Linked Life Data

16684133

Source:http://linkedlifedata.com/resource/pubmed/id/16684133

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2006-5-10
pubmed:abstractText
One of the most common chemicals that behaves as an endocrine disruptor is the compound 4,4'-isopronylidenediphenol, called bisphenol-A (BPA). We previously reported that prenatal and postnatal exposure to BPA potentiated central dopaminergic neurotransmission, resulting in supersensitivity to psychostimulant-induced pharmacological actions. Many recent findings have supported the idea that astrocytes, which are a subpopulation of glial cells, play a critical role in neuronal transmission in the central nervous system. The present study aimed to investigate the role of neurone-astrocyte communication in the enhancement of dopaminergic neurotransmission induced by BPA. We found that treatment of mouse purified astrocytes and neurone/glia cocultures with BPA in vitro caused the activation of astrocytes, as detected by a stellate morphology and an increase in levels of glial fibrillary acidic protein. A low concentration of BPA significantly enhanced the Ca2+ responses to dopamine in both neurones and astrocytes. Furthermore, a high concentration of BPA markedly induced the activation of caspase-3, which is a marker of neuronal apoptotic cell death in mouse midbrain neurone/glia cocultures. By contrast, treatment with 17beta-oestradiol (E2) had no such effects. Prenatal and neonatal exposure to BPA led to an enhancement of the dopamine-dependent rewarding effect induced by morphine. These findings provide evidence that BPA alters dopamine responsiveness in neurones and astrocytes and that, at least in part, it may contribute to potentiate the development of psychological dependence on drugs of abuse.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0953-8194
pubmed:author
pubmed:issnType
Print
pubmed:volume
18
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
434-44
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16684133-Analgesics, Opioid, pubmed-meshheading:16684133-Animals, pubmed-meshheading:16684133-Astrocytes, pubmed-meshheading:16684133-Calcium, pubmed-meshheading:16684133-Cell Communication, pubmed-meshheading:16684133-Cell Death, pubmed-meshheading:16684133-Dopamine, pubmed-meshheading:16684133-Dose-Response Relationship, Drug, pubmed-meshheading:16684133-Estradiol, pubmed-meshheading:16684133-Estrogen Receptor Modulators, pubmed-meshheading:16684133-Estrogens, Non-Steroidal, pubmed-meshheading:16684133-Female, pubmed-meshheading:16684133-Male, pubmed-meshheading:16684133-Mice, pubmed-meshheading:16684133-Mice, Inbred ICR, pubmed-meshheading:16684133-Morphine, pubmed-meshheading:16684133-Neurons, pubmed-meshheading:16684133-Phenols, pubmed-meshheading:16684133-Pregnancy, pubmed-meshheading:16684133-Prenatal Exposure Delayed Effects, pubmed-meshheading:16684133-Reward, pubmed-meshheading:16684133-Substance-Related Disorders, pubmed-meshheading:16684133-Synaptic Transmission
pubmed:year
2006
pubmed:articleTitle
Dynamic changes in dopaminergic neurotransmission induced by a low concentration of bisphenol-A in neurones and astrocytes.
pubmed:affiliation
Department of Toxicology, Hoshi University School of Pharmacy and Pharmaceutical Sciences, Tokyo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't