Effects of apomorphine and β-carbolines on firing rate of neurons in the ventral pallidum in the rats

► Apomorphine decreased unit activity of neurons in the ventral pallidum. ► β-Carbolines harmine, harmane and noreharmane did not alter neural activity. ► β-Carbolines prevented the apomorphine-induced inhibition of pallidal neurons. The ventral pallidum (VP) is a critical element of the mesocorticolimbic system that is inter-connected with motor and limbic structures and may be considered as an interface between motivational and effector neural signals. Dopamine is important in behavioral output of the VP, and dysfunctioning its dopamine quantity leads to various neuropsychiatric disorders. Understanding neural substrate underlying this phenomenon has become an important affair in recent years. In this study, neuronal activities were recorded from the VP in presence or absence of the mixed dopamine D1/D2 receptor agonist, apomorphine, and/or β-carbolines, using an extracellular single-unit recording technique. We reported that subcutaneous administration of apomorphine (0.5 mg/kg) decreased neural activity in the VP. In addition, neither harmine (7.8 mg/kg; i.p.) nor harmane (4 mg/kg; i.p.) and norharmane (2.5 mg/kg; i.p.) had any effect on neural firing in the VP. Finally, pretreatment with β-carbolines prevented the apomorphine-induced inhibition on VP firing rate. Thus, according to the results of aforementioned study and our results in the present study, we can conclude that presumably most responses in the VP are D2 dopamine dependent. Although the β-carbolines were unable to alter neural activity in the VP, interestingly, pretreatment with β-carbolines protect decreasing in firing rate of neurons in the VP followed by apomorphine administration. This protective effect could be explained by interaction between β-carbolines and dopaminergic mechanisms.