Abstract
We investigated the involvement of calcium-dependent enzymes, protein kinase C (PKC) and calcium-calmodulin-dependent protein kinase II (CaMKII), in the signaling pathway triggered by the activation of presynaptic alpha7-type nicotinic acetylcholine receptors by exogenous choline, leading to downregulation of the evoked acetylcholine (ACh) release in mouse motor synapses. Blockade of PKC with chelerythrine neither changed the evoked release of ACh by itself nor prevented the inhibitory effect of choline. The CaMKII blocker KN-62 did not affect synaptic activity but fully prevented the choline-induced downregulation of ACh release.
Highlights
Choline comes from the products of the hydrolysis of acetylcholine (ACh) neurotransmitter by acetylcholinesterase in cholinergic synapses
We have established recently that choline (0.1 mM) downregulates the evoked ACh release in mouse neuromuscular synapses via Ca2+-dependent Ca2+ efflux from the store through ryanodine receptors and the activation of the SK-type KCa channels of terminals, resulting in downregulation of ACh release [4]. It was unclear whether Ca2+-dependent enzymes, such as protein kinase C (PKC) and/or calcium-calmodulin-dependent protein kinase type II (CaMKII), are involved in this cascade
The aim of this study was to assess the changes in choline-evoked ACh release in mouse motor synapses, together with the blockade of calmodulin and Ca2+-dependent enzymes, protein kinase C (PKC), and calcium-calmodulin-dependent protein kinase II (CaMKII)
Summary
Choline comes from the products of the hydrolysis of acetylcholine (ACh) neurotransmitter by acetylcholinesterase in cholinergic synapses. Along with choline reuptake into the nerve terminals where it is recycled to synthesize ACh, choline plays an important role in the auto-regulation of ACh release by the feedback mechanism This mechanism is associated with the ability of choline to selectively activate presynaptic alpha7-type nicotinic acetylcholine receptors (alpha7-nAChR) [1]. We have established recently that choline (0.1 mM) downregulates the evoked ACh release in mouse neuromuscular synapses via Ca2+-dependent Ca2+ efflux from the store through ryanodine receptors and the activation of the SK-type KCa channels of terminals, resulting in downregulation of ACh release [4] It was unclear whether Ca2+-dependent enzymes, such as protein kinase C (PKC) and/or calcium-calmodulin-dependent protein kinase type II (CaMKII), are involved in this cascade. The aim of this study was to assess the changes in choline-evoked ACh release in mouse motor synapses, together with the blockade of calmodulin and Ca2+-dependent enzymes, protein kinase C (PKC), and calcium-calmodulin-dependent protein kinase II (CaMKII)
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