Abstract
Population spikes associated with the paired pulse ratio protocol were used to measure the presynaptic inhibition of corticostriatal transmission caused by μ-opioid receptor activation. A 1 μM of [ d-Ala 2, N-MePhe 4, Gly-ol 5]-enkephalin (DAMGO), a selective μ-opioid receptor agonist, enhanced paired pulse facilitation by 44±8%. This effect was completely blocked by 2 nM of the selective μ-receptor antagonist d-Phe-Cys-Tyr- d-Trp-Orn-Thr-NH (CTOP). Antagonists of N- and P/Q-type Ca 2+ channels inhibited, whereas antagonists of potassium channels enhanced, synaptic transmission. A 1 μM of ω-conotoxin GVIA, a blocker of N-type Ca 2+ channels, had no effect on the action of DAMGO, but 400 nM ω-agatoxin TK, a blocker of P/Q-type Ca 2+-channels, partially blocked the action of this opioid. However, 5 mM Cs 2+ and 400 μM Ba 2+, unselective antagonists of potassium conductances, completely prevented the action of DAMGO on corticostriatal transmission. These data suggest that presynaptic inhibition of corticostriatal afferents by μ-opioids is mediated by the modulation of K + conductances in corticostriatal afferents.
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