PMID- 26895748
OWN - NLM
STAT- MEDLINE
DCOM- 20170501
LR  - 20180830
IS  - 1097-4652 (Electronic)
IS  - 0021-9541 (Linking)
VI  - 231
IP  - 11
DP  - 2016 Nov
TI  - The Cholinergic Signaling Responsible for the Expression of a Memory-Related 
      Protein in Primary Rat Cortical Neurons.
PG  - 2428-38
LID - 10.1002/jcp.25347 [doi]
AB  - Cholinergic dysfunction in the brain is closely related to cognitive impairment 
      including memory loss. In addition to the degeneration of basal forebrain 
      cholinergic neurons, deficits in the cholinergic receptor signaling may also play 
      an important role. In the present study, to examine the cholinergic signaling 
      pathways responsible for the induction of a memory-related postsynaptic protein, 
      a cholinergic agonist carbachol was used to induce the expression of 
      activity-regulated cytoskeleton associated protein (Arc) in primary rat cortical 
      neurons. After pretreating neurons with various antagonists or inhibitors, the 
      levels of carbachol-induced Arc protein expression were detected by Western blot 
      analysis. The results show that carbachol induces Arc protein expression mainly 
      through activating M1 acetylcholine receptors and the downstream phospholipase C 
      pathway, which may lead to the activation of the MAPK/ERK signaling pathway. 
      Importantly, carbachol-mediated M2 receptor activation exerts negative effects on 
      Arc protein expression and thus counteracts the enhanced effects of M1 
      activation. Furthermore, it is suggested for the first time that M1-mediated 
      enhancement of N-methyl-D-aspartate receptor (NMDAR) responses, leading to Ca(2+) 
      entry through NMDARs, contributes to carbachol-induced Arc protein expression. 
      These findings reveal a more complete cholinergic signaling that is responsible 
      for carbachol-induced Arc protein expression, and thus provide more information 
      for developing treatments that can modulate cholinergic signaling and 
      consequently alleviate cognitive impairment. J. Cell. Physiol. 231: 2428-2438, 
      2016. (c) 2016 Wiley Periodicals, Inc.
CI  - (c) 2016 Wiley Periodicals, Inc.
FAU - Chen, Tsan-Ju
AU  - Chen TJ
AD  - Department of Physiology, School of Medicine, College of Medicine, Kaohsiung 
      Medical University, Kaohsiung, Taiwan.
FAU - Chen, Shun-Sheng
AU  - Chen SS
AD  - Department of Neurology, Chang Gung Memorial Hospital, Kaohsiung Medical Center, 
      Chang Gung University College of Medicine, Kaohsiung, Taiwan.
FAU - Wang, Dean-Chuan
AU  - Wang DC
AD  - Department of Sports Medicine, College of Medicine, Kaohsiung Medical University, 
      Kaohsiung, Taiwan.
FAU - Hung, Hui-Shan
AU  - Hung HS
AD  - Department of Physiology, School of Medicine, College of Medicine, Kaohsiung 
      Medical University, Kaohsiung, Taiwan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160308
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Cytoskeletal Proteins)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Receptor, Muscarinic M1)
RN  - 0 (Receptor, Muscarinic M2)
RN  - 0 (Receptors, Cholinergic)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 0 (activity regulated cytoskeletal-associated protein)
RN  - 8Y164V895Y (Carbachol)
RN  - EC 2.7.10.2 (src-Family Kinases)
RN  - EC 3.1.4.- (Type C Phospholipases)
RN  - N9YNS0M02X (Acetylcholine)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Acetylcholine/*metabolism
MH  - Animals
MH  - Animals, Newborn
MH  - Calcium/metabolism
MH  - Carbachol/pharmacology
MH  - Cells, Cultured
MH  - Cerebral Cortex/*cytology
MH  - Cytoskeletal Proteins/*metabolism
MH  - *Memory/drug effects
MH  - Models, Biological
MH  - Nerve Tissue Proteins/*metabolism
MH  - Neurons/drug effects/*metabolism
MH  - Phosphorylation/drug effects
MH  - Rats
MH  - Receptor, Muscarinic M1/antagonists & inhibitors
MH  - Receptor, Muscarinic M2/antagonists & inhibitors
MH  - Receptors, Cholinergic
MH  - Receptors, N-Methyl-D-Aspartate/metabolism
MH  - *Signal Transduction/drug effects
MH  - Type C Phospholipases/metabolism
MH  - src-Family Kinases/antagonists & inhibitors/metabolism
EDAT- 2016/02/21 06:00
MHDA- 2017/05/02 06:00
CRDT- 2016/02/21 06:00
PHST- 2015/09/09 00:00 [received]
PHST- 2016/02/17 00:00 [accepted]
PHST- 2016/02/21 06:00 [entrez]
PHST- 2016/02/21 06:00 [pubmed]
PHST- 2017/05/02 06:00 [medline]
AID - 10.1002/jcp.25347 [doi]
PST - ppublish
SO  - J Cell Physiol. 2016 Nov;231(11):2428-38. doi: 10.1002/jcp.25347. Epub 2016 Mar 
      8.