Antagonism by CPP, (±)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid, of β-phenylethylamine (PEA)-induced hypermotility in mice of different strains

Trace amine-associated receptor 1—Family archetype or iconoclast?

“…In rodents PEA elicits AMPH-like behavior (Hirano et al, 1989;Janssen et al, 1999) at doses of ∼50 mg/kg (intraperitoneal) characterized by hyperactivity, occasional walking backward, rearing, sniffing, gnawing, and licking (Dourish, 1982;Boulton, 1982;Lapin, 1996). At higher doses (75-100 mg/kg) repetitive, stereotypical behaviors, predominate including 'wet dog' shaking, excessive grooming and head movement, seizures, labored breathing, salivation, and straub tail.…”

“…Furthermore, pharmacologic manipulations (Borison et al, 1974;Borison et al, 1975;Boulton, 1976a;Philips & Boulton, 1979;Stoff et al, 1984;Boulton et al, 1990;Juorio et al 1991a;Juorio et al 1991b) and lesioning studies Juorio & Jones, 1981;Greenshaw et al, 1985;Greenshaw et al, 1986;Greenshaw et al, 1986;Juorio et al, 1987; can significantly influence TA turnover and levels with physiological (Becu-Villalobos, 1987;Cheng, 1990;Hirashima, 1999;Lee et al, 2003) and behavioral (Dourish, 1982;Lapin, 1996;Rex et al, 2004;Suo et al, 2006) consequences.…”

Contribution of β-phenethylamine, a component of chocolate and wine, to dopaminergic neurodegeneration: implications for the pathogenesis of Parkinson’s disease

“…Another signifi cant observation was that administration of β-PEA in rodents reduces striatal dopamine content and induces disorders such as akinesia, catalepsy and other motor abnormalities [28,31,32] , similar to those of parkinsonian rodents [6] . However, no reports are available on the extent of dopaminergic neuronal cell death after administration of β-PEA.…”

“…β-PEA, when administered intraventricularly, increases the extracellular dopamine levels in the striatum [35] , and acute administration results in increases in locomotor activity and stereotypic behavior in rodents [31,32] . Importantly, only longterm administration or high doses of β-PEA induces loss of dopamine in the nigrostriatum leading to motor disabilities similar to those of PD, whereas acute or sub-acute doses of β-PEA in rodents increase dopamine levels and induce hypermotility [32] .…”

“…Importantly, only longterm administration or high doses of β-PEA induces loss of dopamine in the nigrostriatum leading to motor disabilities similar to those of PD, whereas acute or sub-acute doses of β-PEA in rodents increase dopamine levels and induce hypermotility [32] . Thus, β-PEA may be comparable with parkinsonian neurotoxins such as MPP + , which when unilaterally infused into the SNc, initially results in release of dopamine into the striatum causing contralateral rotational bias [36] .…”