The pharmacological profile of cannabigerol (CBG), which acid form constitutes the main precursor of the most abundant cannabinoids, has been scarcely studied. It has been reported to target αadrenoceptor and 5-HT receptor. The locus coeruleus (LC) and the dorsal raphe nucleus (DRN) are the main serotonergic (5-HT) and noradrenergic (NA) areas in the rat brain, respectively. We aimed to study the effect of CBG on the firing rate of LC NA cells and DRN 5-HT cells and on α-adrenergic and 5-HT autoreceptors by electrophysiological techniques in male Sprague-Dawley rat brain slices. The effect of CBG on the novelty-suppressed feeding test (NSFT) and the elevated plus maze test (EPMT) and the involvement of the 5-HT receptor was also studied. CBG (30 μM, 10 min) slightly changed the firing rate of NA cells but failed to alter the inhibitory effect of NA (1-100 µM). However, in the presence of CBG the inhibitory effect of the selective α-adrenoceptor agonist UK14304 (10 nM) was decreased. Perfusion with CBG (30 μM, 10 min) did not change the firing rate of DRN 5-HT cells or the inhibitory effect of 5-HT (100 μM, 1 min) but it reduced the inhibitory effect of ipsapirone (100 nM). CBG failed to reverse ipsapirone-induced inhibition whereas perfusion with the 5-HT receptor antagonist WAY100635 (30 nM) completely restored the firing rate of DRN 5-HT cells. In the EPMT, CBG (10 mg/kg, i.p.) significantly increased the percentage of time the rats spent on the open arms and the number of head-dipping but it reduced the anxiety index. In the NSFT, CBG decreased the time latency to eat in the novel environment but it did not alter home-cage consumption. The effect of CBG on the reduction of latency to feed was prevented by pretreatment with WAY100635 (1 mg/kg, i.p.). In conclusion, CBG hinders the inhibitory effect produced by selective α-adrenoceptor and 5-HT receptor agonists on the firing rate of NA-LC and 5-HT-DRN neurons by a yet unknown indirect mechanism in rat brain slices and produces anxiolytic-like effects through 5-HT receptor.