Monitoring and Modulating Inflammation-Associated Alterations in Synaptic Plasticity: Role of Brain Stimulation and the Blood-Brain Interface

Abstract

Inflammation of the central nervous system can be triggered by endogenous and exogenous stimuli such as local or systemic infection, trauma, and stroke. In addition to neurodegeneration and cell death, alterations in physiological brain functions are often associated with neuroinflammation. Robust experimental evidence has demonstrated that inflammatory cytokines affect the ability of neurons to express plasticity. It has been well-established that inflammation-associated alterations in synaptic plasticity contribute to the development of neuropsychiatric symptoms. Nevertheless, diagnostic approaches and interventional strategies to restore inflammatory deficits in synaptic plasticity are limited. Here, we review recent findings on inflammation-associated alterations in synaptic plasticity and the potential role of the blood-brain interface, i.e., the blood-brain barrier, in modulating synaptic plasticity. Based on recent findings indicating that brain stimulation promotes plasticity and modulates vascular function, we argue that clinically employed non-invasive brain stimulation techniques, such as transcranial magnetic stimulation, could be used for monitoring and modulating inflammation-induced alterations in synaptic plasticity.

Keywords: interleukin 10; lipopolysaccharide; synaptic plasticity; transcranial magnetic stimulation.

Figure 1

Blood–brain communication is a crucial regulatory element in neural circuit function. Neurons and glial cells bilaterally influence their function through various mediators, such as neurotransmitters, metabolites and brain derived cytokines. Moreover, soluble and cellular blood components can enter the central nervous system, when the permeability of the blood–brain interface changes. This intruiging blood–brain interaction can influence distinct features of neural circuits, e.g., network activity and the expression of synaptic plasticity.