Article date: September 1972
By: G. BUSTOS, R. H. ROTH in Volume 46, Issue 1, pages 101-115
. A simple in vitro system was developed to study the effect of γ‐hydroxybutyrate on nerve cell depolarization‐induced release of labelled dopamine, noradrenaline and 5‐hydroxytryptamine from brain slices.
. The release of 3H‐dopamine formed in rat striatal slices incubated with 3H‐tyrosine was followed either by transferring the slices through successive media or by using a superfusion system. A one to three minute exposure to K+ (53 mm) caused up to a thirty fold increase in the release of newly synthesized 3H‐dopamine. This K+‐induced release was antagonized when γ‐hydroxybutyrate (1 × 10−3m) was present in the medium.
. Potassium (53 mm) increased (eighteen to thirty fold) the release of 3H‐dopamine from striatal slices initially loaded by preincubation with 3H‐dopamine. However, the K+‐induced release of this pool of dopamine was not antagonized by γ‐hydroxybutyrate.
. Potassium (53 mm) also increased the release from striatal slices of 3H‐5‐hydroxytryptamine newly synthesized from 3H‐tryptophan. This K+‐induced release of 5‐hydroxytryptamine was also not inhibited by γ‐hydroxybutyrate.
. The release of newly synthesized 3H‐noradrenaline from hypothalamic slices was also increased by K+. This K+‐induced release, however, unlike that of 5‐hydroxytryptamine, was antagonized when γ‐hydroxybutyrate was present in the superfusion medium.
. Removal of Ca++ had no effect on K+‐induced release of 3H‐dopamine when followed by transferring the slices through successive media. This K+‐induced release was abolished, however, when Mg++ (12 mm) was present in the medium.
. The removal of Ca++ from the superfusion medium abolished almost completely the K+‐induced release from striatal slices of either newly synthesized 3H‐dopamine or preloaded 3H‐dopamine. This is presumably due to a more effective washout of tissue Ca++ by the superfusion technique.
. The ability of γ‐hydroxybutyrate to antagonize the K+‐induced release of monoamines from brain slices does not appear to be unique to the release of newly synthesized dopamine from the striatum.
. A simple in vitro system was developed to study the effect of γ‐hydroxybutyrate on nerve cell depolarization‐induced release of labelled dopamine, noradrenaline and 5‐hydroxytryptamine from brain slices.
. The release of 3H‐dopamine formed in rat striatal slices incubated with 3H‐tyrosine was followed either by transferring the slices through successive media or by using a superfusion system. A one to three minute exposure to K+ (53 mm) caused up to a thirty fold increase in the release of newly synthesized 3H‐dopamine. This K+‐induced release was antagonized when γ‐hydroxybutyrate (1 × 10−3m) was present in the medium.
. Potassium (53 mm) increased (eighteen to thirty fold) the release of 3H‐dopamine from striatal slices initially loaded by preincubation with 3H‐dopamine. However, the K+‐induced release of this pool of dopamine was not antagonized by γ‐hydroxybutyrate.
. Potassium (53 mm) also increased the release from striatal slices of 3H‐5‐hydroxytryptamine newly synthesized from 3H‐tryptophan. This K+‐induced release of 5‐hydroxytryptamine was also not inhibited by γ‐hydroxybutyrate.
. The release of newly synthesized 3H‐noradrenaline from hypothalamic slices was also increased by K+. This K+‐induced release, however, unlike that of 5‐hydroxytryptamine, was antagonized when γ‐hydroxybutyrate was present in the superfusion medium.
. Removal of Ca++ had no effect on K+‐induced release of 3H‐dopamine when followed by transferring the slices through successive media. This K+‐induced release was abolished, however, when Mg++ (12 mm) was present in the medium.
. The removal of Ca++ from the superfusion medium abolished almost completely the K+‐induced release from striatal slices of either newly synthesized 3H‐dopamine or preloaded 3H‐dopamine. This is presumably due to a more effective washout of tissue Ca++ by the superfusion technique.
. The ability of γ‐hydroxybutyrate to antagonize the K+‐induced release of monoamines from brain slices does not appear to be unique to the release of newly synthesized dopamine from the striatum.
DOI: 10.1111/j.1476-5381.1972.tb06853.x
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