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Increased forebrain beta-adrenergic ligand binding induced by trimethyltin.

Authors
  • Messing, R B
  • Sparber, S B
Type
Published Article
Journal
Toxicology Letters
Publisher
Elsevier
Publication Date
Jan 01, 1986
Volume
32
Issue
1-2
Pages
107–112
Identifiers
PMID: 3016948
Source
Medline
License
Unknown

Abstract

Systemic injection of the organometal neurotoxin trimethyltin (TMT) into rats causes impairments in learning and memory. However, there is a discontinuity in dose-response functions, such that the deficit which emerges with a higher, acutely toxic dose, is qualitatively different from the impairment induced after lower doses. To investigate synaptic receptor changes associated with behavioral deficits, neurotransmitter-receptor ligand binding assays were done in forebrain areas of rats given TMT (3.6 or 7.5 mg/kg). Binding of the beta-adrenergic ligand, dihydroalprenolol in frontal cortex and amygdala/pyriform cortex was an inverted U-shaped function of TMT dose, with rats given the median dose exhibiting increased binding. The curvilinear dose-response functions in behavioral and biochemical assays suggest that altered forebrain noradrenergic neurotransmission could play a role in behavioral deficits.

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