NSD 1034: An amino acid decarboxylase inhibitor with a stimulatory action on dopamine synthesis not mediated by classical dopamine receptors

1988 ◽  
Vol 338 (2) ◽  
Author(s):  
H. Nissbrandt ◽  
G. Engberg ◽  
H. Wikstr�m ◽  
T. Magnusson ◽  
A. Carlsson
Keyword(s):  
Amino Acid ◽  
Dopamine Receptors ◽  
Dopamine Synthesis ◽  
Acid Decarboxylase ◽  
Decarboxylase Inhibitor ◽  
Stimulatory Action ◽  
Amino Acid Decarboxylase

Changes in serotonin contents in brain affect metabolic heat production of rabbits in cold

1978 ◽  
Vol 235 (1) ◽  
pp. R41-R47
Author(s):  
M. T. Lin ◽  
I. H. Pang ◽  
S. I. Chern ◽  
W. Y. Chia
Keyword(s):  
Blood Flow ◽  
Amino Acid ◽  
Heat Loss ◽  
Acid Decarboxylase ◽  
Evaporative Heat Loss ◽  
Decarboxylase Inhibitor ◽  
Ambient Temperatures ◽  
Amino Acid Decarboxylase ◽  
Metabolic Heat ◽  
Normal Limits

Elevating serotonin (5-HT) contents in brain with 5-hydroxytryptophan (5-HTP) reduced rectal temperature (Tre) in rabbits after peripheral decarboxylase inhibition with the aromatic-L-amino-acid decarboxylase inhibitor R04-4602 at two ambient temperatures (Ta), 2 and 22 degrees C. The hypothermia was brought about by both an increase in respiratory evaporative heat loss (Eres) and a decrease in metabolic rate (MR) in the cold. At a Ta of 22 degrees C, the hypothermia was achieved solely due to an increase in heat loss. Depleting brain contents of 5-HT with intraventricular, 5,7-dihydroxytryptamine (5,7-DHT) produced an increased Eres and ear blood flow even at Ta of 2 degrees C. Also, MR increased at all but the Ta of 32 degrees C. However, depleting the central and peripheral contents of 5-HT with p-chlorophenylalanine (pCPA) produced lower MR accompanied by lower Eres in the cold compared to the untreated control. Both groups of pCPA-treated and 5,7-DHT-treated animals maintained their Tre within normal limits. The data suggest that changes in 5-HT content in brain affects the MR of rabbits in the cold. Elevating brain content of 5-HT tends to depress the MR response to cold, while depleting brain content of 5-HT tends to enhance the MR response to cold.

Regulation of Aromatic l-Amino Acid Decarboxylase by Dopamine Receptors in the Rat Brain

1992 ◽  
Vol 58 (2) ◽  
pp. 636-641 ◽  
Author(s):  
M. Y. Zhu ◽  
A. V. Juorio ◽  
I. A. Paterson ◽  
A. A. Boulton
Keyword(s):  
Amino Acid ◽  
Rat Brain ◽  
Dopamine Receptors ◽  
Acid Decarboxylase ◽  
Amino Acid Decarboxylase

Aromatic L-Amino Acid Decarboxylase Is Modulated by D1 Dopamine Receptors in Rat Retina

1990 ◽  
Vol 54 (3) ◽  
pp. 787-791 ◽  
Author(s):  
Zvani L. Rossetti ◽  
Christopher P. Silvia ◽  
Dimitrij Krajnc ◽  
Norton H. Neff ◽  
Maria Hadjiconstantinou
Keyword(s):  
Amino Acid ◽  
Dopamine Receptors ◽  
Acid Decarboxylase ◽  
Rat Retina ◽  
Amino Acid Decarboxylase ◽  
D1 Dopamine Receptors

Aromatic L-Amino Acid Decarboxylase Activity of Mouse Striatum Is Modulated via Dopamine Receptors

1993 ◽  
Vol 60 (6) ◽  
pp. 2175-2180 ◽  
Author(s):  
M. Hadjiconstantinou ◽  
T. A. Wemlinger ◽  
C. P. Sylvia ◽  
J. P. Hubble ◽  
N. H. Neff
Keyword(s):  
Amino Acid ◽  
Dopamine Receptors ◽  
Acid Decarboxylase ◽  
Decarboxylase Activity ◽  
Amino Acid Decarboxylase ◽  
Mouse Striatum

An aromatic l-amino acid decarboxylase inhibitor blocks l-dopa-induced air-stepping in neonatal rats

1996 ◽  
Vol 94 (2) ◽  
pp. 234-237
Author(s):  
Carlos O. Arnaiz ◽  
Lynette L. Taylor ◽  
Donald J. Stehouwer ◽  
Carol Van Hartesveldt
Keyword(s):  
Amino Acid ◽  
Acid Decarboxylase ◽  
Neonatal Rats ◽  
Decarboxylase Inhibitor ◽  
Amino Acid Decarboxylase

L-DOPA–Chlorpromazine Antagonism on Running Activity in Mice

1974 ◽  
Vol 52 (1) ◽  
pp. 114-118 ◽  
Author(s):  
Peter Derkach ◽  
Louis Larochelle ◽  
Detlef Bieger ◽  
Oleh Hornykiewicz
Keyword(s):  
Amino Acid ◽  
Dopamine Receptors ◽  
Dose Response ◽  
Response Curve ◽  
Antagonistic Effect ◽  
Dose Effect ◽  
Main Mechanism ◽  
Acid Decarboxylase ◽  
Amino Acid Decarboxylase ◽  
Running Activity

An attempt was made to study the nature of the antagonistic effect of chlorpromazine on running activity induced by L-3, 4-dihydroxyphenylalanine (L-DOPA) in mice. Dose–effect relations for L-DOPA, given alone and in combination with chlorpromazine, were determined in male albino mice pretreated with an inhibitor of the extracerebral aromatic L-amino acid decarboxylase. Chlorpromazine produced a marked depression in the maximal running response to L-DOPA and a flattening in the slope of the L-DOPA dose–response curve. The results are compatible with a noncompetitive blockade of central dopamine receptors by chlorpromazine as the main mechanism of the drug's anti-L-DOPA activity.

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