Effect of β-phenylethylamine on extracellular concentrations of dopamine in the nucleus accumbens and prefrontal cortex

It is known that psychostimulants stimulate dopamine transmission in the nucleus accumbens. In the present study, we examined the effects of systemically administered β-phenylethylamine (β-PEA), a psychomotor-stimulating trace amine, on dopamine concentrations in the nucleus accumbens and prefrontal cortex in freely moving rats, using an in vivo microdialysis technique. Intraperitoneal administration of β-PEA (12.5 and 25 mg/kg) significantly increased extracellular dopamine levels in the nucleus accumbens shell. The observed increase in the dopamine concentration in nucleus accumbens shell dialysate after intraperitoneal administration of 25 mg/kg β-PEA was inhibited by pre-treatment with a dopamine uptake inhibitor, GBR12909 (10 mg/kg, i.p.). In contrast, β-PEA (25 mg/kg, i.p.) did not affect dopamine release in the nucleus accumbens core. Although a high dose of β-PEA (50 mg/kg) significantly increased dopamine levels in the nucleus accumbens core, the dopamine increasing effect of β-PEA was more potent in the nucleus accumbens shell. Systemic administration of 12.5 and 25 mg/kg β-PEA also increased extracellular dopamine levels in the prefrontal cortex of rats. However, systemic 25 mg/kg β-PEA-induced increases in extracellular dopamine levels were not blocked by GBR12909 within the prefrontal cortex. These results suggest that β-PEA has a greater effect in the shell than in the core and low-dose β-PEA stimulates dopamine release in the nucleus accumbens shell through uptake by a dopamine transporter. Similarly, β-PEA increased extracellular dopamine levels in the prefrontal cortex. Thus, β-PEA may increase extracellular dopamine concentrations in the mesocorticolimbic pathway.