Effect of 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP) on monoamine neurotransmitters in mouse brain & heart

Raye Ann Wallace, Robert Boldry, Thomas Schmittgen, Duane Miller, Norman Uretsky

Research output: Contribution to journalArticle

64 Citations (Scopus)

Abstract

The effect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was studied on dopamine (DA), norepinephrine (NE), serotonin (5HT) and γ-aminobutyric acid (GABA) neurons in mouse brain and on NE neurons of mouse heart. MPTP (45 mg/kg) was administered s.c. to mice twice daily for 2 consecutive days. This dosage regimen produced a decrease in the forebrain concentrations of DA and NE at 7 and 20 days after injection. In contrast, the forebrain concentrations of 5HT and GABA were not significantly decreased at either time. MPTP administration also produced a marked decrease in the uptake of 3H-DA into striatal slices and 3H-NE into cerebral cortical slices. In contrast, the uptake of 3H-NE into hypothalamic slices and the uptake of 3H-5HT into slices from several brain regions were not altered. MPTP initially reduced the concentration of NE in the heart, but unlike the persistent decreases in the forebrain concentrations of NE and DA, the NE concentration in the heart returned to control levels at approximately 20 days after MPTP administration. These results, showing that MPTP can produce a long lasting and selective decrease in the forebrain concentrations of NE and DA and in the uptake of radioactive DA and NE into brain slices, suggest that MPTP can cause the destruction of catecholamine neurons in mouse brain. In contrast, MPTP administration does not appear to produce long term changes in either 5HT or GABA neurons.

Original languageEnglish (US)
Pages (from-to)285-291
Number of pages7
JournalLife Sciences
Volume35
Issue number3
DOIs
StatePublished - Jul 16 1984
Externally publishedYes

Fingerprint

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
Neurotransmitter Agents
Brain
Norepinephrine
Dopamine
Prosencephalon
Neurons
gamma-Aminobutyric Acid
GABAergic Neurons
Aminobutyrates
Corpus Striatum
Level control
Catecholamines
Serotonin

All Science Journal Classification (ASJC) codes

  • Pharmacology

Cite this

Effect of 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP) on monoamine neurotransmitters in mouse brain & heart. / Ann Wallace, Raye; Boldry, Robert; Schmittgen, Thomas; Miller, Duane; Uretsky, Norman.

In: Life Sciences, Vol. 35, No. 3, 16.07.1984, p. 285-291.

Research output: Contribution to journalArticle

Ann Wallace, Raye ; Boldry, Robert ; Schmittgen, Thomas ; Miller, Duane ; Uretsky, Norman. / Effect of 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP) on monoamine neurotransmitters in mouse brain & heart. In: Life Sciences. 1984 ; Vol. 35, No. 3. pp. 285-291.
@article{f353de3e51884968b648c3ed84b7c5ae,
title = "Effect of 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP) on monoamine neurotransmitters in mouse brain & heart",
abstract = "The effect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was studied on dopamine (DA), norepinephrine (NE), serotonin (5HT) and γ-aminobutyric acid (GABA) neurons in mouse brain and on NE neurons of mouse heart. MPTP (45 mg/kg) was administered s.c. to mice twice daily for 2 consecutive days. This dosage regimen produced a decrease in the forebrain concentrations of DA and NE at 7 and 20 days after injection. In contrast, the forebrain concentrations of 5HT and GABA were not significantly decreased at either time. MPTP administration also produced a marked decrease in the uptake of 3H-DA into striatal slices and 3H-NE into cerebral cortical slices. In contrast, the uptake of 3H-NE into hypothalamic slices and the uptake of 3H-5HT into slices from several brain regions were not altered. MPTP initially reduced the concentration of NE in the heart, but unlike the persistent decreases in the forebrain concentrations of NE and DA, the NE concentration in the heart returned to control levels at approximately 20 days after MPTP administration. These results, showing that MPTP can produce a long lasting and selective decrease in the forebrain concentrations of NE and DA and in the uptake of radioactive DA and NE into brain slices, suggest that MPTP can cause the destruction of catecholamine neurons in mouse brain. In contrast, MPTP administration does not appear to produce long term changes in either 5HT or GABA neurons.",
author = "{Ann Wallace}, Raye and Robert Boldry and Thomas Schmittgen and Duane Miller and Norman Uretsky",
year = "1984",
month = "7",
day = "16",
doi = "10.1016/0024-3205(84)90112-7",
language = "English (US)",
volume = "35",
pages = "285--291",
journal = "Life Sciences",
issn = "0024-3205",
publisher = "Elsevier Inc.",
number = "3",

