The contribution of calcium/calmodulin-dependent protein-kinase II (CaMKII) to short-term plasticity at the neuromuscular junction

• Published in: Brain research bulletin 2010-04, Vol.81 (6), p.613-616
• Main Authors: Mukhamedyarov, Marat A, Kochunova, Julia O, Yusupova, Elvina R, Haidarov, Bulat A, Zefirov, Andrey L, Palotás, András
• Format: Article
• Language: English
• Subjects: Acetylcholine - metabolism; Animals; Anura; Benzylamines - pharmacology; Calcium-Calmodulin-Dependent Protein Kinase Type 2 - antagonists & inhibitors; Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism; Calcium/calmodulin-dependent protein-kinase II (CaMKII); Electric Stimulation; Evoked Potentials; Excitatory Postsynaptic Potentials; KN-93; Microelectrodes; Neurology; Neuromuscular junction; Neuromuscular Junction - drug effects; Neuromuscular Junction - physiology; Neuronal Plasticity - drug effects; Neuronal Plasticity - physiology; Neurotransmitter release; Paired-pulse facilitation; Presynaptic Terminals - drug effects; Presynaptic Terminals - physiology; Protein Kinase Inhibitors - pharmacology; Rana ridibunda; Short-term depression; Short-term synaptic plasticity; Sulfonamides - pharmacology; Synaptic Transmission - drug effects; Synaptic Transmission - physiology; Time Factors
• ISSN: 0361-9230; 1873-2747
• DOI: 10.1016/j.brainresbull.2009.12.010

Abstract Calcium/calmodulin-dependent protein-kinase II (CaMKII) is a ubiquitous intracellular enzyme, which is implicated in learning and memory mechanisms in the central nervous system, however its contribution to peripheral cholinergic neurotransmission is not well characterized. This study evaluated the impact of CaMKII on the function of frog neuromuscular synapse using electrophysiological recordings. Application of the selective CaMKII inhibitor KN-93 (5 μM) did not significantly alter the parameters of evoked and spontaneous quantal acetylcholine release under low-frequency stimulation (0.03 Hz). KN-93, on the other hand, produced pronounced changes in short-term synaptic plasticity: particularly, KN-93 inhibits the second component of paired-pulse facilitation (interpulse intervals of 100 ms and longer) and strengthens the depression of synaptic transmission under high-frequency stimulation (50 Hz). These results imply that CaMKII plays an important role in presynaptic functions at the frog neuromuscular junction, and potentiates quantal acetylcholine release under high-frequency activity.