Glutamate is the primary excitatory neurotransmitter in the central nervous system, and it is released by neurons in response to various stimuli. When glutamate is released, it binds to and activates receptors on the postsynaptic neuron, leading to an influx of positively charged ions such as calcium and sodium into the neuron. This influx of ions depolarizes the postsynaptic membrane, increasing the likelihood that the neuron will fire an action potential.

Glutamate is stored in synaptic vesicles within the presynaptic neuron, and its release is tightly regulated by a variety of processes. When an action potential reaches the presynaptic terminal, it triggers the opening of voltage-gated calcium channels, allowing calcium ions to enter the neuron. The influx of calcium causes the synaptic vesicles containing glutamate to fuse with the presynaptic membrane, releasing glutamate into the synaptic cleft.

The release of glutamate is critical for many aspects of neural function, including learning and memory, sensory processing, and motor control. Dysregulation of glutamate release or receptor function has been implicated in a range of neurological and psychiatric disorders, including epilepsy, stroke, and schizophrenia.

Overall, the release of glutamate is a tightly regulated process that plays a critical role in neural communication and function. Understanding the mechanisms that control glutamate release and receptor function is essential for developing treatments for neurological and psychiatric disorders.