}

TY - JOUR

T1 - Effect of 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP) on monoamine neurotransmitters in mouse brain & heart

AU - Ann Wallace, Raye

AU - Boldry, Robert

AU - Schmittgen, Thomas

AU - Miller, Duane

AU - Uretsky, Norman

PY - 1984/7/16

Y1 - 1984/7/16

N2 - The effect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was studied on dopamine (DA), norepinephrine (NE), serotonin (5HT) and γ-aminobutyric acid (GABA) neurons in mouse brain and on NE neurons of mouse heart. MPTP (45 mg/kg) was administered s.c. to mice twice daily for 2 consecutive days. This dosage regimen produced a decrease in the forebrain concentrations of DA and NE at 7 and 20 days after injection. In contrast, the forebrain concentrations of 5HT and GABA were not significantly decreased at either time. MPTP administration also produced a marked decrease in the uptake of 3H-DA into striatal slices and 3H-NE into cerebral cortical slices. In contrast, the uptake of 3H-NE into hypothalamic slices and the uptake of 3H-5HT into slices from several brain regions were not altered. MPTP initially reduced the concentration of NE in the heart, but unlike the persistent decreases in the forebrain concentrations of NE and DA, the NE concentration in the heart returned to control levels at approximately 20 days after MPTP administration. These results, showing that MPTP can produce a long lasting and selective decrease in the forebrain concentrations of NE and DA and in the uptake of radioactive DA and NE into brain slices, suggest that MPTP can cause the destruction of catecholamine neurons in mouse brain. In contrast, MPTP administration does not appear to produce long term changes in either 5HT or GABA neurons.

AB - The effect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was studied on dopamine (DA), norepinephrine (NE), serotonin (5HT) and γ-aminobutyric acid (GABA) neurons in mouse brain and on NE neurons of mouse heart. MPTP (45 mg/kg) was administered s.c. to mice twice daily for 2 consecutive days. This dosage regimen produced a decrease in the forebrain concentrations of DA and NE at 7 and 20 days after injection. In contrast, the forebrain concentrations of 5HT and GABA were not significantly decreased at either time. MPTP administration also produced a marked decrease in the uptake of 3H-DA into striatal slices and 3H-NE into cerebral cortical slices. In contrast, the uptake of 3H-NE into hypothalamic slices and the uptake of 3H-5HT into slices from several brain regions were not altered. MPTP initially reduced the concentration of NE in the heart, but unlike the persistent decreases in the forebrain concentrations of NE and DA, the NE concentration in the heart returned to control levels at approximately 20 days after MPTP administration. These results, showing that MPTP can produce a long lasting and selective decrease in the forebrain concentrations of NE and DA and in the uptake of radioactive DA and NE into brain slices, suggest that MPTP can cause the destruction of catecholamine neurons in mouse brain. In contrast, MPTP administration does not appear to produce long term changes in either 5HT or GABA neurons.

UR - http://www.scopus.com/inward/record.url?scp=0021240702&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0021240702&partnerID=8YFLogxK

U2 - 10.1016/0024-3205(84)90112-7

DO - 10.1016/0024-3205(84)90112-7

M3 - Article

VL - 35

SP - 285

EP - 291

JO - Life Sciences

JF - Life Sciences

SN - 0024-3205

IS - 3

ER -