Abstract:
:It is now established that (1) concentrations of 2-phenylethylamine (PEA) are greatly increased in brain following administration of monoamine oxidase inhibitor (MAOI) antidepressants; (2) PEA is a metabolite of the MAOI antidepressant phenelzine; and (3) PEA may be a neuromodulator of catecholamine activity. On the basis of these observations, the effects of long term increases in brain PEA on catecholamine receptors have been assessed. Both PEA and antidepressants induced a reduction in the behavioural response to the beta 2 adrenoceptor agonist salbutamol. Radioligand binding measurements revealed that 28 day administration of PEA in combination with the type B MAOI (-)-deprenyl results in a decrease in the density of beta 1 adrenoceptors but not beta 2 adrenoceptors in rat cerebral cortex and cerebellum. (-)-Deprenyl alone also induced a significant decrease in beta 1-adrenoceptors but when PEA was added to this treatment there was a further decrease in beta 1-adrenoceptor density. Only changes in beta 1 adrenoceptor density were evident following 28 day administration of MAOI antidepressants. PEA also induced a decrease in the density of D1-like dopamine (DA) receptors in the rat striatum. MAOI antidepressants induced a decrease in the density of both D1-like and D2-like DA receptors. These data are discussed in terms of a possible role of PEA-catecholamine interactions in antidepressant drug action.
journal_name
Neurochem Resjournal_title
Neurochemical researchauthors
Paetsch PR,Greenshaw AJdoi
10.1007/BF00966762subject
Has Abstractpub_date
1993-09-01 00:00:00pages
1015-22issue
9eissn
0364-3190issn
1573-6903journal_volume
18pub_type
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