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The ionized glutamate receptor (GluRs) is an cation channel of heterogeneity typolymers that mediates the conduction of most excitable neurotransmitteres in the central nervous system.
different types of subjects can be divided into different subject subsypes according to their sub-base combinations.
different subtypes of synapse-subject subtypes mediated synth function and plasticity.
example, GluA1 (a subject sub-base) is necessary for synaptic long-range enhancement (LTP), while GluA2 is involved in long-range suppression (LTD).
addition, glutamate-like subtypes of functional abnormalities and imbalances are closely related to many neuropsychiast diseases, such as Alzheimer's and Huntington's disease.
, little is known about the regulatory mechanism of glutamate-subject subsystic balance.
Yongqing, a researcher at the Institute of Genetics and Developmental Biology of the Chinese Academy of Sciences, has been working on molecular mechanisms for sudden-triggering parenting for a long time.
the team found that two types of glutamate subtypes (A and B) expressed in the nerve muscle synapses of fruit flies were antagonist to each other at synhaplic expression levels, while the total number of synapses remained the same.
ultra-resolution microscopy technology reveals that type A and type B subjects are located in synapses with congenial double rings.
in the process of temperature-induced synhapus plasticity, the expression of type A receptors increases, while the expression of type B receptors decreases.
To further explore the signaling path paths that regulate the subtype balance of the subject, the team screened the candidate genes and found that the dunce gene that specifically knocks down the code cAMP phosphate disgase after the synapse induces the elevation of the type A-type subject and the decrease of the type B-type subject.
this study reveals the direct role of the post-synact cAMP signal path in regulating the glutamate-like subtype balance associated with synhaplic plasticity, which makes people have a deep understanding of the molecular regulatory mechanism of synhaplic plasticity.
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