Abstract
Synapses change their strength in response to specific activity patterns. This functional plasticity is assumed to be the brain's primary mechanism for information storage. We used optogenetic stimulation of rat hippocampal slice cultures to induce long-term potentiation (LTP), long-term depression (LTD), or both forms of plasticity in sequence. Two-photon imaging of spine calcium signals allowed us to identify stimulated synapses and to follow their fate for the next 7 days. We found that plasticity-inducing protocols affected the synapse's chance for survival: LTP increased synaptic stability, LTD destabilized synapses, and the effect of the last stimulation protocol was dominant over earlier stimulations. Interestingly, most potentiated synapses were resistant to depression-inducing protocols delivered 24 hr later. Our findings suggest that activity-dependent changes in the transmission strength of individual synapses are transient, but have long-lasting consequences for synaptic lifetime.
Highlights
Graded changes in synaptic strength, driven by specific activity patterns, are a candidate mechanism for information storage in the brain (Chaudhuri and Fiete, 2016)
On CA1 pyramidal cells expressing GCaMP6s and mCerulean, active spines were identified by imaging stimulation-induced excitatory postsynaptic calcium transients (EPSCaTs)
complex spike bursts (CSBs) in the reporter neuron were time-locked with large calcium transients in the stretch of dendrite adjacent to the postsynaptic spine (Figure 1B, middle column), suggesting that synchronized CSBs were occurring in neighboring neurons
Summary
Graded changes in synaptic strength, driven by specific activity patterns, are a candidate mechanism for information storage in the brain (Chaudhuri and Fiete, 2016). A prevailing theory is that graded changes in synaptic strength persist as a memory trace of former activity. At the level of individual synapses, dramatic fluctuations in spine volume over time scales of hours to days cast doubt on whether information can be stored for long periods in the analog strength of synapses (Holtmaat and Caroni, 2016; Berry and Nedivi, 2017). An alternative hypothesis is that over longer time periods, information is stored not in the strength but in the number of connections, which, at the level of individual synapses, would manifest as a change in synaptic lifetime. Supporting evidence comes from the findings that long term depression (LTD) decreases synaptic lifetime (Nagerl et al, 2004; Bastrikova et al, 2008; Wiegert and Oertner, 2013) and that spine structure becomes stabilized and growth persists up to 3 days after induction of long term potentiation (LTP) (De Roo et al, 2008; Hill and Zito, 2013)
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