Table 1.

Neurological activities of carvone.

Molecules	Origins	Models Used	Experimental Approaches	Key Results	References
(S)-(+)-Carvone and (R)-(−)-carvone	Purchased	Male Swiss mice	Pentobarbital-induced sleeping time Locomotor activity assessed in an activity cage PTZ-induced convulsions Pentobarbital-induced hypnosis PTZ-induced seizure PIC-induced seizure	LD50 = 484.2 mg/kg for (S)-(+)-carvone LD50 = 426.6 mg/kg for (R)-(−)-carvone Both enantiomers induced depressive effects Both enantiomers significantly reduced ambulation At 100 mg/kg, (R)-(−)-carvone was more effective than (S)-(+)-carvone in increasing pentobarbital sleeping duration At 200 mg/kg, (S)-(+)-carvone improved the latency of convulsions produced by PTZ and PIC (S)-(+)-carvone and (R)-(−)-carvone have depressant effects in the CNS (S)-(+)-carvone has anticonvulsant-like activity	[9]
(+)-carvone, (−)-carvone	Not reported	The sciatic nerve of the frog (Rana ridibunda) from both sex	Three-chambered recording bath for the assessment of local anesthetic activity	Both carvone enantiomers elicited comparable responses The action potential of the evoked compound was abolished in 6 to 7 min and had an immediate recovery of 83% to 87% Both carvones acted in the same way as lidocaine (10 mM) No recovery of the action potential of the elicited compound, when nerves have been exposed to carvones for more than 6–7 min The unusual neurotoxic effect of C+ and C− may be a disadvantage for their use in clinical practice	[10]
(+)-carvone, (−)-carvone	Purchased	Adult male Wistar rats	Sucrose-gap apparatus (ex vivo assay) for CAP-inhibitory effect	C- was less potent (IC50 = 10.7 ± 0.07 mM) in reducing nerve excitability than C+ (IC50 = 8.7 ± 0.1 mM) Both enantiomers acted in a similar manner The structure–function relationship of the enantiomers was linked to the CAP inhibitory action	[11]
(R)-(−)- carvone and (S)-(+)-carvone	Purchased	Cultures of cortical neurons prepared from the cerebral cortices of fetal rats	[3H] Flunitrazepam Binding Cell viability assay	Both isomers blocked GABA-induced activation of [3H] Flunitrazepam binding The doses required to produce negative receptor modulation were not lethal The insecticidal effect of carvones can be explained by their interaction with the GABAA receptor at its non-competitive blocker region	[12]