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Rhodiola rosea Impairs Acquisition and Expression of Conditioned Place Preference Induced by Cocaine.

Titomanlio F, Manzanedo C, Rodríguez-Arias M, Mattioli L, Perfumi M, Miñarro J, Aguilar MA - Evid Based Complement Alternat Med (2013)

Bottom Line: A novel approach to the treatment of adverse effects of drugs of abuse is one which makes use of natural products.Rhodiola did not induce motivational effects by itself but attenuated the acquisition and expression of cocaine-induced CPP.Moreover, it was found that RHO did not block reinstatement.

View Article: PubMed Central - PubMed

Affiliation: Pharmacognosy Unit, School of Pharmacy, University of Camerino, Via Madonna delle Carceri 9, 62032 Camerino, Italy.

ABSTRACT
A novel approach to the treatment of adverse effects of drugs of abuse is one which makes use of natural products. The present study investigated the effect of Rhodiola rosea L. hydroalcoholic extract (RHO) on cocaine-induced hyperactivity and conditioned place preference (CPP) in mice. In a first experiment, mice received RHO (15, 20 or 25 mg/kg, IG), cocaine (25 mg/kg, i.p.) (COC), or a combination of both drugs (COC + RHO15, COC + RHO20, and COC + RHO25), and their locomotor activity was evaluated. In a second experiment, the effects of RHO on the acquisition, expression, and reinstatement of cocaine CPP (induced by drug priming or social defeat stress) were evaluated. RHO alone did not increase activity but potentiated the hyperactivity induced by cocaine. Rhodiola did not induce motivational effects by itself but attenuated the acquisition and expression of cocaine-induced CPP. Moreover, it was found that RHO did not block reinstatement. The results indicate that RHO is effective in reducing the rewarding properties of cocaine but is ineffective in preventing priming or stress-induced cocaine reinstatement. In light of these findings, the benefits of Rhodiola rosea L. as a treatment of cocaine addiction would seem to be limited.

No MeSH data available.


Related in: MedlinePlus

Effects of RHO on cocaine-induced hyperactivity. Mice (n = 8 per group) were placed in the actimeter for a 30-min adaptation period (0–30 min). Afterwards, two groups received IG vehicle (Veh-sal and Coc), two groups received IG RHO 15 mg/kg (RHO15 + Coc, RHO15), two groups RHO 20 mg/kg (RHO20 + Coc, RHO20), and two groups RHO 25 mg/kg (RHO25 + Coc, RHO25), and their motor activity was registered over another hour (31–60, 61–90 min). Finally, the first two groups received a IP injection of saline (Veh-Sal) or cocaine 25 mg/kg (Coc), and the groups treated with RHO received an IP injection of cocaine 25 mg/kg (RHO15 + Coc, RHO20 + Coc, and RHO25 + Coc) or saline (RHO 15, RHO 20, and RHO 25), and their motor activity was registered over a further hour (91–120, 121–150 min). (a) represents the motor activity of all groups over the complete time of testing (0–150 min) and shows the time of RHO and cocaine administration in the corresponding groups. (b) represents the data for the last hour of the test (after cocaine administration to the corresponding groups). Values are means ± SEM. *P < 0.05; **P < 0.01; significant difference with respect to the values of the control (Veh-sal) group at the same time test.
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fig1: Effects of RHO on cocaine-induced hyperactivity. Mice (n = 8 per group) were placed in the actimeter for a 30-min adaptation period (0–30 min). Afterwards, two groups received IG vehicle (Veh-sal and Coc), two groups received IG RHO 15 mg/kg (RHO15 + Coc, RHO15), two groups RHO 20 mg/kg (RHO20 + Coc, RHO20), and two groups RHO 25 mg/kg (RHO25 + Coc, RHO25), and their motor activity was registered over another hour (31–60, 61–90 min). Finally, the first two groups received a IP injection of saline (Veh-Sal) or cocaine 25 mg/kg (Coc), and the groups treated with RHO received an IP injection of cocaine 25 mg/kg (RHO15 + Coc, RHO20 + Coc, and RHO25 + Coc) or saline (RHO 15, RHO 20, and RHO 25), and their motor activity was registered over a further hour (91–120, 121–150 min). (a) represents the motor activity of all groups over the complete time of testing (0–150 min) and shows the time of RHO and cocaine administration in the corresponding groups. (b) represents the data for the last hour of the test (after cocaine administration to the corresponding groups). Values are means ± SEM. *P < 0.05; **P < 0.01; significant difference with respect to the values of the control (Veh-sal) group at the same time test.

Mentions: The results regarding the effect of RHO on cocaine-induced hyperactivity are represented in Figure 1. The ANOVA showed a significant effect of the variable time (F(4,224) = 43.358; P < 0.001), treatment (F(7,56) = 3.674; P < 0.002), and the interaction time × treatment (F(28,224) = 8.145; P < 0.001). The Bonferroni post hoc comparison showed that cocaine increased motor activity in comparison with the vehicle during the 30 min after its administration (P < 0.05). The groups treated with cocaine plus RHO also showed an increase in activity with respect to controls (P < 0.001), and the groups RHO15 + Coc and RHO20 + Coc presented more activity than the groups RHO15 and RHO20, respectively (P < 0.05 and P < 0.001). Between 31 and 60 min after cocaine administration, only the groups treated with RHO20 + Coc and RHO25 + Coc showed an increase in activity in comparison to controls (P < 0.001), and the group RHO20 + Coc also displayed more activity than RHO20 group (P < 0.001).


