KAPPA-OPIOID RECEPTOR ACTIVATION MODULATES CA2-TERMINALS( CURRENTS AND SECRETION IN ISOLATED NEUROENDOCRINE NERVE)

Whole-cell patch-clamp recordings were performed together with time-re solved measurements of membrane capacitance (C-m) in nerve terminals a cutely dissociated from neurohypophysis of adult rats to investigate m odulation of Ca2+ currents and secretion by activation of opioid recep tors. Bath superfusion of the kappa-opioid agonists U69,593 (0.3-1 mu M), dynorphin A (1 mu M), or U50,488H (1-3 mu M) reversibly suppressed the peak amplitude of Ca2+ currents 32.7 +/- 2.7% (in 41 of 66 termin als), 37.4 +/- 5.3% (in 5 of 8 terminals), and 33.5 +/- 8.1% (in 5 of 10 terminals), respectively. In contrast, tests in 11 terminals reveal ed no effect of the mu-opioid agonist [D-Pen(2,5)]-enkephalin (1-3 mu M; n = 7) or of the delta-agonist Tyr-D-Ala-Gly-N-Me-Phe-Gly-ol (1 mu M; n = 4) on Ca2+ currents. Three components of high-threshold current were distinguished on the basis of their sensitivity to blockade by o mega-conotoxin GVIA, nicardipine, and omega-conotoxin MVIIC, N-, L-, a nd P/Q-type current, respectively.