Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-3-19
pubmed:abstractText
Chronic exposure to cadmium causes central nervous system disorders, e.g. olfactory dysfunction. To clarify cadmium toxicity in synaptic neurotransmission in the brain, the movement of cadmium in the synapses was examined using in vivo microdialysis. One and 24 h after injection of (109)CdCl(2) into the amygdala of rats, (109)Cd release into the extracellular space was facilitated by stimulation with high K(+), suggesting that cadmium taken up by amygdalar neurons is released into the synaptic clefts in a calcium- and impulse-dependent manner. Moreover, to examine the action of cadmium in the synapses, the amygdala was perfused with artificial cerebrospinal fluid containing 10-30 microM CdCl(2). The release of excitatory neurotransmitters, i.e. glutamate and aspartate, into the extracellular space was decreased during perfusion with cadmium, while the release of inhibitory neurotransmitters, i.e. glycine and gamma-amino butyric acid (GABA), into the extracellular space was increased during the period. These results suggest that cadmium released from the amygdalar neuron terminals affect the degree and balance of excitation-inhibition in synaptic neurotransmission.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
16
pubmed:volume
894
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
336-9
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Cadmium toxicity in synaptic neurotransmission in the brain.
pubmed:affiliation
Department of Radiobiochemistry, School of Pharmaceutical Sciences, University of Shizuoka, 52-1 Yada, 422-8526, Shizuoka, Japan.
pubmed:publicationType
Journal Article