Anti-CX3CL1 polyclonal antibody [Biotin]

Psychological stress can precipitate depression, and emerging preclinical data suggest a link between stress-induced alterations in microglia function and development of depressive-like behaviors. Microglia are highly dynamic, and play an integral role in maintaining neuronal homeostasis and synaptic plasticity. In this capacity, microglial dysfunction represents a compelling avenue through which stress might disrupt neuronal integrity and induce psychopathology. This review examines preclinical and clinical postmortem findings that indicate microglia-neuron interactions contribute to stress-induced synaptic deficits and associated behavioral and cognitive consequences. We focus on pathways that are implicated in microglia-mediated neuronal remodeling, including CSF1-CSF1R, CX3CL1-CX3CR1, and CD11b (CR3)-C3, as well as purinergic signaling via P2RX7 and P2RY12. We also highlight sex differences in stress effects on microglia, and the potential for microglia in the development of sex-specific treatments for depressive disorders.

This study aims to explore the role of fractalkine/CX3C chemokine receptor 1 (CX3CR1) signaling pathway in the recovery of neurological functioning after an early ischemic stroke in rats. After establishment of permanent middle cerebral artery occlusion (pMCAO) models, 50 rats were divided into blank, sham, model, positive control and CX3CR1 inhibitor groups. Neurological impairment, walking and grip abilities, and cortical and hippocampal infarctions were evaluated by Zea Longa scoring criterion, beam-walking assay and grip strength test, and diffusion -weighted magnetic resonance imaging. qRT-PCR and Western blotting were performed to detect mRNA and protein expressions. ELISA was conducted to measure concentration of sFractalkine (sFkn), interleukin-1p (IL-1 beta) and TNF-alpha.. The recovery rate of neurological functioning impairment and reduced walking and grip abilities was faster in the positive control and CX3CR1 inhibitor groups than the model group. The model, positive control and CX3CR1 inhibitor groups showed increased mRNA and protein expression of chemokine C-X3-C motif ligand 1 (CX3CL1) and CX3CR1, concentration of sFkn, IL-1 beta and TNF-alpha, and size of cortical and cerebral infarctions while decreased expression of NGF and BDNF compared with the blank and sham groups. Compared with the model group, the mRNA and protein expression of CX3CL1 and CX3CR1, concentration of sFkn, IL-1 beta and TNF-alpha, and size of cortical and cerebral infarctions decreased while expression of NGF and BDNF increased in the positive control and CX3CR1 inhibitor groups. Thus, the study suggests that inhibition of fractalkine/CX3CR1 signaling pathway promotes the recovery of neurological functioning after the occurrence of an early ischemic stroke. (C) 2017 Elsevier Inc. All rights reserved.