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Responsible editorZyme Nerve has plasticity to meet the basic needs of learning and memory
.
The negative feedback synaptic homeostasis plasticity mechanism is like a sentinel that can stabilize the function of the neural circuit, so as to ensure the normal operation of the nervous system while ensuring the flexibility of learning and memory
.
The homeostatic regulation of presynaptic neurotransmitter release is a basic form of stabilizing the plasticity of neural activity.
Presynaptic homeostatic depression (PHD) can adaptively reduce the intensity of synaptic neurotransmitter release
.
Studies have proposed that PHD adjusts the nervous system's excessive glutamate release in a steady state by adaptively reducing presynaptic release
.
This theory speculates that there is an autoreceptor for glutamate before the synapse that releases glutamate
.
Recently, the Dion Dickman laboratory of the University of Southern California published an article titled Autocrine inhibition by a glutamate-gated chloride channel mediates presynaptic homeostatic depression in Science Advances
.
The study established the establishment of glutamate-gated chloride channels for PHD, and revealed the regulatory mechanism in PHD
.
This work used the neuromuscular junction of Drosophila larvae as a model to systematically screen all neuronal glutamate receptors in the Drosophila genome, and finally determined the glutamate-gated chloride channel (GluClα) required for PHD expression.
)
.
The GluClα mutation completely suppressed the PHD caused by the overexpression of the glutamate vector
.
Pharmacology, genetics and calcium imaging experiments show that GluClα acts locally at the end of axons to drive the expression of PHD
.
Unexpectedly, GluClα localizes on the synaptic vesicles and follows the vesicles
.
With the release of synaptic vesicles, GluClα acts on the presynaptic membrane, binds to glutamate and drives presynaptic inhibition through dependent anion conductance
.
Therefore, as a sensor and effector of PHD, GluClα adaptively inhibits the release of neurotransmitters by generating inhibitory signal mechanisms at the nerve presynaptic terminals
.
Figure 2.
GluClα localizes on synaptic vesicles and transfers with the vesicles
.
The steady-state control of glutamate levels in the nervous system is essential
.
Excessive glutamate in the nervous system can cause excitotoxicity, seizures, stroke, and is an important pathological mechanism in neurodegenerative diseases
.
This article shows that the adaptive plasticity mechanism of nerve presynapses can be used as an important direction for future research on the steady-state control of glutamate and other neurotransmitters
.
Original link: https:// Platemaker: Notes for reprinting on the 11th [Non-original article] The copyright of this article belongs to the author of the article.
Personal forwarding and sharing are welcome.
Reprinting without permission is prohibited.
The author has all legal rights, and offenders must be investigated
.
.
The negative feedback synaptic homeostasis plasticity mechanism is like a sentinel that can stabilize the function of the neural circuit, so as to ensure the normal operation of the nervous system while ensuring the flexibility of learning and memory
.
The homeostatic regulation of presynaptic neurotransmitter release is a basic form of stabilizing the plasticity of neural activity.
Presynaptic homeostatic depression (PHD) can adaptively reduce the intensity of synaptic neurotransmitter release
.
Studies have proposed that PHD adjusts the nervous system's excessive glutamate release in a steady state by adaptively reducing presynaptic release
.
This theory speculates that there is an autoreceptor for glutamate before the synapse that releases glutamate
.
Recently, the Dion Dickman laboratory of the University of Southern California published an article titled Autocrine inhibition by a glutamate-gated chloride channel mediates presynaptic homeostatic depression in Science Advances
.
The study established the establishment of glutamate-gated chloride channels for PHD, and revealed the regulatory mechanism in PHD
.
This work used the neuromuscular junction of Drosophila larvae as a model to systematically screen all neuronal glutamate receptors in the Drosophila genome, and finally determined the glutamate-gated chloride channel (GluClα) required for PHD expression.
)
.
The GluClα mutation completely suppressed the PHD caused by the overexpression of the glutamate vector
.
Pharmacology, genetics and calcium imaging experiments show that GluClα acts locally at the end of axons to drive the expression of PHD
.
Unexpectedly, GluClα localizes on the synaptic vesicles and follows the vesicles
.
With the release of synaptic vesicles, GluClα acts on the presynaptic membrane, binds to glutamate and drives presynaptic inhibition through dependent anion conductance
.
Therefore, as a sensor and effector of PHD, GluClα adaptively inhibits the release of neurotransmitters by generating inhibitory signal mechanisms at the nerve presynaptic terminals
.
Figure 2.
GluClα localizes on synaptic vesicles and transfers with the vesicles
.
The steady-state control of glutamate levels in the nervous system is essential
.
Excessive glutamate in the nervous system can cause excitotoxicity, seizures, stroke, and is an important pathological mechanism in neurodegenerative diseases
.
This article shows that the adaptive plasticity mechanism of nerve presynapses can be used as an important direction for future research on the steady-state control of glutamate and other neurotransmitters
.
Original link: https:// Platemaker: Notes for reprinting on the 11th [Non-original article] The copyright of this article belongs to the author of the article.
Personal forwarding and sharing are welcome.
Reprinting without permission is prohibited.
The author has all legal rights, and offenders must be investigated
.
