NDLI: σ$_{1}$ Receptor Subtype Is Involved in the Facilitation of Cortical Dopaminergic Transmission in the Rat Brain

Content Provider	Springer Nature Link
Author	Kobayashi, Tetsuya Matsu, Kiyoshi Murai, Masaaki Mita, Shiro
Copyright Year	1997
Abstract	Our previous studies have shown that three sigma (σ) receptor ligands, (+)-N-allylnormetazocine ((+)-SKF-10,047), (±)-pentazocine and 1,3-di(2-tolyl)guanidine (DTG) differently regulated the dopamine (DA) transmission in the rat brain. In the present study, we attempted to clarify the role of σ$_{1}$ receptor subtype in the regulation of DA transmission using a novel and selective σ$_{1}$ receptor agonist, 1-(3,4-dimethoxyphenethyl)-4-(3-phenylpropyl)piperazine dihydrochloride (SA4503) in the rat brain. Acute administration of SA4503 (1.0 mg/kg, p.o.) significantly increased DA and 3,4-dihydroxyphenylacetic acid (DOPAC) levels in the rat frontal cortex, but not in the other six regions, hippocampus, striatum, midbrain, cerebellum, medulla/pons and hypothalamus. The increase of cortical DA level elicited by SA4503 was fully reversed by N,N-dipropyl-2-(4-methoxy-3-(2-phenylethoxy)phenyl)ethylamine (NE-100) (0.25 mg/kg, p.o.), a putative σ$_{1}$ receptor antagonist. In addition, SA4503 (1.0 mg/kg, p.o.) showed an increase of cortical L-3,4-dihydroxyphenylalanine (L-DOPA) accumulation under the inhibition of dopa decarboxylase activity with m-hydrobenzylhydrazine (NSD-1015), suggesting that SA4503 has activated the cortical DA synthesis rate. These results suggest that the σ$_{1}$ receptor subtype plays an important role in the facilitation of cortical DA transmission. In addition, this phenomenon is partially involved in the augmentation of DA synthesis rate.
Starting Page	1105
Ending Page	1109
Page Count	5
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	22
Issue Number	9
e-ISSN	15736903
Language	English
Publisher	Kluwer Academic Publishers-Plenum Publishers
Publisher Date	1997-01-01
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Neurosciences Neurology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

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