I got confused when reading the mechanism of Synaptic plasticity - (Glutamate neurotransmitter Physiological role) - necessary of learning & memory.
In some literature, they are telling that NMDA will get activated, leads to Ca2+ entry, which phophorylate the AMPA receptor. AMPA removes the Blackade of Mg2+ from NMDA & thus more NMDA will activated which multiplies the response - LTP - synaptic plasticity. As well as for the activation of AMPA, NMDA activation is must required.
While other material suggests that, During resting potential AMPA are in active stage while NMDA are blocked by Mg2+.
So can anybody suggest me the exact mechanism of synaptic plasticity???
Just in a nutshell, AMPA is activated first, because it doesn't have a block (such as Mg+), and therefore it can make a depolarization that might be enough to remove the Mg block from NMDA. AMPA has a fast time-scale, with fast activation and inactivation. NMDA is activated in a much slower time-scale and it inactivated in almost a sec. So if AMPA can acitave NMDA, that for a second AP, you will get a much higher response, because, you don't need to remove the Mg+ block, as NMDA is still active. So this is the high-school case of plasticity. But for a bigger picture you need to see into the actions of mGluR-s, because they can facilitate of act as depressors for synaptic transmission. I hope it helped!
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