ANALYSIS OF β-PHENYLETHYLAMINE AND CHANGES OF ITS LEVEL IN THE BRAIN AFTER ADMINISTRATION OF METHAMPHETAMINE

1999 Fiscal Year Final Research Report Summary

• Project/Area Number: 10670390
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Legal medicine
• Research Institution: SHIMANE MEDICAL UNIVERSITY
• Principal Investigator: KIMURA Kojiro Shimane Medical Univ. Legal Med., Professor, 医学部, 教授 (30153191)
• Co-Investigator(Kenkyū-buntansha): YAKABE Tomohiro Shimane Medical Univ. Legal Med., Assistant, 医学部, 助手 (40314645) ; ETO Hideaki Shimane Medical Univ. Legal Med., Assistant, 医学部, 助手 (80244094) ; TAKAHASHI Setsunori Shimane Medical Univ. Legal Med., Assistant, 医学部, 助手 (90032226)
• Project Period (FY): 1998 – 1999
• Keywords: Forensic toxicology / Neuro toxicology / Gas chromatography / mass spectrometry / Microdialysis / β-Phenylethylamine / Methamphetamine

Research Abstract

The structure is similar to dopamine and stimulant drug on β-phenyl-ethylamine (PEA) which is an endogenous chemical compound. The change of the PEA concentration in the b rain may be concerned in the mental retardation expression, while PEA affects it as a dopaminergic neurotoxin, and influence of stimulant drugs on PEA also seems to be very important in order to evaluate nerve cell change behavioral effects, etc..
In this study, we measured the basic value of PEA concentration in extracellular fluid obtained from rat striatum by using microdialysis method combined with gas chromatography/mass spectrometry. Simultaneously, the changes of PEA concentration in various parts of the brain after methamphetamine (MA) administration was also examined.
1) A sensitive and reliable analytical method was established by means of 3-phenyl-1-propylamine as an internal standard and pentafluorobenzaldehyde as a derivative agent. The basal level of PEA in extracellular fluid of rat striatum was around 260.54 pg/ml.
2) Extracellular PEA level in rat striatum gradually increased with a slight decrease at the time of 24th after administration of 20 mg/kg of MA. This finding indicated that the competitive antagonization of monoamine oxydase B by amphetamine which is a potent metabolite of MA or inhibition of reup take of PEA would occur during the examination. The basal levels of PEA in intracellular fluid were slightly higher in the striatum and hypothalamus than the other parts of the brain. The PEA concentrations in the striatum, hippocampus, hypothalamus, mesencephalon and pons, etc. were gradually decreased after administration of MA, so that the micro-degeneration of neural cells would generate by MA administration. On the other hand, no remarkable changes In histo-pathological examinations were observed in the various parts of the brains at the time of 6 or 12hr after 10 mg/kg of MA administration.