The central nervous system (CNS), historically considered an immunological sanctuary, has its gateways selectively opened to systemic signaling that reaches the CNS from the vascular compartment. Coagulation proteins and immune mediators revealed novel mechanisms of action from the neurovascular unit: metabolic coupling, tissue repair, host defense, and tumor suppression (physiologically) or metabolic failure, maladaptive plasticity, neuroinflammation, and tumor aidance (pathologically). Resident non-neuronal cells and extracellular matrix (ECM), face the arterial supply, the venous drainage, and, as recently demonstrated, also the lymphatic compartment. Moreover, the interstitial fluid (ISF) and the cerebrospinal fluid (CSF) are progressively gaining attention for their putative role in the sleep/wake cycles and neurodegeneration.
We want to address the role of the integrated synaptic plasticity, completing the simplistic neuronal model. Astrocytic gliotransmission and microglial scavenging role directly prompt plastic changes. The metabolic and hormonal coupling from the astrocytic glia limitans to the brain parenchyma is also actively modulated by synaptic activity, ECM composition, and the vascular cells (endothelium, pericytes, smooth muscle cells) functional state. Oligodendrocytes and their precursors (OPCs) are pivotal to avoid circuitry miswiring and to prompt learning processes. To overcome pathological stressors also the circulating elements, as leukocytes and platelets are essential. The molecular mediators that can influence synaptic transmission are indeed not limited to the classic transmitters and ionic concentrations but should include chemokines and cytokines, growth factors, the thrombin/plasmin axis, complement factors, matrix metalloproteinases (MMPs), and protease-activated receptors (PARs).
The role of these cellular and molecular components widen the multifactorial approach to neurological diseases and could furnish precious hints for new models of neurodegeneration, neuro-inflammation and neuro-oncology. The systems biology approach could lead to novel targets acquisition and drug discovery. The present Special Issue invites Authors experts in the field of neuroscience, to submit their manuscripts critically investigating the integrated CNS plasticity (neuronal – non neuronal). The Issue will collect the latest developments in understanding the role played by each cellular and non-cellular component of the CNS from bench to bedside, with a particular focus on glial cells and the regulation of the neurovascular unit.
The central nervous system (CNS), historically considered an immunological sanctuary, has its gateways selectively opened to systemic signaling that reaches the CNS from the vascular compartment. Coagulation proteins and immune mediators revealed novel mechanisms of action from the neurovascular unit: metabolic coupling, tissue repair, host defense, and tumor suppression (physiologically) or metabolic failure, maladaptive plasticity, neuroinflammation, and tumor aidance (pathologically). Resident non-neuronal cells and extracellular matrix (ECM), face the arterial supply, the venous drainage, and, as recently demonstrated, also the lymphatic compartment. Moreover, the interstitial fluid (ISF) and the cerebrospinal fluid (CSF) are progressively gaining attention for their putative role in the sleep/wake cycles and neurodegeneration.
We want to address the role of the integrated synaptic plasticity, completing the simplistic neuronal model. Astrocytic gliotransmission and microglial scavenging role directly prompt plastic changes. The metabolic and hormonal coupling from the astrocytic glia limitans to the brain parenchyma is also actively modulated by synaptic activity, ECM composition, and the vascular cells (endothelium, pericytes, smooth muscle cells) functional state. Oligodendrocytes and their precursors (OPCs) are pivotal to avoid circuitry miswiring and to prompt learning processes. To overcome pathological stressors also the circulating elements, as leukocytes and platelets are essential. The molecular mediators that can influence synaptic transmission are indeed not limited to the classic transmitters and ionic concentrations but should include chemokines and cytokines, growth factors, the thrombin/plasmin axis, complement factors, matrix metalloproteinases (MMPs), and protease-activated receptors (PARs).
The role of these cellular and molecular components widen the multifactorial approach to neurological diseases and could furnish precious hints for new models of neurodegeneration, neuro-inflammation and neuro-oncology. The systems biology approach could lead to novel targets acquisition and drug discovery. The present Special Issue invites Authors experts in the field of neuroscience, to submit their manuscripts critically investigating the integrated CNS plasticity (neuronal – non neuronal). The Issue will collect the latest developments in understanding the role played by each cellular and non-cellular component of the CNS from bench to bedside, with a particular focus on glial cells and the regulation of the neurovascular unit.
