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Decrease of Acetylcholine Release from Cortical Slices in Aged Rats: Investigations into Its Reversal by Phosphatidylserine
Author(s) -
Vannucchi Maria Giuliana,
Casamenti Fiorella,
Pepeu Giancarlo
Publication year - 1990
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1990.tb04565.x
Subject(s) - acetylcholine , stimulation , physostigmine , endocrinology , medicine , chemistry , phosphatidylserine , choline , cholinesterase , incubation , biology , phospholipid , biochemistry , membrane
The release of total acetylcholine (ACh) and [ 3 H]ACh was investigated in electrically stimulated cortical slices prepared from 4‐ and 18‐month‐old male Wistar rats. The slices were prelabeled with [ 3 H]choline ([ 3 H]Ch) and perfused with Krebs solution containing physostigmine. Total ACh was measured and the nature of the tritium efflux identified by HPLC. The total tritium content in the slices at the end of the incubation period was half as great in the old as in young rats. A linear relationship was found between stimulation frequencies (2, 5, and 10 Hz) and fractional [ 3 H]ACh release in both young and old rats. In the latter the release was significantly smaller. At 10 Hz stimulation frequency the ratio between the two 2‐min stimulation periods, S 2 /S 1 , was higher in the 18‐month‐old rats than in the young rats. Specific activity of the evoked ACh release was significantly smaller in S 2 than in S 1 in 4‐month‐old rats only. These findings indicate that the young synthetize ACh from endogenous unlabeled Ch more than older rats. In 18‐month‐old rats both the evoked total ACh and [ 3 H]ACh release, expressed as picograms per minute, showed an approximately 50% decrease in both S 1 and S 2 stimulation periods, with no significant difference in specific activity. Phosphatidylserine (PtdSer) administration (15 mg/kg, i.p. daily) for 1 week to 18‐month‐old rats prevented the reduction in total evoked ACh release but not the reduction in evoked [ 3 H]ACh release. The specific activity of ACh release was therefore significantly smaller than that of the young and untreated old rats. This finding indicates that PtdSer is able to increase the availability of endogenous choline for de novo ACh synthesis and release. PtdSer treatment also prevented impairment of the passive avoidance conditioned response observed in old rats.