Fig. 4.

The increase in TFL to intra-CeA clonidine microinfusion is dependent upon the α₂-noradrenergic receptor subtype. Saline microinjection followed by clonidine (1.25μg), an α₂-noradrenergic receptor agonist, resulted in a significant increase in TFL. Microinjection of the α₂-noradrenergic receptor antagonist idazoxan (9μg) blocked the effect of subsequently microinjected clonidine (1.25μg). Microinjection of idazoxan followed by saline microinjection resulted in a TFL that did not significantly differ from baseline. Microinjection of the α₁-noradrenergic receptor antagonist WB-4101 (12μg) did not block the effect of subsequently microinjected clonidine (1.25μg). Microinjection of WB-4101 (12μg) followed by saline injection did not result in a significant alteration of baseline TFL, N = 5−8 per group. There were no differences among the groups in baseline latencies (ANOVA). There was no significant difference in post-treatment TFL between the saline/clonidine and WB-4101/clonidine groups (ANOVA). (**p<0.01, values averaged over 30 min post-injection time period compared with baseline, Student's t-test for correlated means). clon = clonidine, ida = idazoxan, WB = WB-4101.