Activation of pre- and postsynaptic protein kinase C during tetraethylammonium-induced long-term potentiation in the CA1 field of the hippocampus. 2000

G M Ramakers, and P Pasinelli, and M van Beest, and A van der Slot, and W H Gispen, and P N De Graan
Rudolf Magnus Institute for Neurosciences, Department of Medical Pharmacology, Universiteitsweg 100, 3584 CG, Utrecht, The Netherlands. g.m.j.ramakers@med.uu.nl

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.

UI MeSH Term Description Entries
D009419 Nerve Tissue Proteins Proteins, Nerve Tissue,Tissue Proteins, Nerve
D009435 Synaptic Transmission The communication from a NEURON to a target (neuron, muscle, or secretory cell) across a SYNAPSE. In chemical synaptic transmission, the presynaptic neuron releases a NEUROTRANSMITTER that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across ELECTRICAL SYNAPSES. Neural Transmission,Neurotransmission,Transmission, Neural,Transmission, Synaptic
D009543 Nifedipine A potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure. Adalat,BAY-a-1040,Bay-1040,Cordipin,Cordipine,Corinfar,Fenigidin,Korinfar,Nifangin,Nifedipine Monohydrochloride,Nifedipine-GTIS,Procardia,Procardia XL,Vascard,BAY a 1040,BAYa1040,Bay 1040,Bay1040,Monohydrochloride, Nifedipine,Nifedipine GTIS
D010766 Phosphorylation The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety. Phosphorylations
D011493 Protein Kinase C An serine-threonine protein kinase that requires the presence of physiological concentrations of CALCIUM and membrane PHOSPHOLIPIDS. The additional presence of DIACYLGLYCEROLS markedly increases its sensitivity to both calcium and phospholipids. The sensitivity of the enzyme can also be increased by PHORBOL ESTERS and it is believed that protein kinase C is the receptor protein of tumor-promoting phorbol esters. Calcium Phospholipid-Dependent Protein Kinase,Calcium-Activated Phospholipid-Dependent Kinase,PKC Serine-Threonine Kinase,Phospholipid-Sensitive Calcium-Dependent Protein Kinase,Protein Kinase M,Calcium Activated Phospholipid Dependent Kinase,Calcium Phospholipid Dependent Protein Kinase,PKC Serine Threonine Kinase,Phospholipid Sensitive Calcium Dependent Protein Kinase,Phospholipid-Dependent Kinase, Calcium-Activated,Serine-Threonine Kinase, PKC
D002121 Calcium Channel Blockers A class of drugs that act by selective inhibition of calcium influx through cellular membranes. Calcium Antagonists, Exogenous,Calcium Blockaders, Exogenous,Calcium Channel Antagonist,Calcium Channel Blocker,Calcium Channel Blocking Drug,Calcium Inhibitors, Exogenous,Channel Blockers, Calcium,Exogenous Calcium Blockader,Exogenous Calcium Inhibitor,Calcium Channel Antagonists,Calcium Channel Blocking Drugs,Exogenous Calcium Antagonists,Exogenous Calcium Blockaders,Exogenous Calcium Inhibitors,Antagonist, Calcium Channel,Antagonists, Calcium Channel,Antagonists, Exogenous Calcium,Blockader, Exogenous Calcium,Blocker, Calcium Channel,Blockers, Calcium Channel,Calcium Blockader, Exogenous,Calcium Inhibitor, Exogenous,Channel Antagonist, Calcium,Channel Blocker, Calcium,Inhibitor, Exogenous Calcium
D002148 Calmodulin-Binding Proteins Proteins which bind calmodulin. They are found in many tissues and have a variety of functions including F-actin cross-linking properties, inhibition of cyclic nucleotide phosphodiesterase and calcium and magnesium ATPases. Caldesmon,Calspectin,CaM-BP(80),Caldesmon (77),Calmodulin Binding Proteins,Proteins, Calmodulin-Binding
D006624 Hippocampus A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation. Ammon Horn,Cornu Ammonis,Hippocampal Formation,Subiculum,Ammon's Horn,Hippocampus Proper,Ammons Horn,Formation, Hippocampal,Formations, Hippocampal,Hippocampal Formations,Hippocampus Propers,Horn, Ammon,Horn, Ammon's,Proper, Hippocampus,Propers, Hippocampus,Subiculums
D000818 Animals Unicellular or multicellular, heterotrophic organisms, that have sensation and the power of voluntary movement. Under the older five kingdom paradigm, Animalia was one of the kingdoms. Under the modern three domain model, Animalia represents one of the many groups in the domain EUKARYOTA. Animal,Metazoa,Animalia
D013570 Synaptic Membranes Cell membranes associated with synapses. Both presynaptic and postsynaptic membranes are included along with their integral or tightly associated specializations for the release or reception of transmitters. Membrane, Synaptic,Membranes, Synaptic,Synaptic Membrane

Related Publications

G M Ramakers, and P Pasinelli, and M van Beest, and A van der Slot, and W H Gispen, and P N De Graan
June 1989, Trends in pharmacological sciences,
G M Ramakers, and P Pasinelli, and M van Beest, and A van der Slot, and W H Gispen, and P N De Graan
April 1992, Proceedings of the National Academy of Sciences of the United States of America,
G M Ramakers, and P Pasinelli, and M van Beest, and A van der Slot, and W H Gispen, and P N De Graan
March 1996, Science (New York, N.Y.),
G M Ramakers, and P Pasinelli, and M van Beest, and A van der Slot, and W H Gispen, and P N De Graan
August 1994, Hippocampus,
G M Ramakers, and P Pasinelli, and M van Beest, and A van der Slot, and W H Gispen, and P N De Graan
February 1997, Brain research,
G M Ramakers, and P Pasinelli, and M van Beest, and A van der Slot, and W H Gispen, and P N De Graan
June 1988, The Journal of physiology,
G M Ramakers, and P Pasinelli, and M van Beest, and A van der Slot, and W H Gispen, and P N De Graan
February 1995, Proceedings of the National Academy of Sciences of the United States of America,
G M Ramakers, and P Pasinelli, and M van Beest, and A van der Slot, and W H Gispen, and P N De Graan
March 1996, Science (New York, N.Y.),
G M Ramakers, and P Pasinelli, and M van Beest, and A van der Slot, and W H Gispen, and P N De Graan
September 2012, Journal of integrative neuroscience,
G M Ramakers, and P Pasinelli, and M van Beest, and A van der Slot, and W H Gispen, and P N De Graan
August 1992, Neuroscience,
Copied contents to your clipboard!