-independent, since it also occurred in cells isolated from mice deficient in both types of TNF receptors. A TNF mutant in which the three amino acids critical for the lectin-like activity were replaced by an alanine did not show any significant effect on membrane conductance. Moreover, a synthetic 17-amino acid peptide of TNF, which was previously shown to exert lectin-like activity, also increased the ion permeability in these cells. The amiloride sensitivity of the observed activity suggests a binding of TNF to an endogenous ion channel rather than channel formation by TNF itself. This may have important implications in mechanisms of TNF-mediated vascular pathology.

Published
1999

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