Synaptic Plasticity Shapes Brain Connectivity: Implications for Network Topology.

Mario Stampanoni Bassi,Diego Centonze,Fabio Buttari,Luana Gilio,Ennio Iezzi

doi:10.3390/ijms20246193

Abstract

Studies of brain network connectivity improved understanding on brain changes and adaptation in response to different pathologies. Synaptic plasticity, the ability of neurons to modify their connections, is involved in brain network remodeling following different types of brain damage (e.g., vascular, neurodegenerative, inflammatory). Although synaptic plasticity mechanisms have been extensively elucidated, how neural plasticity can shape network organization is far from being completely understood. Similarities existing between synaptic plasticity and principles governing brain network organization could be helpful to define brain network properties and reorganization profiles after damage. In this review, we discuss how different forms of synaptic plasticity, including homeostatic and anti-homeostatic mechanisms, could be directly involved in generating specific brain network characteristics. We propose that long-term potentiation could represent the neurophysiological basis for the formation of highly connected nodes (hubs). Conversely, homeostatic plasticity may contribute to stabilize network activity preventing poor and excessive connectivity in the peripheral nodes. In addition, synaptic plasticity dysfunction may drive brain network disruption in neuropsychiatric conditions such as Alzheimer’s disease and schizophrenia. Optimal network architecture, characterized by efficient information processing and resilience, and reorganization after damage strictly depend on the balance between these forms of plasticity.

Highlights

The functional properties of the brain are largely determined by the characteristics of its neurons and the pattern of synaptic connections between them
While long-term potentiation (LTP) is anti-homeostatic and represents a possible substrate for hubs generation, we propose that homeostatic plasticity, in particular synaptic scaling, may intervene to maintain low connectivity in the peripheral nodes of the network
The recurrence of seizures has been associated with imbalanced excitatory and inhibitory synaptic transmission leading to hypersynchronized neuronal activity [88,89], and epileptogenesis has been linked to altered expression of hippocampal LTP and long-term depression (LTD) at glutamatergic and GABAergic synapses, respectively [90]

Summary

Introduction

The functional properties of the brain are largely determined by the characteristics of its neurons and the pattern of synaptic connections between them. Comprehension of brain networks organization has been fueled by the application of procedures able to investigate brain connectivity in vivo [1,2] based on new theoretical/mathematical approaches (i.e., graph theory) to extract several measures that describe network architecture and functioning [3,4]. This approach led to the identification of specific features of brain networks, such as modularity and the presence of network hubs, that provide efficient information processing and elevated resistance to damage [5]. This perspective may be helpful to understand how networks adapt in response to brain damage and to explain mechanisms of network disruption in neuropsychiatric conditions such as Alzheimer’s disease and schizophrenia

Brain Network Organization

Synaptic Plasticity

Synaptic Plasticity and Brain Network Organization

Synaptic Plasticity Promotes Brain Network Reorganization after Damage

Conclusions