Synaptic Clustering and Memory Formation

Abstract

In the study of memory engrams, synaptic memory allocation is a newly emerged theme that focuses on how specific synapses are engaged in the storage of a given memory. Cumulating evidence from imaging and molecular experiments indicates that the recruitment of synapses that participate in the encoding and expression of memory is neither random nor uniform. A hallmark observation is the emergence of groups of synapses that share similar response properties and/or similar input properties and are located within a stretch of a dendritic branch. This grouping of synapses has been termed “synapse clustering” and has been shown to emerge in many different memory-related paradigms, as well as in in vitro studies. The clustering of synapses may emerge from synapses receiving similar input, or via many processes which allow for cross-talk between nearby synapses within a dendritic branch, leading to cooperative plasticity. Clustered synapses can act in concert to maximally exploit the nonlinear integration potential of the dendritic branches in which they reside. Their main contribution is to facilitate the induction of dendritic spikes and dendritic plateau potentials, which provide advanced computational and memory-related capabilities to dendrites and single neurons. This review focuses on recent evidence which investigates the role of synapse clustering in dendritic integration, sensory perception, learning, and memory as well as brain dysfunction. We also discuss recent theoretical work which explores the computational advantages provided by synapse clustering, leading to novel and revised theories of memory. As an eminent phenomenon during memory allocation, synapse clustering both shapes memory engrams and is also shaped by the parallel plasticity mechanisms upon which it relies.

The Subcortical-Allocortical- Neocortical continuum for the Emergence and Morphological Heterogeneity of Pyramidal Neurons in the Human Brain

“…Ramified spines have additional functional possibilities by displaying postsynaptic receptors on different parts of the spine heads ( Verzi and Noris, 2009 ) with likely temporal and spatial specificity and signaling microdomains ( Newpher and Ehlers, 2009 ; Chen and Sabatini, 2012 ). Synaptic amplification involving clustered dendritic spines would also enhance input cooperativity among coactive inputs at neighboring synapses ( Harnett et al, 2012 ; Yadav et al, 2012 ), influencing network plasticity, learning, and memory ( Frank et al, 2018 ; Kastellakis and Poirazi, 2019 ; for the dendritic mechanisms linking memories and overlapping allocations of synaptic resources see also Kastellakis et al, 2016 ).…”

“…Clustered synapses can act in concert to maximally exploit the non-linear integration potential of the dendritic branches in which they reside. Their main contribution is to facilitate the induction of dendritic spikes and dendritic plateau potentials, which provide advanced computational and memory-related capabilities to dendrites and single neurons” ( Kastellakis and Poirazi, 2019 ). In conjunction, these findings indicate that the diversity of operations in pyramidal spines provide an exceptional repertoire for the integration of postsynaptic potentials at each spiny dendritic segment and more “functional output codes” for each cell.…”

Memory consolidation and improvement by synaptic tagging and capture in recurrent neural networks

“…Nevertheless, there can also be local protein synthesis in the dendrites 72 – 75 , which could confine the here identified protein-dependent dynamics of consolidation and improvement to specific dendritic branches of a neuron. However, due to synaptic clustering 76 , local protein synthesis would not necessarily yield different results as compared to our model.…”

The effect of maslinic acid on cognitive dysfunction induced by cholinergic blockade in mice

“…Synaptic plasticity is associated with cognitive function (Kastellakis & Poirazi, 2019). T,hus we investigated the effect of maslinic acid on synaptic plasticity by measuring the LTP in the hippocampal slices treated with maslinic acid (1, 10 and 30 μM) for 2 hr (Figure 2).…”