Cadmium toxicity in synaptic neurotransmission in the brain

Abstract

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 109CdCl 2 into the amygdala of rats, 109Cd 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 μM 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 γ-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.