The effect of [Ca2+] and [H+] on the functional recovery of rat brain synaptosomes from anoxic insult in vitro.

Abstract

The energy status (as measured by the ATP/ADP ratio), oxidative metabolism (14CO2 output) and neurotransmitter synthesis ( [14C]acetylcholine production) by rat brain synaptosomes utilizing [U-14C]glucose has been studied. The ability of anoxia in vitro to permanently alter these parameters was investigated with reference to external [Ca2+] and [H+]. It has previously been shown that anoxic damage to synaptosomal preparations is only apparent when their metabolism is stimulated by veratridine [Harvey, Booth & Clark (1982) Biochem. J. 206, 433-439]. It is concluded that low [Ca2+] ameliorates, and high [H+] exacerbates, the damage sustained by veratridine-stimulated anoxic synaptosomes. The combined effects of low pH, anoxia and veratridine stimulation on synaptosomal metabolism most closely approximated to the irreversible damage to brain metabolism observed during acute hypoxia in vivo [Booth, Harvey & Clark (1983) J. Neurochem. 40, 106-110]. Suitably treated synaptosomal preparations may therefore be usefully employed as models to study impaired neurotransmitter synthesis in vivo.

• Authors: S A Harvey, R F Booth, J B Clark
• Journal: The Biochemical journal (Biochem J) Vol. 212 Issue 2 Pg. 289-95 (May 15 1983) ISSN: 0264-6021 [Print] England
• PMID: 6882373 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Adenosine Diphosphate
• Veratridine
• Hydrogen
• Adenosine Triphosphate
• Acetylcholine
• Oxygen
• Calcium

Topics

• Acetylcholine (biosynthesis)
• Adenosine Diphosphate (metabolism)
• Adenosine Triphosphate (metabolism)
• Animals
• Brain (drug effects, metabolism)
• Calcium (pharmacology)
• Hydrogen (pharmacology)
• Male
• Oxygen (metabolism)
• Rats
• Synaptosomes (drug effects, metabolism)
• Veratridine (pharmacology)