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UPTAKE OF RADIOCALCIUM BY NERVE ENDINGS ISOLATED FROM RAT BRAIN: PHARMACOLOGICAL STUDIES
Author(s) -
GRIPENBERG J.,
HEIN E.,
JANSSON S.E.
Publication year - 1980
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1980.tb10936.x
Subject(s) - calcium , chemistry , striatum , endocrinology , potassium , medicine , dopamine , depolarization , free nerve ending , haloperidol , biophysics , biology , organic chemistry
1 The uptake of radiocalcium by nerve‐ending particles isolated from the striatum of rat brain was studied using lanthanum as a quenching agent. 2 High potassium‐induced calcium uptake occurred in two phases: an initial rapid phase and a late slow phase. Following preincubation with CaCl 2 2.2 mmol/l for 1 h, dopamine at 1 to 2 × 10 −4 mol/l reduced the high potassium‐induced calcium uptake which occurred during the initial rapid phase by 66 and 25% at 2 and 4 s of incubation, respectively, but had no effect on the late slow uptake phase. 3 Haloperidol at 1 × 10 −6 mol/l abolished the inhibitory effect of dopamine on the initial rapid phase of the high potassium‐induced calcium uptake. Haloperidol per se had no effect on the calcium uptake. 4 Dibutyryl cyclic adenosine monophosphate at 2.5 × 10 −3 mol/l or prostaglandin E 1 (PGE 1 ) at 1 × 10 −5 mol/l had no effect on the initial rapid phase of the high potassium‐induced calcium uptake by striatal synaptosomes. Neither of these agents affect calcium uptake by whole brain synaptosomes. 5 It appears that in the striatum, dopamine regulates the depolarization‐induced influx of calcium in presynaptic nerve endings. This mechanism could constitute a feed‐back inhibition for transmitter release in the striatum.