Evidence suggests a clear role for the amygdala endocannabinoid system in pain processing. Harmaline has been also known as the main nociceptive agent extracted from the Peganum harmala plant. In this study, the role of basolateral amygdala (BLA) cannabinoid CB1 receptors in pain sensitivity of harmaline-treated mice were assessed using tail-flick and hot plate methods in adolescent male NMRI mice. Intraperitoneal administration of two higher doses of harmaline (6 and 8 mg/kg) increased tail-flick latency, suggesting an antinociceptive activity. The same result was observed for the higher dose of harmaline in the hot plate test. Intra-BLA microinjection of CB1 receptor agonist ACPA (1 and 1.5 ng/mouse) or (1.5 ng/mouse) enhanced the ineffective dose-response of harmaline on pain threshold in the tail-flick or hot plate tests, respectively. Microinjection of two higher doses of CB1 receptor antagonist AM251 (0.5 and 1 ng/mouse) attenuated the antinociceptive activity of harmaline (8 ng/mouse) in both tail-flick and hot plate tests. Meanwhile, ACPA and AM251 did not alter latency to withdraw from the noxious stimulus in both tests, by themselves. It should be noted that the analgesic dose of the drugs alone or in combination did not affect locomotor activity. The obtained results highlight that BLA CB1 receptors mediate the antinociceptive activity of harmaline.