Background:

The G-protein coupled receptor 55 (GPR55) is a cannabinoid/lysophospholipid target expressed in several tissues in mammals, including the central nervous system (CNS). Its actions in CNS are only partially known and include anxiety, spatial memory, reward, and pain. A recent study reported that systemic O-1602 (a GPR55 agonist) blocked the nicotine- induced conditioned place preference (CPP), but the knockdown of GPR55 in the nucleus accumbens did not modify the actions of O-1602, so its site of action remains obscure. GPR55 is expressed significantly in the dorsal hippocampus, a structure involved in the context-association to drugs-reward.

Objective:

To preliminary analyze the potential participation of dorsal- hippocampal GPR55 in the nicotine-induced CPP.

Method:

Male Wistar rats were implanted in dorsal hippocampus to receive: (i) vehicle (dimethyl sulfoxide 10%); (ii) ML184 (0.48 nmol; GPR55 agonist); or (iii) CID16020046 (1.16 nmol; GPR55 antagonist) during the conditioning phase in the nicotine-mediated CPP paradigm.

Results:

Animals from the vehicle group exhibited an increased time in the nicotine-paired chamber compared with its baseline (p < 0.05). In contrast, both ML184 and CIDl6020046 prevented the nicotine-induced CPP (p > 0.05).

Conclusion:

Under our experimental conditions, pharmacological manipulation of GPR55 in the dorsal hippocampus prevented the nicotine-induced CPP due to mechanisms that remain to be identified.

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