Research reportModulation of the effects of the cannabinoid agonist, ACPA, on spatial and non-spatial novelty detection in mice by dopamine D1 receptor drugs infused into the basolateral amygdala

- ACPA decreases spatial change detection and reaction to non-spatial novelty.
- SKF38393 (intra-BLA; at highest dose) impaired spatial and non-spatial detection.
- SCH23390 (intra-BLA; at lowest dose) impaired spatial and non-spatial detection.
- SKF38393 restored ACPA-induced spatial and non-spatial memory deficit.
- SCH23390 potentiated impairment of spatial and non-spatial memory by ACPA.

AimThe amygdala is a major target of midbrain dopaminergic neurons and is implicated in learning and memory processes. This study investigates the effect of basolateral amygdale (BLA) dopamine receptors on spatial and non-spatial novelty detection deficit, induced by a selective CB1 cannabinoid receptor agonist (Arachidonylcyclopropylamide; ACPA), during a non-associative task.MethodsMale mice weighing 30-35 g were used. Open field procedure was employed to assess the spatial and non-spatial memory retention.ResultsOur data showed that post-training intraperitoneal injection of ACPA (0.02 mg/kg), intra-BLA microinjection of SKF38393 (D1 dopamine receptor agonist; at higher dose, 0.1 μg/mouse) and SCH23390 (D1 dopamine receptor antagonist; at lowest dose, 0.005 μg/mouse) impaired both spatial and non-spatial novelty detection. Moreover, intra-BLA microinjection of subthreshold dose of SKF38393 or SCH23390 restored and potentiated the spatial and non-spatial novelty detection impairment caused by ACPA, respectively.ConclusionOur results suggested that the ACPA induced impairment of memory retention, may occur through BLA D1 dopamine receptors.