TY - JOUR
T1 - Effect of β-phenylethylamine on extracellular concentrations of dopamine in the nucleus accumbens and prefrontal cortex
AU - Murata, Mikio
AU - Katagiri, Nobuyuki
AU - Ishida, Kota
AU - Abe, Kenji
AU - Ishikawa, Masago
AU - Utsunomiya, Iku
AU - Hoshi, Keiko
AU - Miyamoto, Ken ichi
AU - Taguchi, Kyoji
PY - 2009/5/7
Y1 - 2009/5/7
N2 - 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.
AB - 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.
KW - Dopamine uptake inhibitor
KW - In vivo microdialysis
KW - Nucleus accumbens shell
KW - Prefrontal cortex
KW - β-phenylethylamine
UR - http://www.scopus.com/inward/record.url?scp=67349114224&partnerID=8YFLogxK
U2 - 10.1016/j.brainres.2009.03.002
DO - 10.1016/j.brainres.2009.03.002
M3 - Article
C2 - 19285043
AN - SCOPUS:67349114224
SN - 0006-8993
VL - 1269
SP - 40
EP - 46
JO - Brain Research
JF - Brain Research
ER -