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Differential effects between one week and four weeks exposure to same mass of SO2 on synaptic plasticity in rat hippocampus

Author:
Yao, Gaoyi, Yun, Yang, Sang, Nan
Source:
Environmental toxicology 2016 v.31 no.7 pp. 820-829
ISSN:
1520-4081
Subject:
adverse effects, air, air pollution, breathing, cAMP-dependent protein kinase, gene expression, glutamate receptors, hippocampus, messenger RNA, mortality, neuroplasticity, neurotoxicity, pollutants, protein kinase C, protein synthesis, rats, risk, signal transduction, sulfur dioxide, synapse
Abstract:
Sulfur dioxide (SO₂) is a ubiquitous air pollutant. The previous studies have documented the adverse effects of SO₂ on nervous system health, suggesting that acutely SO₂ inhalation at high concentration may be associated with neurotoxicity and increase risk of hospitalization and mortality of many brain disorders. However, the remarkable features of air pollution exposure are lifelong duration and at low concentration; and it is rarely reported that whether there are different responses on synapse when rats inhaled same mass of SO₂ at low concentration with a longer term. In this study, we evaluated the synaptic plasticity in rat hippocampus after exposure to same mass of SO₂ at various concentrations and durations (3.5 and 7 mg/m³, 6 h/day, for 4 weeks; and 14 and 28 mg/m³, 6 h/day, for 1 week). The results showed that the mRNA level of synaptic plasticity marker Arc, glutamate receptors (GRIA1, GRIA2, GRIN1, GRIN2A, and GRIN2B) and the protein expression of memory related kinase p‐CaMKпα were consistently inhibited by SO₂ both in 1 week and 4 weeks exposure cases; the protein expression of presynaptic marker synaptophysin, postsynaptic density protein 95 (PSD‐95), protein kinase A (PKA), and protein kinase C (PKC) were increased in 1 week exposure case, and decreased in 4 weeks exposure case. Our results indicated that SO₂ inhalation caused differential synaptic injury in 1 week and 4 weeks exposure cases, and implied the differential effects might result from different PKA‐ and/or PKC‐mediated signal pathway. © 2014 Wiley Periodicals, Inc. Environ Toxicol 31: 820–829, 2016.
Agid:
5232063