Effects of Postnatal Trimethyltin or Triethyltin Treatment on CNS Catecholamine, GABA, and Acetylcholine Systems in the Rat

Richard Mailman, Martin R. Krigman, Gerald D. Frye, Israel Hanin

Research output: Contribution to journalArticle

44 Citations (Scopus)

Abstract

Abstract: The effects on brain neurochemistry of two neurotoxic tin compounds, trimethyltin (TMT) hydroxide and triethyltin (TET) sulfate, were examined. Long‐Evans rats were treated with TMT hydroxide (1 mg/kg, i.p.) on alternate days from day 2 to 29 of life. These treatments caused a weight deficit of 10–20% by the time the animals were killed on day 55 by head‐focused microwave irradiation. These TMT treatments are known to cause severe neuronal loss in the hippocampus and lesser damage in other brain regions. Accordingly, the concentration of γ‐aminobutyric acid (GABA) was decreased in the hippocampus; however, acetylcholine and choline concentrations were unaffected. These data suggest that TMT‐induced effects on GABA systems are greater than that due simply to generalized neuronal loss. The TMT treatments also caused a significant decrease in dopamine concentrations in the striatum, but did not alter the concentrations of dihydroxyphenylacetic acid or homovanillic acid, the acidic metabolites of dopamine. Conversely, concentrations of dopamine and norepinephrine in the brain stem and norepinephrine in the cerebellum were not altered. Despite reports in the literature of TMT‐induced neuronal damage in areas of the cortex, no effects on GABA, acetylcholine, or choline levels were found in the cortical areas examined, or in the hypothalamus. TET sulfate (0.3 mg/kg/day) was administered for 6 consecutive days of every week during days 2–29 of life. This dose is lower than that needed to cause intramyelin edema, yet it does result in long‐term behavioral changes. Despite this, no changes in the concentration of any of the measured neurotransmitters or their metabolites were detected. In concert, these data demonstrate that neurochemical methods should not be used as neurological “screens,” but rather to define specific mechanisms suggested by detailed behavior, pharmacological, and/or physiological studies. 1983 International Society for Neurochemistry

Original languageEnglish (US)
Pages (from-to)1423-1429
Number of pages7
JournalJournal of neurochemistry
Volume40
Issue number5
DOIs
StatePublished - Jan 1 1983

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gamma-Aminobutyric Acid
Acetylcholine
Catecholamines
Neurochemistry
Rats
Dopamine
Brain
Metabolites
Choline
Hippocampus
Norepinephrine
Tin Compounds
Aminobutyrates
Homovanillic Acid
Microwave irradiation
Microwaves
Cerebellum
Hypothalamus
Brain Stem
Neurotransmitter Agents

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Cellular and Molecular Neuroscience

Cite this

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title = "Effects of Postnatal Trimethyltin or Triethyltin Treatment on CNS Catecholamine, GABA, and Acetylcholine Systems in the Rat",
abstract = "Abstract: The effects on brain neurochemistry of two neurotoxic tin compounds, trimethyltin (TMT) hydroxide and triethyltin (TET) sulfate, were examined. Long‐Evans rats were treated with TMT hydroxide (1 mg/kg, i.p.) on alternate days from day 2 to 29 of life. These treatments caused a weight deficit of 10–20{\%} by the time the animals were killed on day 55 by head‐focused microwave irradiation. These TMT treatments are known to cause severe neuronal loss in the hippocampus and lesser damage in other brain regions. Accordingly, the concentration of γ‐aminobutyric acid (GABA) was decreased in the hippocampus; however, acetylcholine and choline concentrations were unaffected. These data suggest that TMT‐induced effects on GABA systems are greater than that due simply to generalized neuronal loss. The TMT treatments also caused a significant decrease in dopamine concentrations in the striatum, but did not alter the concentrations of dihydroxyphenylacetic acid or homovanillic acid, the acidic metabolites of dopamine. Conversely, concentrations of dopamine and norepinephrine in the brain stem and norepinephrine in the cerebellum were not altered. Despite reports in the literature of TMT‐induced neuronal damage in areas of the cortex, no effects on GABA, acetylcholine, or choline levels were found in the cortical areas examined, or in the hypothalamus. TET sulfate (0.3 mg/kg/day) was administered for 6 consecutive days of every week during days 2–29 of life. This dose is lower than that needed to cause intramyelin edema, yet it does result in long‐term behavioral changes. Despite this, no changes in the concentration of any of the measured neurotransmitters or their metabolites were detected. In concert, these data demonstrate that neurochemical methods should not be used as neurological “screens,” but rather to define specific mechanisms suggested by detailed behavior, pharmacological, and/or physiological studies. 1983 International Society for Neurochemistry",
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Effects of Postnatal Trimethyltin or Triethyltin Treatment on CNS Catecholamine, GABA, and Acetylcholine Systems in the Rat. / Mailman, Richard; Krigman, Martin R.; Frye, Gerald D.; Hanin, Israel.

