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The effects of lanthanum chloride administration in newborn chicks on glutamate uptake and release by brain
Insights
Acute lanthanum chloride exposure in newborn chicks inhibits glutamate uptake and release in brain synaptosomes. This suggests lanthanum intoxication disrupts crucial neurotransmitter functions by affecting calcium binding.
Area of Science:
- Neuroscience
- Toxicology
- Biochemistry
Background:
- Glutamate is a primary excitatory neurotransmitter in the brain.
- Synaptosomes are isolated nerve terminals used to study neurotransmitter transport.
- Lanthanum is a rare-earth element with known biological effects.
Purpose of the Study:
- To investigate the effects of acute lanthanum chloride administration on glutamate uptake and release in chick brain synaptosomes.
- To explore the role of calcium in lanthanum-induced alterations of neurotransmitter function.
Main Methods:
- Acute intraperitoneal injection of lanthanum chloride (250 mg/kg) in newborn chicks.
- Isolation of brain synaptosomes.
- Measurement of [14C]glutamate uptake and release under various conditions (e.g., presence of Ca2+, high K+).
Main Results:
- Lanthanum chloride significantly inhibited the high-affinity uptake of [14C]glutamate by isolated brain synaptosomes.
- A marked decrease in the release of preloaded [14C]glutamate was observed.
- Inhibition of glutamate release was noted in the presence of external Ca2+ or high K+ stimulation.
Conclusions:
- Acute lanthanum intoxication impairs glutamate neurotransmission in developing chick brains.
- Lanthanum may interfere with synaptic vesicle release mechanisms, potentially by affecting calcium binding to the synaptosomal membrane.
- These findings highlight the neurotoxic potential of lanthanum chloride on developing nervous systems.
Abstract:
Acute i.p. administration of lanthanum chloride to newborn chicks at a single dose of 250 mg/kg body weight causes inhibition of the high affinity uptake of [14C]glutamate by isolated brain synaptosomes. There is also a marked decrease in the release of preloaded [14C]glutamate from brain synaptosomes in the presence of externally available Ca2+ (1.2 mM) or a high K+ concentration (71 mM). The inhibition of glutamate release has been discussed in relation to depletion of Ca2+ binding to the synaptosomal membrane under lanthanum intoxication.