Functional damage of dopamine nerve terminals following intrastriatal kainic acid injection.

The release of [3H]dopamine ([3H]DA) previously taken up into rat striatal slices was studied one week after a monolateral intrastriatal injection of kainic acid (KA). Different releasing stimuli (electrical pulses, veratrine, high-K+) were applied. The electrically evoked release in the KA-lesioned striata was drastically reduced with respect to the unlesioned contralateral striata. In contrast, KA had no effect on the release of [3H]DA evoked by veratrine or high-K+. In unlesioned striatal slices, depolarized with 15 mM KCl, apomorphine reduced and (-)sulpiride increased the release of [3H]DA. The effect of apomorphine was antagonized by (-)sulpiride indicating the presence of an autoreceptor system similar to that seen in unlesioned striata stimulated electrically. However, the effects of apomorphine and of (-)sulpiride were dramatically reduced in K+-depolarized slices prepared from KA-lesioned striata. The results suggest that the axon terminals in KA-treated areas remain intact in several of their properties but may be damaged in some critical processes.