CX3CL1 Human ELISA Kit

y With the rise of e-cigarette use, teen nicotine exposure is becoming more widespread. Findings from clinical and preclinical studies show that the adolescent brain is particularly sensitive to nicotine. Animal studies have demonstrated that adolescent nicotine exposure increases reinforcement for cocaine and other drugs. However, the mechanisms that underlie these behaviors are poorly understood. Here, we report reactive microglia are critical regulators of nicotine-induced increases in adolescent cocaine self-administration. Nicotine has dichotomous, age-dependent effects on microglial morphology and immune transcript profiles. A multistep signaling mechanism involving D2 receptors and CX3CL1 mediates nicotine-induced increases in cocaine self-administration and microglial activation. Moreover, nicotine depletes presynaptic markers in a manner that is microglia-, D2- and CX3CL1-dependent. Taken together, we demonstrate that adolescent microglia are uniquely susceptible to perturbations by nicotine, necessary for nicotine-induced increases in cocaine-seeking, and that D2 receptors and CX3CL1 play a mechanistic role in these phenomena.

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.