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

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 Bull

journal_title

Brain research bulletin

authors

Mukhamedyarov MA,Kochunova JO,Yusupova ER,Haidarov BA,Zefirov AL,Palotás A

doi

10.1016/j.brainresbull.2009.12.010

subject

Has Abstract

pub_date

2010-04-05 00:00:00

pages

613-6

issue

6

eissn

0361-9230

issn

1873-2747

pii

S0361-9230(09)00403-1

journal_volume

81

pub_type

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