The efflux of previously accumulated [3H]‐spermine from brain slices was measured using a continuous perfusion system. The spontaneous efflux was biphasic, consisting of an initial rapid efflux followed by a much slower release.
The slices were depolarized by the addition to the medium of high potassium concentrations, ouabain or veratrine.
At concentrations greater than 30 mM, potassium evoked a striking increase in the release of [3H]‐spermine. Following uptake in the presence of 5.7 × 10−9M[3H]‐spermine, K+‐evoked release was dependent on the presence of calcium ions. Release of spermine after uptake at 5.6 × 10−8m or 5.0 × 10−7m was not calcium‐dependent.
The calcium‐dependent, K+‐stimulated release of spermine was inhibited in the presence of diphenylhydantoin (5 × 10−3m) or ruthenium red (10−3 m).
Following uptake of 5.7 × 10−9m [3H]‐spermine in a sodium‐free medium, the calcium‐dependent, K+‐stimulated release was significantly inhibited.
Ouabain (10−4m) caused a large but calcium‐independent increase in the efflux of [3H]‐spermine.
Veratrine‐induced release was less substantial but was increased in a calcium‐free medium. Release evoked by veratrine was abolished in the absence of sodium.
These results are discussed with respect to a possible ‘neurotransmitter’ or ‘neuromodulator’ role for spermine.