Glutamate toxicity studies: simultaneous recording of single neuron O2 consumption, intracellular Ca2 + concentration and mitochondrial membrane potential

Neurons are excitable cells. After synaptic activity and action potentials are generated, neurons must produce a large amount of ATP to drive ion pumps to increase intracellular Na + and Ca2 + levels. Glutamic acid (Glu) is an important neurotransmitter, responsible for rapid synaptic transmission and long-term changes in synaptic transmission strength, and participates in processes such as cognition and memory; but if glutamate receptors are excessively activated, glutamic acid will Lead to toxic reactions such as disruption of ion balance and cell death.

In this paper, to clarify the mechanism of glutamate neurotoxicity, non-invasive micro-measurement technology and laser confocal technology are combined, and neurons in the cerebral cortex of rat pups are used as tested samples. O2 electrode) to detect the O2 consumption (ie O2 influx) of a single neuron, and the confocal laser technique to detect its intracellular Ca2 + concentration and mitochondrial membrane potential.

The study found that under the action of glutamate, the intracellular Ca2 + concentration increased, and then the O2 consumption increased, during which the mitochondrial membrane potential also changed accordingly. This conclusion directly confirms the following glutamate toxicity mechanism model: glutamate receptors can cause Ca2 + influx after activation, leading to the loss of intracellular ATP.

Combining non-damaging micro-measurement technology with laser confocal technology to detect changes in ion molecules or other information inside and outside biological samples has become an important means to reveal the mechanism of life processes.