Cadmium toxicity in synaptic neurotransmission in the brain

Chronic exposure to cadmium causes central nervous system disorders, e.g. o lfactory dysfunction. To clarify cadmium toxicity in synaptic neurotransmis sion in the brain, the movement of cadmium in the synapses was examined usi ng in vivo microdialysis. One and 24 h after injection of (CdCl2)-Cd-109 in to the amygdala of rats, Cd-109 release into the extracellular space was fa cilitated by stimulation with high K+, suggesting that cadmium taken up by amygdalar neurons is released into the synaptic clefts in a calcium- and im pulse-dependent manner. Moreover, to examine the action of cadmium in the s ynapses, the amygdala was perfused with artificial cerebrospinal fluid cont aining 10-30 muM CdCl2. The release of excitatory neurotransmitters, i.e, g lutamate and aspartate, into the extracellular space was decreased during p erfusion with cadmium, while the release of inhibitory neurotransmitters, i .e, glycine and gamma -amino butyric acid (GABA), into the extracellular sp ace was increased during the period. These results suggest that cadmium rel eased from the amygdalar neuron terminals affect the degree and balance of excitation-inhibition in synaptic neurotransmission. (C) 2001 Elsevier Scie nce BN. All rights reserved.