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 microM) 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.
journal_name
Brain Res Bulljournal_title
Brain research bulletinauthors
Mukhamedyarov MA,Kochunova JO,Yusupova ER,Haidarov BA,Zefirov AL,Palotás Adoi
10.1016/j.brainresbull.2009.12.010subject
Has Abstractpub_date
2010-04-05 00:00:00pages
613-6issue
6eissn
0361-9230issn
1873-2747pii
S0361-9230(09)00403-1journal_volume
81pub_type
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