In: Journal of neurochemistry, Vol. 40, No. 5, 01.01.1983, p. 1423-1429.

Research output: Contribution to journalArticle

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N2 - Abstract: The effects on brain neurochemistry of two neurotoxic tin compounds, trimethyltin (TMT) hydroxide and triethyltin (TET) sulfate, were examined. Long‐Evans rats were treated with TMT hydroxide (1 mg/kg, i.p.) on alternate days from day 2 to 29 of life. These treatments caused a weight deficit of 10–20% by the time the animals were killed on day 55 by head‐focused microwave irradiation. These TMT treatments are known to cause severe neuronal loss in the hippocampus and lesser damage in other brain regions. Accordingly, the concentration of γ‐aminobutyric acid (GABA) was decreased in the hippocampus; however, acetylcholine and choline concentrations were unaffected. These data suggest that TMT‐induced effects on GABA systems are greater than that due simply to generalized neuronal loss. The TMT treatments also caused a significant decrease in dopamine concentrations in the striatum, but did not alter the concentrations of dihydroxyphenylacetic acid or homovanillic acid, the acidic metabolites of dopamine. Conversely, concentrations of dopamine and norepinephrine in the brain stem and norepinephrine in the cerebellum were not altered. Despite reports in the literature of TMT‐induced neuronal damage in areas of the cortex, no effects on GABA, acetylcholine, or choline levels were found in the cortical areas examined, or in the hypothalamus. TET sulfate (0.3 mg/kg/day) was administered for 6 consecutive days of every week during days 2–29 of life. This dose is lower than that needed to cause intramyelin edema, yet it does result in long‐term behavioral changes. Despite this, no changes in the concentration of any of the measured neurotransmitters or their metabolites were detected. In concert, these data demonstrate that neurochemical methods should not be used as neurological “screens,” but rather to define specific mechanisms suggested by detailed behavior, pharmacological, and/or physiological studies. 1983 International Society for Neurochemistry

AB - Abstract: The effects on brain neurochemistry of two neurotoxic tin compounds, trimethyltin (TMT) hydroxide and triethyltin (TET) sulfate, were examined. Long‐Evans rats were treated with TMT hydroxide (1 mg/kg, i.p.) on alternate days from day 2 to 29 of life. These treatments caused a weight deficit of 10–20% by the time the animals were killed on day 55 by head‐focused microwave irradiation. These TMT treatments are known to cause severe neuronal loss in the hippocampus and lesser damage in other brain regions. Accordingly, the concentration of γ‐aminobutyric acid (GABA) was decreased in the hippocampus; however, acetylcholine and choline concentrations were unaffected. These data suggest that TMT‐induced effects on GABA systems are greater than that due simply to generalized neuronal loss. The TMT treatments also caused a significant decrease in dopamine concentrations in the striatum, but did not alter the concentrations of dihydroxyphenylacetic acid or homovanillic acid, the acidic metabolites of dopamine. Conversely, concentrations of dopamine and norepinephrine in the brain stem and norepinephrine in the cerebellum were not altered. Despite reports in the literature of TMT‐induced neuronal damage in areas of the cortex, no effects on GABA, acetylcholine, or choline levels were found in the cortical areas examined, or in the hypothalamus. TET sulfate (0.3 mg/kg/day) was administered for 6 consecutive days of every week during days 2–29 of life. This dose is lower than that needed to cause intramyelin edema, yet it does result in long‐term behavioral changes. Despite this, no changes in the concentration of any of the measured neurotransmitters or their metabolites were detected. In concert, these data demonstrate that neurochemical methods should not be used as neurological “screens,” but rather to define specific mechanisms suggested by detailed behavior, pharmacological, and/or physiological studies. 1983 International Society for Neurochemistry

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