Korean J Physiol Pharmacol.  2009 Jun;13(3):147-151. 10.4196/kjpp.2009.13.3.147.

Role of Dopamine Receptors on Electroencephalographic Changes Produced by Repetitive Apomorphine Treatments in Rats

• Jang HS
• Kim JY
• Kim SH
• Lee MG

• KMID: 2071664
• DOI: http://doi.org/10.4196/kjpp.2009.13.3.147

Abstract

Repeated psychostimulants induce electroencephalographic (EEG) changes, which reflect adaptation of the neural substrate related to dopaminergic pathways. To study the role of dopamine receptors in EEG changes, we examined the effect of apomorphine, the dopamine D1 receptor antagonist, SCH-23390, and the D2 receptor antagonist, haloperidol, on EEG in rats. For single and repeated apomorphine treatment groups, the rats received saline or apomorphine for 4 days followed by a 3-day withdrawal period and then apomorphine (2.5 mg/kg, i.p.) challenge after pretreatment with saline, SCH-23390, or haloperidol on the day of the experiment. EEGs from the frontal and parietal cortices were recorded. On the frontal cortex, apomorphine decreased the power of all the frequency bands in the single treatment group, and increased the theta (4.5~8 Hz) and alpha (8~13 Hz) powers in the repeated treatment group. Changes in both groups were reversed to the control values by SCH-23390. On the parietal cortex, single apomorphine treatment decreased the power of some frequency bands, which were reversed by haloperidol but not by SCH-23390. Repeated apomorphine treatment did not produce significant changes in the power profile. These results show that adaptation of dopamine pathways by repeated apomorphine treatment could be identified with EEG changes such as increases in theta and alpha power of the frontal cortex, and this adaptation may occur through changes in the D1 receptor and/or the D2 receptor.

Keyword

Apomorphine; Dopamine D1 receptor; Dopamine D2 receptor; SCH-23390; Haloperidol; EEG; Rat

MeSH Terms

Animals
Apomorphine
Benzazepines
Dopamine
Electroencephalography
Haloperidol
Rats
Receptors, Dopamine
Receptors, Dopamine D1
Receptors, Dopamine D2
Apomorphine
Benzazepines
Dopamine
Haloperidol
Receptors, Dopamine
Receptors, Dopamine D1
Receptors, Dopamine D2

Figure

• 

  Fig. 1. EEG band powers of the frontal cortex after apomorphine (APO) treatment in single (S) and repeated (R) apomorphine treatment groups. (A) Band powers in the control state and 25~30 min after APO injection; (B) Band powers in the control state and 55~60 min after APO injection. Each point and bar represent the mean±S.E.M. ∗Significantly different from the control state; #Significantly different between R and S groups (p<0.05 by ANOVA, t-test).

• 

  Fig. 2. EEG band powers of the frontal cortex 25~30 min after apomorphine (APO) injection in single (S, upper panel, A and C) and repeated (R, lower panel, B and D) treatment groups pretreated with: SCH-2390 (SCH, A and B) and haloperidol (HAL, C and D). Each point and bar represent the mean±S.E.M. ∗Significantly different from the control state; #Significantly different from saline (SAL) pretreatment (p<0.05 by ANOVA, t-test).

• 

  Fig. 3. EEG band powers of the parietal cortex after apomorphine (APO) treatment in single (S) and repeated (R) apomorphine treatment groups. (A) Band powers in the control state and 25~30 min after APO injection; (B) Band powers in the control state and 55~60 min after APO injection. Each point and bar represent the mean±S.E.M. ∗Significantly different from the control state (p<0.05 by ANOVA, t-test).

• 

  Fig. 4. EEG band powers of the parietal cortex 25~30 min after apomorphine (APO) injection in single (S, upper panel, A and C) and repeated (R, lower panel, B and D) treatment groups pretreated with: SCH-2390 (SCH, A and B) and haloperidol (HAL, C and D). Each point and bar represent the mean±S.E.M. ∗Significantly different from the control state; #Significantly different from saline (SAL) pretreatment (p<0.05 by ANOVA, t-test).

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