PMID- 26826585
OWN - NLM
STAT- MEDLINE
DCOM- 20161213
LR  - 20161230
IS  - 1872-6240 (Electronic)
IS  - 0006-8993 (Linking)
VI  - 1635
DP  - 2016 Mar 15
TI  - Suppression of outward K(+) currents by activating dopamine D1 receptors in rat 
      retinal ganglion cells through PKA and CaMKII signaling pathways.
PG  - 95-104
LID - S0006-8993(16)30016-6 [pii]
LID - 10.1016/j.brainres.2016.01.039 [doi]
AB  - Dopamine plays an important role in regulating neuronal functions in the central 
      nervous system by activating the specific G-protein coupled receptors. Both D1 
      and D2 dopamine receptors are extensively distributed in the retinal neurons. In 
      the present study, we investigated the effects of D1 receptor signaling on 
      outward K(+) currents in acutely isolated rat retinal ganglion cells (RGCs) by 
      patch-clamp techniques. Extracellular application of SKF81297 (10 muM), a specific 
      D1 receptor agonist, significantly and reversibly suppressed outward K(+) 
      currents of the cells, which was reversed by SCH23390 (10 muM), a selective D1 
      receptor antagonist. We further showed that SKF81297 mainly suppressed the 
      glybenclamide (Gb)- and 4-aminopyridine (4-AP)-sensitive K(+) current components, 
      but did not show effect on the tetraethylammonium (TEA)-sensitive one. Both 
      protein kinase A (PKA) and calcium/calmodulin-dependent protein kinase II 
      (CaMKII) signaling pathways were likely involved in the SKF81297-induced 
      suppression of the K(+) currents since either Rp-cAMP (10 muM), a cAMP/PKA 
      signaling inhibitor, or KN-93 (10 muM), a specific CaMKII inhibitor, eliminated 
      the SKF81297 effect. In contrast, neither protein kinase C (PKC) nor 
      mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase 
      (ERK) signaling pathway seemed likely to be involved because both the PKC 
      inhibitor bisindolylmaleimide IV (Bis IV) (10 muM) and the MAPK/ERK1/2 inhibitor 
      U0126 (10 muM) did not block the SKF81297-induced suppression of the K(+) 
      currents. These results suggest that activation of D1 receptors suppresses the 
      Gb- and 4-AP-sensitive K(+) current components in rat RGCs through the 
      intracellular PKA and CaMKII signaling pathways, thus modulating the RGC 
      excitability.
CI  - Copyright (c) 2016 Elsevier B.V. All rights reserved.
FAU - Li, Qian
AU  - Li Q
AD  - Institutes of Brain Science, Fudan University, Shanghai 200032, China; Institute 
      of Neurobiology, Fudan University, Shanghai 200032, China; State Key Laboratory 
      of Medical Neurobiology, Fudan University, Shanghai 200032, China; Collaborative 
      Innovation Center for Brain Science, Fudan University, Shanghai 200032, China. 
      Electronic address: 14110700008@fudan.edu.cn.
FAU - Wu, Na
AU  - Wu N
AD  - Institutes of Brain Science, Fudan University, Shanghai 200032, China; Department 
      of Ophthalmology at Eye & ENT Hospital, Fudan University, Shanghai 200031, China; 
      State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200032, 
      China; Shanghai Key Laboratory of Visual Impairment and Restoration, Fudan 
      University, Shanghai 200031, China; Collaborative Innovation Center for Brain 
      Science, Fudan University, Shanghai 200032, China. Electronic address: 
      tgf_b@sina.cn.
FAU - Cui, Peng
AU  - Cui P
AD  - Institutes of Brain Science, Fudan University, Shanghai 200032, China; Institute 
      of Neurobiology, Fudan University, Shanghai 200032, China; State Key Laboratory 
      of Medical Neurobiology, Fudan University, Shanghai 200032, China; Collaborative 
      Innovation Center for Brain Science, Fudan University, Shanghai 200032, China. 
      Electronic address: 14111520017@fudan.edu.cn.
