Abstract
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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have