NAT COMMUN: How is memory consolidated? 

Neuromodulation agents control not only the synactic transmission of neurons, but also the internal excitability of neurons, whose dysfunction can lead to neurological diseases.
their abundance are controlled by a delicate balance between production and degradation.
Although it is generally assumed that neuromodulation promotes the production of neuromodulants to affect signal transmission, a rapid chemical degradation process may control the time curve in which neuromodulants act to optimize the processing of information within neuron circuits.
therefore, changes in the degradation rate can affect the signal conduction of neuromodulation agents, but the presence of this plastic form has not yet been determined.
previous studies have shown that the abundance of inner cannabinin, which regulates synactal delivery retrograde, is controlled by a delicate balance between internal cannabinin synthesis and degradation.
Although it is common assumption that "on-demand" release determines the signaling of cannabinin, their rapid degradation is expected to control the time curve of the internal cannabinin action and may affect the conduction of neuron signals.
recently, researchers published in the journal Nature Communications showed that memory formation through fear conditions selectively accelerated the degradation of cannabinin in the brain.
led to a persistent increase in GABA release, which is what drives endorphin degradation changes.
, Gq-DREADD's activation of the small brain's Pocon wild cells enhances the internal cannabinin signal and impairs memory consolidation.
therefore, the results identified a previously unconcensed interaction between GABA and the cannabinin system, in which GABA signals accelerate the degradation of cannabinin and trigger a learning-induced plasticity.
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