Persistent Signalling and Changes in Presynaptic Function in Long-Term Potentiation

2007 ◽  
pp. 176-207 ◽  
Author(s):  
Antonio Malgaroli ◽  
Roberto Malinow ◽  
Howard Schulman ◽  
Richard W. Tsien
Keyword(s):  
Long Term Potentiation ◽  
Presynaptic Function ◽  
Term Potentiation

scholarly journals Glutamate release is inhibitory and unnecessary for the long-term potentiation of presynaptic function

2017 ◽  
Author(s):  
Zahid Padamsey ◽  
Rudi Tong ◽  
Nigel Emptage
Keyword(s):  
Glutamate Release ◽  
Learning Rule ◽  
Long Term Potentiation ◽  
Neuronal Dendrites ◽  
Presynaptic Function ◽  
Term Potentiation ◽  
Presynaptic Plasticity ◽  
Presynaptic Nmda Receptors

AbstractLong-term potentiation (LTP) and long-term depression (LTD) of transmitter release probability (Pr) are thought to be triggered by the activation of glutamate receptors. Here, we demonstrate that glutamate release at CA3-CA1 synapses is in fact inhibitory and unnecessary for increases in Pr. Instead, at active presynaptic terminals, postsynaptic depolarization alone can increase Pr by promoting the release of nitric oxide from neuronal dendrites in a manner dependent on L-type voltage-gated Ca2+ channels. The release of glutamate, in contrast, decreases Pr by activating presynaptic NMDA receptors (NMDAR). Thus, net changes in Pr are determined by the combined effect of both LTP-promoting and LTD-promoting processes, that is, by the amount of glutamate release and postsynaptic depolarization that accompany presynaptic activity, respectively. Neither of these processes directly depends on the activation of postsynaptic NMDARs. We further show that presynaptic changes can be captured by a simple learning rule, in which the role of presynaptic plasticity is to ensure that the ability for a presynaptic terminal to release glutamate is matched with its ability to predict postsynaptic spiking.

scholarly journals Glutamate is required for depression but not potentiation of long-term presynaptic function

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Zahid Padamsey ◽  
Rudi Tong ◽  
Nigel Emptage
Keyword(s):  
Transmitter Release ◽  
Glutamate Release ◽  
Long Term Potentiation ◽  
Voltage Gated ◽  
Presynaptic Function ◽  
Hebbian Plasticity ◽  
Term Potentiation ◽  
Presynaptic Plasticity ◽  
Ca2 Channels

Hebbian plasticity is thought to require glutamate signalling. We show this is not the case for hippocampal presynaptic long-term potentiation (LTPpre), which is expressed as an increase in transmitter release probability (Pr). We find that LTPpre can be induced by pairing pre- and postsynaptic spiking in the absence of glutamate signalling. LTPpre induction involves a non-canonical mechanism of retrograde nitric oxide signalling, which is triggered by Ca2+ influx from L-type voltage-gated Ca2+ channels, not postsynaptic NMDA receptors (NMDARs), and does not require glutamate release. When glutamate release occurs, it decreases Pr by activating presynaptic NMDARs, and promotes presynaptic long-term depression. Net changes in Pr, therefore, depend on two opposing factors: (1) Hebbian activity, which increases Pr, and (2) glutamate release, which decreases Pr. Accordingly, release failures during Hebbian activity promote LTPpre induction. Our findings reveal a novel framework of presynaptic plasticity that radically differs from traditional models of postsynaptic plasticity.

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