Abstract
This paper gives experimental evidence involving protein kinase C (PKC) in the inhibitory effects of adenosine (ADO) upon the spontaneous transmitter release at the frog neuromuscular junction. In the presence of two PKC inhibitors--polymyxin B (5 x 10(-6) mol/l) and H-7 (10(-5) mol/l), both adenosine (5 x 10(-5) mol/l) and its stable analogue 1-PIA (5 x 10(-8) mol/l), significantly increased the rate of the spontaneous release of acetylcholine quanta. Even when PKC was activated with OAG (5 x 10(-6) mol/l) or TPA (162 x 10(-9) mol/l) and quantal release was increased greatly, ADO still inhibited release. ADO deaminase increased the PKC-induced activation of the transmitter release significantly.
MeSH terms
-
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
-
Acetylcholine / metabolism*
-
Acetylcholine / physiology
-
Adenosine / pharmacology*
-
Animals
-
Diglycerides / pharmacology*
-
Glycerides / pharmacology*
-
In Vitro Techniques
-
Isoquinolines / pharmacology
-
Neuromuscular Junction / drug effects
-
Neuromuscular Junction / metabolism*
-
Neuromuscular Junction / physiology
-
Piperazines / pharmacology
-
Polymyxin B / pharmacology*
-
Polymyxins / pharmacology*
-
Protease Inhibitors / pharmacology
-
Protein Kinase C / metabolism
-
Protein Kinase C / physiology*
-
Rana ridibunda
Substances
-
Diglycerides
-
Glycerides
-
Isoquinolines
-
Piperazines
-
Polymyxins
-
Protease Inhibitors
-
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine
-
1-oleoyl-2-acetylglycerol
-
Protein Kinase C
-
Polymyxin B
-
Adenosine
-
Acetylcholine