PMID- 2422345
OWN - NLM
STAT- MEDLINE
DCOM- 19860623
LR  - 20151119
IS  - 0022-3565 (Print)
IS  - 0022-3565 (Linking)
VI  - 237
IP  - 2
DP  - 1986 May
TI  - Effects of secretagogues on ATP levels and protein carboxyl methylation in rat 
      brain synaptosomes.
PG  - 569-76
AB  - The influence of various substances which are known to alter free intracellular 
      calcium concentrations on protein carboxyl methyltransferase (PCM) activity was 
      investigated in rat brain synaptosomes. The synaptosomes were labeled with 
      L-[3H]methionine and the 3H-methyl esters of proteins were formed from the methyl 
      donor S-[3H]adenosyl-L-methionine ([3H]AdoMet). The calcium ionophore A23187 and 
      ouabain decreased PCM activity and the decrease produced by A23187 was 
      antagonized by ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid 
      and MnCl2. On the other hand, ruthenium red, an inhibitor of calcium uptake, 
      stimulated PCM activity. These data suggest that PCM activity is inversely 
      related to the free cytoplasmic calcium concentration. Veratridine, A23187 and 
      elevated potassium ions decreased the levels of ATP and [3H]AdoMet. The 
      A23187-mediated decrease in ATP levels and the reduced [3H]AdoMet formation was 
      antagonized by ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid 
      and MnCl2. Inhibition of metabolic activity of the synaptosomes by NaCN led to: 
      decreased ATP levels; inhibition of [3H]AdoMet formation; and inhibition of PCM 
      activity. These data suggest that the decrease in protein methylation produced by 
      secretagogues is associated with an increase in the concentration of free 
      intracellular calcium which results in a decrease in the metabolically active 
      pool of ATP. This leads to a decreased rate of AdoMet formation, a cosubstrate 
      for PCM and a resultant decrease in PCM activity.
FAU - Bjorndahl, J M
AU  - Bjorndahl JM
FAU - Rutledge, C O
AU  - Rutledge CO
LA  - eng
GR  - 5606/PHS HHS/United States
GR  - NS 16364/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Pharmacol Exp Ther
JT  - The Journal of pharmacology and experimental therapeutics
JID - 0376362
RN  - 0 (Chlorides)
RN  - 0 (Manganese Compounds)
RN  - 0 (Proteins)
RN  - 10028-17-8 (Tritium)
RN  - 11103-72-3 (Ruthenium Red)
RN  - 37H9VM9WZL (Calcimycin)
RN  - 42Z2K6ZL8P (Manganese)
RN  - 526U7A2651 (Egtazic Acid)
RN  - 5ACL011P69 (Ouabain)
RN  - 71-62-5 (Veratridine)
RN  - 7LP2MPO46S (S-Adenosylmethionine)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - 979-92-0 (S-Adenosylhomocysteine)
RN  - EC 2.1.1.- (Protein Methyltransferases)
RN  - EC 2.1.1.- (Protein O-Methyltransferase)
RN  - K72T3FS567 (Adenosine)
RN  - O5DDB9Z95G (Sodium Cyanide)
RN  - QQE170PANO (manganese chloride)
RN  - RWP5GA015D (Potassium)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Adenosine/analysis
MH  - Adenosine Triphosphate/*analysis
MH  - Animals
MH  - Brain/*metabolism
MH  - Brain Chemistry/drug effects
MH  - Calcimycin/pharmacology
MH  - Calcium/metabolism
MH  - *Chlorides
MH  - Egtazic Acid/pharmacology
MH  - Female
MH  - In Vitro Techniques
MH  - Manganese/pharmacology
MH  - *Manganese Compounds
MH  - Methylation
MH  - Ouabain/pharmacology
MH  - Potassium/pharmacology
MH  - Protein Methyltransferases/*analysis
MH  - Protein O-Methyltransferase/*analysis
MH  - Proteins/*metabolism
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Ruthenium Red/pharmacology
MH  - S-Adenosylhomocysteine/analysis
MH  - S-Adenosylmethionine/analysis/metabolism
MH  - Sodium Cyanide/pharmacology
MH  - Synaptosomes/*metabolism
MH  - Tritium
MH  - Veratridine/pharmacology
EDAT- 1986/05/01 00:00
MHDA- 1986/05/01 00:01
CRDT- 1986/05/01 00:00
PHST- 1986/05/01 00:00 [pubmed]
PHST- 1986/05/01 00:01 [medline]
PHST- 1986/05/01 00:00 [entrez]
PST - ppublish
SO  - J Pharmacol Exp Ther. 1986 May;237(2):569-76.