Rhodiola rosea Impairs Acquisition and Expression of Conditioned Place Preference Induced by Cocaine.

Titomanlio F, Manzanedo C, Rodríguez-Arias M, Mattioli L, Perfumi M, Miñarro J, Aguilar MA - Evid Based Complement Alternat Med (2013)

Effects of RHO on cocaine-induced hyperactivity. Mice (n = 8 per group) were placed in the actimeter for a 30-min adaptation period (0–30 min). Afterwards, two groups received IG vehicle (Veh-sal and Coc), two groups received IG RHO 15 mg/kg (RHO15 + Coc, RHO15), two groups RHO 20 mg/kg (RHO20 + Coc, RHO20), and two groups RHO 25 mg/kg (RHO25 + Coc, RHO25), and their motor activity was registered over another hour (31–60, 61–90 min). Finally, the first two groups received a IP injection of saline (Veh-Sal) or cocaine 25 mg/kg (Coc), and the groups treated with RHO received an IP injection of cocaine 25 mg/kg (RHO15 + Coc, RHO20 + Coc, and RHO25 + Coc) or saline (RHO 15, RHO 20, and RHO 25), and their motor activity was registered over a further hour (91–120, 121–150 min). (a) represents the motor activity of all groups over the complete time of testing (0–150 min) and shows the time of RHO and cocaine administration in the corresponding groups. (b) represents the data for the last hour of the test (after cocaine administration to the corresponding groups). Values are means ± SEM. *P < 0.05; **P < 0.01; significant difference with respect to the values of the control (Veh-sal) group at the same time test.
© Copyright Policy - open-access
Related In: Results  -  Collection

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fig1: Effects of RHO on cocaine-induced hyperactivity. Mice (n = 8 per group) were placed in the actimeter for a 30-min adaptation period (0–30 min). Afterwards, two groups received IG vehicle (Veh-sal and Coc), two groups received IG RHO 15 mg/kg (RHO15 + Coc, RHO15), two groups RHO 20 mg/kg (RHO20 + Coc, RHO20), and two groups RHO 25 mg/kg (RHO25 + Coc, RHO25), and their motor activity was registered over another hour (31–60, 61–90 min). Finally, the first two groups received a IP injection of saline (Veh-Sal) or cocaine 25 mg/kg (Coc), and the groups treated with RHO received an IP injection of cocaine 25 mg/kg (RHO15 + Coc, RHO20 + Coc, and RHO25 + Coc) or saline (RHO 15, RHO 20, and RHO 25), and their motor activity was registered over a further hour (91–120, 121–150 min). (a) represents the motor activity of all groups over the complete time of testing (0–150 min) and shows the time of RHO and cocaine administration in the corresponding groups. (b) represents the data for the last hour of the test (after cocaine administration to the corresponding groups). Values are means ± SEM. *P < 0.05; **P < 0.01; significant difference with respect to the values of the control (Veh-sal) group at the same time test.
Mentions: The results regarding the effect of RHO on cocaine-induced hyperactivity are represented in Figure 1. The ANOVA showed a significant effect of the variable time (F(4,224) = 43.358; P < 0.001), treatment (F(7,56) = 3.674; P < 0.002), and the interaction time × treatment (F(28,224) = 8.145; P < 0.001). The Bonferroni post hoc comparison showed that cocaine increased motor activity in comparison with the vehicle during the 30 min after its administration (P < 0.05). The groups treated with cocaine plus RHO also showed an increase in activity with respect to controls (P < 0.001), and the groups RHO15 + Coc and RHO20 + Coc presented more activity than the groups RHO15 and RHO20, respectively (P < 0.05 and P < 0.001). Between 31 and 60 min after cocaine administration, only the groups treated with RHO20 + Coc and RHO25 + Coc showed an increase in activity in comparison to controls (P < 0.001), and the group RHO20 + Coc also displayed more activity than RHO20 group (P < 0.001).

Bottom Line: A novel approach to the treatment of adverse effects of drugs of abuse is one which makes use of natural products.Rhodiola did not induce motivational effects by itself but attenuated the acquisition and expression of cocaine-induced CPP.Moreover, it was found that RHO did not block reinstatement.

View Article: PubMed Central - PubMed

Affiliation: Pharmacognosy Unit, School of Pharmacy, University of Camerino, Via Madonna delle Carceri 9, 62032 Camerino, Italy.

ABSTRACT
A novel approach to the treatment of adverse effects of drugs of abuse is one which makes use of natural products. The present study investigated the effect of Rhodiola rosea L. hydroalcoholic extract (RHO) on cocaine-induced hyperactivity and conditioned place preference (CPP) in mice. In a first experiment, mice received RHO (15, 20 or 25 mg/kg, IG), cocaine (25 mg/kg, i.p.) (COC), or a combination of both drugs (COC + RHO15, COC + RHO20, and COC + RHO25), and their locomotor activity was evaluated. In a second experiment, the effects of RHO on the acquisition, expression, and reinstatement of cocaine CPP (induced by drug priming or social defeat stress) were evaluated. RHO alone did not increase activity but potentiated the hyperactivity induced by cocaine. Rhodiola did not induce motivational effects by itself but attenuated the acquisition and expression of cocaine-induced CPP. Moreover, it was found that RHO did not block reinstatement. The results indicate that RHO is effective in reducing the rewarding properties of cocaine but is ineffective in preventing priming or stress-induced cocaine reinstatement. In light of these findings, the benefits of Rhodiola rosea L. as a treatment of cocaine addiction would seem to be limited.

No MeSH data available.


Related in: MedlinePlus