Figure 6. A1 receptor antagonism does not affect the ADP.

A, mAHPs and ADPs (averages of 5 traces) that each follow a 5-spike train (arrowheads, spikes truncated) evoked by a 80 ms depolarizing pulse (+170 pA) before (Pre-drug, left) and during superfusion of 1 μm apamin (middle) and 10 μm CPT in the continued presence of 1 μm apamin (right). B, ADP amplitude in supraoptic nucleus neurones (n= 5) before (Pre-drug, left) and during superfusion of 1 μm apamin (middle) and 10 μm CPT in the continued presence of 1 μm apamin (right), showing that A1 adenosine receptor antagonism does not affect ADP amplitude when the mAHP is reduced by apamin. C, mAHPs and ADPs (average of 5 traces) that each follow a 5-spike train (arrowheads) evoked 9 s apart by a 80-ms depolarizing pulse (+200 pA) before (Pre-CPT, black) and during (dotted line) superfusion of 10 μm CPT. A conditioning train (arrow) of 25 spikes (at 25 Hz) was evoked by a corresponding number of 5 ms, +500 pA DC pulses. D, bar graphs showing mean mAHP amplitude (n= 8) before (Pre-train) and after (Post-train) the 25-spike conditioning train before (Pre-CPT, left) and during superfusion of 10 μm CPT (right). Two-way repeated measures ANOVA showed that the conditioning train had no effect on mAHP amplitude (P= 0.97) but that CPT reduced mAHP amplitude (P= 0.05), independent of the conditioning train (P= 0.51). *P < 0.05, two-way repeated measures ANOVA. E, bar graphs showing mean ADP amplitude (n= 4) before (Pre-train) and after (Post-train) the 25 spike conditioning train before (Pre-CPT, left) and during superfusion of 10 μm CPT (right), showing that activity-dependent inhibition of the ADP was not altered by 10 μm CPT. A separate two-way repeated measured ANOVA showed no effect of CPT on ADP amplitude (P= 0.92) but revealed a significant inhibition by the conditioning train (P= 0.01) that was independent of CPT treatment (P= 0.92). *P < 0.05, Student–Newman–Keuls test.