FAU - Gao, Feng
AU  - Gao F
AD  - Institutes of Brain Science, Fudan University, Shanghai 200032, China; Department 
      of Ophthalmology at Eye & ENT Hospital, Fudan University, Shanghai 200031, China; 
      State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200032, 
      China; Shanghai Key Laboratory of Visual Impairment and Restoration, Fudan 
      University, Shanghai 200031, China; Collaborative Innovation Center for Brain 
      Science, Fudan University, Shanghai 200032, China. Electronic address: 
      fenggao@fudan.edu.cn.
FAU - Qian, Wen-Jing
AU  - Qian WJ
AD  - Institutes of Brain Science, Fudan University, Shanghai 200032, China; Institute 
      of Neurobiology, Fudan University, Shanghai 200032, China; State Key Laboratory 
      of Medical Neurobiology, Fudan University, Shanghai 200032, China; Collaborative 
      Innovation Center for Brain Science, Fudan University, Shanghai 200032, China. 
      Electronic address: 15111520021@fudan.edu.cn.
FAU - Miao, Yanying
AU  - Miao Y
AD  - Institutes of Brain Science, Fudan University, Shanghai 200032, China; Institute 
      of Neurobiology, Fudan University, Shanghai 200032, China; State Key Laboratory 
      of Medical Neurobiology, Fudan University, Shanghai 200032, China; Collaborative 
      Innovation Center for Brain Science, Fudan University, Shanghai 200032, China. 
      Electronic address: yymiao@fudan.edu.cn.
FAU - Sun, Xing-Huai
AU  - Sun XH
AD  - Institutes of Brain Science, Fudan University, Shanghai 200032, China; Department 
      of Ophthalmology at Eye & ENT Hospital, Fudan University, Shanghai 200031, China; 
      State Key Laboratory of Medical Neurobiology, Fudan University, Shanghai 200032, 
      China; Shanghai Key Laboratory of Visual Impairment and Restoration, Fudan 
      University, Shanghai 200031, China; Collaborative Innovation Center for Brain 
      Science, Fudan University, Shanghai 200032, China. Electronic address: 
      xhsun@shmu.edu.cn.
FAU - Wang, Zhongfeng
AU  - Wang Z
AD  - Institutes of Brain Science, Fudan University, Shanghai 200032, China; Department 
      of Ophthalmology at Eye & ENT Hospital, Fudan University, Shanghai 200031, China; 
      Institute of Neurobiology, Fudan University, Shanghai 200032, China; State Key 
      Laboratory of Medical Neurobiology, Fudan University, Shanghai 200032, China; 
      Shanghai Key Laboratory of Visual Impairment and Restoration, Fudan University, 
      Shanghai 200031, China; Collaborative Innovation Center for Brain Science, Fudan 
      University, Shanghai 200032, China. Electronic address: zfwang@fudan.edu.cn.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160127
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Benzazepines)
RN  - 0 (Potassium Channels)
RN  - 0 (Receptors, Dopamine D1)
RN  - 0 (SCH 23390)
RN  - 71636-61-8 (SK&F 81297)
RN  - EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
RN  - EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinase Type 2)
SB  - IM
MH  - Animals
MH  - Benzazepines/pharmacology
MH  - Calcium-Calmodulin-Dependent Protein Kinase Type 2/*metabolism
MH  - Cyclic AMP-Dependent Protein Kinases/*metabolism
MH  - Male
MH  - Potassium Channels/*physiology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Dopamine D1/agonists/antagonists & inhibitors/*physiology
MH  - Retinal Ganglion Cells/drug effects/metabolism/*physiology
MH  - Signal Transduction
OTO - NOTNLM
OT  - Dopamine D1 receptor
OT  - Outward K(+) currents
OT  - Patch-clamp
OT  - Retinal ganglion cell
EDAT- 2016/01/31 06:00
MHDA- 2016/12/15 06:00
CRDT- 2016/01/31 06:00
PHST- 2015/09/18 00:00 [received]
PHST- 2016/01/17 00:00 [revised]
PHST- 2016/01/21 00:00 [accepted]
PHST- 2016/01/31 06:00 [entrez]
PHST- 2016/01/31 06:00 [pubmed]
PHST- 2016/12/15 06:00 [medline]
AID - S0006-8993(16)30016-6 [pii]
AID - 10.1016/j.brainres.2016.01.039 [doi]
PST - ppublish
SO  - Brain Res. 2016 Mar 15;1635:95-104. doi: 10.1016/j.brainres.2016.01.039. Epub 
      2016 Jan 27.