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

G M Ramakers; P Pasinelli; M van Beest; A van der Slot; W H Gispen; P N De Graan

doi:10.1016/s0304-3940(00)01081-8

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

Neurosci Lett. 2000 May 26;286(1):53-6. doi: 10.1016/s0304-3940(00)01081-8.

Authors

G M Ramakers¹, P Pasinelli, M van Beest, A van der Slot, W H Gispen, P N De Graan

Affiliation

¹ Rudolf Magnus Institute for Neurosciences, Department of Medical Pharmacology, Universiteitsweg 100, 3584 CG, Utrecht, The Netherlands. [email protected]

PMID: 10822151
DOI: 10.1016/s0304-3940(00)01081-8

Abstract

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.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

2-Amino-5-phosphonovalerate / pharmacology
4-Aminopyridine / pharmacology
Animals
Calcium Channel Blockers / pharmacology
Calmodulin-Binding Proteins / metabolism
Excitatory Amino Acid Antagonists / pharmacology
Excitatory Postsynaptic Potentials / drug effects
Excitatory Postsynaptic Potentials / physiology
GAP-43 Protein / metabolism
Hippocampus / cytology
Hippocampus / drug effects*
Hippocampus / metabolism*
In Vitro Techniques
Long-Term Potentiation / drug effects*
Long-Term Potentiation / physiology*
Nerve Tissue Proteins / metabolism
Neurogranin
Nifedipine / pharmacology
Phosphorylation
Potassium Channel Blockers
Potassium Channels / drug effects
Potassium Channels / metabolism
Presynaptic Terminals / drug effects*
Presynaptic Terminals / metabolism*
Presynaptic Terminals / ultrastructure
Protein Kinase C / drug effects*
Protein Kinase C / metabolism*
Rats
Signal Transduction / drug effects
Signal Transduction / physiology
Synaptic Membranes / drug effects*
Synaptic Membranes / metabolism*
Synaptic Membranes / ultrastructure
Synaptic Transmission / drug effects
Synaptic Transmission / physiology
Tetraethylammonium / pharmacology*

Substances

Calcium Channel Blockers
Calmodulin-Binding Proteins
Excitatory Amino Acid Antagonists
GAP-43 Protein
Nerve Tissue Proteins
Nrgn protein, rat
Potassium Channel Blockers
Potassium Channels
Neurogranin
Tetraethylammonium
2-Amino-5-phosphonovalerate
4-Aminopyridine
Protein Kinase C
Nifedipine