PMID- 7921629
OWN - NLM
STAT- MEDLINE
DCOM- 19941109
LR  - 20190512
IS  - 0007-1188 (Print)
IS  - 0007-1188 (Linking)
VI  - 112
IP  - 3
DP  - 1994 Jul
TI  - Potentiation by adenosine of ATP-evoked dopamine release via a pertussis 
      toxin-sensitive mechanism in rat phaeochromocytoma PC12 cells.
PG  - 992-7
AB  - 1. The effects of adenosine on adenosine 5'-triphosphate (ATP)-evoked dopamine 
      release from rat phaeochromocytoma PC12 cells was investigated to determine 
      whether adenosine exerts a regulatory effect on the ATP-evoked response. 
      Adenosine potentiated ATP (30 microM)-evoked dopamine release in a 
      concentration-dependent manner over a concentration-range of 1 to 100 microM. 
      Adenosine (100 microM) shifted the concentration-dependence of the ATP-evoked 
      response to the left without affecting the maximal response. 2. Aminophylline, a 
      non-selective adenosine receptor antagonist, and CP66713, a selective antagonist 
      at the A2 subclass of adenosine receptors, abolished the adenosine-induced 
      potentiation. Furthermore, 8-cyclopentyltheophylline, a selective antagonist at 
      the adenosine A1 receptor partially inhibited the adenosine-evoked potentiation. 
      CGS22492, a selective A2 receptor agonist, potentiated ATP-evoked dopamine 
      release whereas N6-cyclohexyladenosine (CHA), a selective A1 receptor agonist, 
      had no effect. 3. Pertussis toxin (PTX), a bacterial exotoxin which catalyzes the 
      ADP-ribosylation of guanosine 5'-triphosphate (GTP)-binding proteins 
      (G-proteins), inhibited the adenosine-induced potentiation of dopamine release. 
      Dibutyryl cyclic AMP (db cyclic AMP), an analogue of cyclic AMP, had no effect on 
      the release on the ATP-evoked response. 4. Adenosine potentiated the ATP-evoked 
      rise in intracellular Ca2+ concentration ([Ca]i) in PC12 cells. This potentiation 
      was also observed with CGS 22492 but not with CHA. PTX completely inhibited the 
      adenosine-induced potentiation of the rise in [Ca]i. 5. On the basis of these 
      findings, we suggest that the adenosine-induced potentiation of ATP-evoked 
      dopamine release was due to an increase in [Ca]i in the cells. Although the 
      potentiation is most likely mediated by a subclass of A2 receptors, the subclass 
      may be different from those previously reported since the potentiation was 
      sensitive to PTX and was not reproduced by db cyclic AMP.
FAU - Koizumi, S
AU  - Koizumi S
AD  - Division of Pharmacology, National Institute of Health Sciences, Tokyo, Japan.
FAU - Watano, T
AU  - Watano T
FAU - Nakazawa, K
AU  - Nakazawa K
FAU - Inoue, K
AU  - Inoue K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Br J Pharmacol
JT  - British journal of pharmacology
JID - 7502536
RN  - 0 (Purinergic P1 Receptor Antagonists)
RN  - 0 (Virulence Factors, Bordetella)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - E0399OZS9N (Cyclic AMP)
RN  - EC 2.4.2.31 (Pertussis Toxin)
RN  - K72T3FS567 (Adenosine)
RN  - SY7Q814VUP (Calcium)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Adenosine/antagonists & inhibitors/*pharmacology
MH  - Adenosine Triphosphate/antagonists & inhibitors/*pharmacology
MH  - Animals
MH  - Calcium/metabolism
MH  - Cyclic AMP/physiology
MH  - Dopamine/*metabolism
MH  - Drug Synergism
MH  - PC12 Cells
MH  - *Pertussis Toxin
MH  - Purinergic P1 Receptor Antagonists
MH  - Rats
MH  - Virulence Factors, Bordetella/*pharmacology
PMC - PMC1910190
EDAT- 1994/07/01 00:00
MHDA- 1994/07/01 00:01
PMCR- 1995/07/01
CRDT- 1994/07/01 00:00
PHST- 1994/07/01 00:00 [pubmed]
PHST- 1994/07/01 00:01 [medline]
PHST- 1994/07/01 00:00 [entrez]
PHST- 1995/07/01 00:00 [pmc-release]
AID - 10.1111/j.1476-5381.1994.tb13179.x [doi]
PST - ppublish
SO  - Br J Pharmacol. 1994 Jul;112(3):992-7. doi: 10.1111/j.1476-5381.1994.tb13179.x.