PMID- 1815825
OWN - NLM
STAT- MEDLINE
DCOM- 19920701
LR  - 20190613
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 567
IP  - 1
DP  - 1991 Dec 13
TI  - Decreased potassium-stimulated release of [3H]D-aspartate from hippocampal slices 
      distinguishes encephalopathy related to acute liver failure from that induced by 
      simple hyperammonemia.
PG  - 165-8
AB  - The calcium-dependent, high (65 mM) potassium-evoked release of the L-glutamate 
      analogue [3H]D-aspartate (D-Asp) was measured in hippocampal slices derived from 
      rats with (a) hepatic encephalopathy (HE) induced with a hepatotoxin, 
      thioacetamide, (b) hyperammonemia produced by i.p. administration of ammonium 
      acetate, and (c) in normal slices preincubated for 30 min with 1 mM ammonium 
      acetate. HE (variant a) inhibited the release by about 30%, which was interpreted 
      to indicate depressed exocytosis of synaptic glutamate. This phenomenon is likely 
      to lead to a decrease of glutamate-mediated neural excitation, which in turn 
      could contribute to the neural inhibition typical of HE. By contrast, and in 
      agreement with earlier reports, hyperammonemia (variant b) did not affect D-Asp 
      release, whereas in vitro treatment of the slices with ammonium acetate (variant 
      c) resulted in a 60% increase of the release. Hence, impairment of synaptic 
      glutamate exocytosis is the phenomenon that distinguishes HE related to toxic 
      liver failure from simple hyperammonemia. This result emphasizes the role of 
      other factors than ammonia in the pathophysiological mechanism of HE.
FAU - Hilgier, W
AU  - Hilgier W
AD  - Medical Research Centre, Polish Academy of Sciences, Warsaw.
FAU - Haugvicova, R
AU  - Haugvicova R
FAU - Albrecht, J
AU  - Albrecht J
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Acetates)
RN  - 075T165X8M (Thioacetamide)
RN  - 10028-17-8 (Tritium)
RN  - 30KYC7MIAI (Aspartic Acid)
RN  - RRE756S6Q2 (ammonium acetate)
RN  - RWP5GA015D (Potassium)
SB  - IM
MH  - Acetates/*pharmacology
MH  - Animals
MH  - Aspartic Acid/*metabolism
MH  - Female
MH  - Hepatic Encephalopathy/chemically induced/*metabolism
MH  - Hippocampus/drug effects/*metabolism
MH  - In Vitro Techniques
MH  - Kinetics
MH  - Potassium/*pharmacology
MH  - Radioisotope Dilution Technique
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Thioacetamide
MH  - Tritium
EDAT- 1991/12/13 00:00
MHDA- 1991/12/13 00:01
CRDT- 1991/12/13 00:00
PHST- 1991/12/13 00:00 [pubmed]
PHST- 1991/12/13 00:01 [medline]
PHST- 1991/12/13 00:00 [entrez]
AID - 0006-8993(91)91451-6 [pii]
AID - 10.1016/0006-8993(91)91451-6 [doi]
PST - ppublish
SO  - Brain Res. 1991 Dec 13;567(1):165-8. doi: 10.1016/0006-8993(91)91451-6.