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.
Bonanno
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G
Istituto di Farmacologia e Farmacognosia, Università di Genova, Italy.
Fedele
E
E
Versace
P
P
Raiteri
M
M
D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D004298:Dopamine / Q000378:metabolism*; D004558:Electric Stimulation; D007608:Kainic Acid / Q000494:pharmacology*; D008297:Male; D009411:Nerve Endings / Q000187:drug effects / Q000378:metabolism*; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000187:drug effects / Q000378:metabolism*; D014702:Veratrine / Q000494:pharmacology
D011954:Receptors, Dopamine; D014702:Veratrine; D001058:Apomorphine; D011188:Potassium; D007608:Kainic Acid; D004298:Dopamine