Activation of pre- and postsynaptic protein kinase C during tetraethylammonium-induced long-term potentiation in the CA1 field of the hippocampus
Autor: | Annemarie van der Slot, Moniek van Beest, Piera Pasinelli, W.H. Gispen, Geert M.J. Ramakers, Pierre N. E. De Graan |
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Rok vydání: | 2000 |
Předmět: |
Potassium Channels
Nifedipine Long-Term Potentiation Presynaptic Terminals Synaptic Membranes Nerve Tissue Proteins In Vitro Techniques Biology Neurotransmission Hippocampus Synaptic Transmission Geneeskunde chemistry.chemical_compound GAP-43 Protein Postsynaptic potential Potassium Channel Blockers Animals 4-Aminopyridine Phosphorylation Gap-43 protein Protein Kinase C Protein kinase C Tetraethylammonium musculoskeletal neural and ocular physiology General Neuroscience Calcium channel Excitatory Postsynaptic Potentials Long-term potentiation Calcium Channel Blockers Rats 2-Amino-5-phosphonovalerate nervous system Biochemistry chemistry Biophysics biology.protein NMDA receptor Calmodulin-Binding Proteins Neurogranin Excitatory Amino Acid Antagonists Signal Transduction |
Zdroj: | Neuroscience letters, 286(1), 53. Elsevier |
ISSN: | 0304-3940 |
Popis: | Tetraethylammonium (TEA) induces a form of long-term potentiation (LTP) that is independent on N -methyl- d -aspartate (NMDA) receptor activation (LTP K ). LTP K may be a suitable chemical model to study molecular mechanisms underlying LTP. We monitored the phosphorylation state of two identified neural-specific protein kinase C (PKC) substrates (the presynaptic protein GAP-43/B-50 and postsynaptic protein RC3) after different chemical depolarisations. TEA induced a long-lasting increase in synaptic efficacy in the CA1 field of the hippocampus and increased the phosphorylation of both GAP-43/B-50 and RC3 (51 and 56.1%, respectively). These effects were blocked by the voltage-dependent calcium channel antagonist nifedipine, but not by the NMDA receptor antagonist AP5. These data show that in LTP K the in situ phosphorylation of pre-and postsynaptic PKC substrates is increased, indicating that NMDA receptor-dependent and NMDA receptor-independent LTP share common Ca 2+ -dependent expression mechanisms, including activation of pre- and postsynaptic PKC. |
Databáze: | OpenAIRE |
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