scholarly journals Beta2-containing nicotinic acetylcholine receptors mediate calcium/calmodulin-dependent protein kinase-II and synapsin I protein levels in the nucleus accumbens after nicotine withdrawal in mice

2013 ◽  
Vol 701 (1-3) ◽  
pp. 1-6 ◽  
Author(s):  
Kia J. Jackson ◽  
M. Imad Damaj
Keyword(s):  
Nucleus Accumbens ◽  
Protein Kinase ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Synapsin I ◽  
Dependent Protein Kinase ◽  
Nicotinic Acetylcholine ◽  
Protein Levels ◽  
Calcium Calmodulin Dependent ◽  
Dependent Protein

scholarly journals CaMKII Is Involved in the Choline-Induced Downregulation of Acetylcholine Release in Mouse Motor Synapses

Acta Naturae ◽  
2017 ◽  
Vol 9 (4) ◽  
pp. 110-113 ◽  
Author(s):  
A. E. Gaydukov ◽  
O. P. Balezina
Keyword(s):  
Protein Kinase ◽  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Inhibitory Effect ◽  
Synaptic Activity ◽  
Ach Release ◽  
Calcium Dependent ◽  
Calcium Calmodulin Dependent ◽  
Kinase C ◽  
Dependent Protein

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.

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