Acute neuroleptic stimulates DOPA decarboxylase in porcine brain in vivo.

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Standard

Acute neuroleptic stimulates DOPA decarboxylase in porcine brain in vivo. / Danielsen, E H; Smith, D; Hermansen, F; Gjedde, A; Cumming, P.

In: Synapse, Vol. 41, No. 2, 2001, p. 172-5.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Danielsen, EH, Smith, D, Hermansen, F, Gjedde, A & Cumming, P 2001, 'Acute neuroleptic stimulates DOPA decarboxylase in porcine brain in vivo.', Synapse, vol. 41, no. 2, pp. 172-5.

APA

Danielsen, E. H., Smith, D., Hermansen, F., Gjedde, A., & Cumming, P. (2001). Acute neuroleptic stimulates DOPA decarboxylase in porcine brain in vivo. Synapse, 41(2), 172-5.

Vancouver

Danielsen EH, Smith D, Hermansen F, Gjedde A, Cumming P. Acute neuroleptic stimulates DOPA decarboxylase in porcine brain in vivo. Synapse. 2001;41(2):172-5.

Author

Danielsen, E H ; Smith, D ; Hermansen, F ; Gjedde, A ; Cumming, P. / Acute neuroleptic stimulates DOPA decarboxylase in porcine brain in vivo. In: Synapse. 2001 ; Vol. 41, No. 2. pp. 172-5.

Bibtex

@article{39bdf8d0b31511debc73000ea68e967b,
title = "Acute neuroleptic stimulates DOPA decarboxylase in porcine brain in vivo.",
abstract = "The activity of DOPA decarboxylase measured in homogenates from rat striatum, or calculated from the rate of tracer decarboxylation measured ex vivo, is stimulated following acute treatment with antagonists of dopamine D2-like receptors. We used compartmental kinetics to test the hypothesis that utilization of the DOPA decarboxylase substrate [(18)F]fluorodopa is potentiated in living striatum following acute treatment with a typical neuroleptic. The kinetics of the tracer uptake were determined in eight anesthetized female pigs (40 kg) and in three animals receiving an infusion of haloperidol (75 microg kg(-1) h(-1)) for 1 h prior to tracer administration and throughout the 2-h positron emission recording. The relative activity of DOPA decarboxylase in striatum was increased threefold by the treatment. This potentiation of DOPA decarboxylation after pharmacological blockade of dopamine D2-like receptors may be used to optimize the utilization of exogenous DOPA in the treatment of Parkinson's disease.",
author = "Danielsen, {E H} and D Smith and F Hermansen and A Gjedde and P Cumming",
year = "2001",
language = "English",
volume = "41",
pages = "172--5",
journal = "Synapse",
issn = "0887-4476",
publisher = "Wiley",
number = "2",

}

RIS

TY - JOUR

T1 - Acute neuroleptic stimulates DOPA decarboxylase in porcine brain in vivo.

AU - Danielsen, E H

AU - Smith, D

AU - Hermansen, F

AU - Gjedde, A

AU - Cumming, P

PY - 2001

Y1 - 2001

N2 - The activity of DOPA decarboxylase measured in homogenates from rat striatum, or calculated from the rate of tracer decarboxylation measured ex vivo, is stimulated following acute treatment with antagonists of dopamine D2-like receptors. We used compartmental kinetics to test the hypothesis that utilization of the DOPA decarboxylase substrate [(18)F]fluorodopa is potentiated in living striatum following acute treatment with a typical neuroleptic. The kinetics of the tracer uptake were determined in eight anesthetized female pigs (40 kg) and in three animals receiving an infusion of haloperidol (75 microg kg(-1) h(-1)) for 1 h prior to tracer administration and throughout the 2-h positron emission recording. The relative activity of DOPA decarboxylase in striatum was increased threefold by the treatment. This potentiation of DOPA decarboxylation after pharmacological blockade of dopamine D2-like receptors may be used to optimize the utilization of exogenous DOPA in the treatment of Parkinson's disease.

AB - The activity of DOPA decarboxylase measured in homogenates from rat striatum, or calculated from the rate of tracer decarboxylation measured ex vivo, is stimulated following acute treatment with antagonists of dopamine D2-like receptors. We used compartmental kinetics to test the hypothesis that utilization of the DOPA decarboxylase substrate [(18)F]fluorodopa is potentiated in living striatum following acute treatment with a typical neuroleptic. The kinetics of the tracer uptake were determined in eight anesthetized female pigs (40 kg) and in three animals receiving an infusion of haloperidol (75 microg kg(-1) h(-1)) for 1 h prior to tracer administration and throughout the 2-h positron emission recording. The relative activity of DOPA decarboxylase in striatum was increased threefold by the treatment. This potentiation of DOPA decarboxylation after pharmacological blockade of dopamine D2-like receptors may be used to optimize the utilization of exogenous DOPA in the treatment of Parkinson's disease.

M3 - Journal article

C2 - 11400183

VL - 41

SP - 172

EP - 175

JO - Synapse

JF - Synapse

SN - 0887-4476

IS - 2

ER -

ID: 14946348