SKF-83566 (0.1 μM-10 μM) causes a concentration-dependent increase in peak evoked extracellular DA concentration ([DA]
o
) evoked by single-pulse stimulation, with a maximum 65% increase in peak evoked [DA]
o
with 5 μM. The EC
50
value of this effect of SKF-83566 is 1.3 μM.SKF-83566 inhibited [
3
H]DA uptake with an IC
50
of 5.73 μM. Moreover, SKF-83566 more potently inhibits the binding of [
3
H]CFT, a cocaine analog, with an IC
50
of 0.51 μM in [
3
H]DA uptake and [
3
H]CFT binding studies.Similarly, in LLc-PK-rDAT cell, SKF-83566 also inhibits [
3
H]CFT binding with an IC
50
of 0.77 μM in LLc-PK-rDAT cell membrane preparations.
SKF 83566 hydrobromide (oral administration; 20 µg/mL; 7 days) alone has no effects on altering LTP (115%). However, combinnation of SKF 83566 and nicotine significantly blocks the enhancement of long-term synaptic potentiation (LTP) induced by pretreatment with nicotine (SKF 83566+nicotine+cocaine, 120%; nicotine+cocaine, 143%).
Animal Model:
Male C57BL6/J mice (6- to 9-wk-old)
Dosage:
20 µg/mL (Together with nicotine for 7 d, followed by the injection of cocaine)
Administration:
Oral administration; 7 days
Result:
Blocked nicotine and cocaine-induced facilitation of LTP.
