PMID- 17448462
OWN - NLM
STAT- MEDLINE
DCOM- 20070919
LR  - 20131121
IS  - 0014-2999 (Print)
IS  - 0014-2999 (Linking)
VI  - 566
IP  - 1-3
DP  - 2007 Jul 2
TI  - Ethanolamine and related amino alcohols increase basal and evoked release of 
      [3H]-D-aspartic acid from synaptosomes by enhancing the filling of synaptic 
      vesicles.
PG  - 103-12
AB  - This research examines the effects of ethanolamine and other amino alcohols on 
      the dynamics of acridine orange (AO), oxonol V, and [3H]-D-aspartic acid in 
      synaptic preparations isolated from mammalian brain. Ethanolamine 
      concentration-dependently enhanced AO release from synaptosomes. Similar effects 
      were observed with methylethanolamine and dimethylethanolamine, but not choline. 
      The enhancement of AO efflux by ethanolamine was independent of extrasynaptosomal 
      calcium (in contrast to KCl-induced AO efflux), was unaffected by tetrodotoxin 
      and did not involve depolarization of the synaptosomal plasma membrane. KCl was 
      unable to release AO from synaptosomes following exposure to ethanolamine, 
      however ethanolamine and other amino alcohols were found to enhance both basal 
      and KCl-evoked release of [3H]-D-aspartic acid from synaptosomes. Using isolated 
      synaptic vesicles we demonstrate that amino alcohols are able to 1) abolish the 
      ATP-dependent intravesicular proton concentration (i.e. stimulate efflux of AO) 
      in a similar way to carbonyl cyanide m-chlorophenylhydrazone (CCCP), 2) increase 
      the ATP-supported transvesicular membrane potential (i.e. quench oxonol V 
      fluorescence) in contrast to CCCP and 3) enhance intravesicular uptake of 
      [3H]-D-aspartic acid. These results suggest that positively charged, membrane 
      impermeant amino alcohol species are generated within synaptic vesicles as they 
      sequester protons. Cationic forms of these amino alcohols boost the 
      transvesicular electrical potential which increases transmitter uptake into 
      synaptic vesicles and facilitates enhancement of basal and evoked release of 
      transmitter. Our data suggest a potential role for ethanolamine and related amino 
      alcohols in the regulation of synaptic vesicle filling. These findings may also 
      have relevance to neuropathophysiological states involving altered production of 
      ethanolamine.
FAU - Liao, Chengyong
AU  - Liao C
AD  - Department of Biological Sciences, Simon Fraser University, 8888 University 
      Drive, Burnaby, BC, Canada V5A 1S6.
FAU - Nicholson, Russell A
AU  - Nicholson RA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20070324
PL  - Netherlands
TA  - Eur J Pharmacol
JT  - European journal of pharmacology
JID - 1254354
RN  - 0 (Ethanolamines)
RN  - 0 (Fluorescent Dyes)
RN  - 0 (Isoxazoles)
RN  - 10028-17-8 (Tritium)
RN  - 30KYC7MIAI (Aspartic Acid)
RN  - 61389-30-8 (oxonol V)
RN  - F30N4O6XVV (Acridine Orange)
SB  - IM
MH  - Acridine Orange/metabolism
MH  - Animals
MH  - Aspartic Acid/*metabolism
MH  - Brain/drug effects/physiology
MH  - Cell Membrane/drug effects/physiology
MH  - Ethanolamines/*pharmacology
MH  - Fluorescent Dyes/metabolism
MH  - Isoxazoles/metabolism
MH  - Male
MH  - Membrane Potentials/drug effects
MH  - Mice
MH  - Mice, Inbred Strains
MH  - Synaptic Vesicles/*drug effects/physiology
MH  - Synaptosomes/*drug effects/physiology
MH  - Tritium
EDAT- 2007/04/24 09:00
MHDA- 2007/09/20 09:00
CRDT- 2007/04/24 09:00
PHST- 2007/01/19 00:00 [received]
PHST- 2007/03/07 00:00 [revised]
PHST- 2007/03/08 00:00 [accepted]
PHST- 2007/04/24 09:00 [pubmed]
PHST- 2007/09/20 09:00 [medline]
PHST- 2007/04/24 09:00 [entrez]
AID - S0014-2999(07)00352-4 [pii]
AID - 10.1016/j.ejphar.2007.03.020 [doi]
PST - ppublish
SO  - Eur J Pharmacol. 2007 Jul 2;566(1-3):103-12. doi: 10.1016/j.ejphar.2007.03.020. 
      Epub 2007 Mar 24.