Immunity: Where do bad emotions come from? It turns out this cell is making a fuss.

In many pathological cases, inflammatory signals in the central nervous system regulate mood.
systemic inflammation leads to the release of inflammatory media in the central nervous system, a process that has been linked to depression in humans and mice.
addition, many neurological disorders are associated with neuroinvestment, for example, levels of inflammation are associated with depression and anxiety in Parkinson's disease.
imaging and post-mortem analysis showed that small glial cell activity may lead to depressive symptoms.
recently, researchers from the Department of Biomedical and Clinical Sciences at the University of Linschepin in Sweden published a study in Immunity entitled Microglial activation elicits a negative affective state through prostaglandin-mediated modulation of striatal neurons, which found that small glial cells activate synth neuron regulation that relies on prostaglandin, which produces negative emotions and interferes with the process.
researchers first injected cre-dependent lyrovirus vectors into Cx3cr1-creER mice to selectively target synth small glial cells.
results show that the use of chlorine nitrogen flat N-oxide (CNO) to active small glial cells in the strium can induce negative emotional state.
, the researchers found that small glial cell activity was necessary to induce negative emotional states caused by systemic inflammation.
to study the effects of small glial cell activity on the excitability of ratchet neurons (MSNs) in the symposome, the researchers used CNO to stimulate Cx3cr1creer-hM3Dq and control mouse back sprite slices.
Subsequently, the current clamp records show that CNO induced small glial cell activation can lead to a decrease in MSN discharge rate, small glial cell activation also reduces the resistance of the membrane, indicating that the increase in the opening of the K-ion channel may be the cause of the decrease in MSN activity.
analysis found that after 1 hour of induced systemic inflammation, the level of IL-6 increased in the synapse and plasma.
directed injection of IL-6 into the stria can cause strong positional aversion, while systemic (intra-peritina) injections do not.
addition, local injection of IL-6R antibody toad monoantigen in the synth can completely eliminate the disgust caused by LPS.
, small glial cell-to-neuron signal transductivity mediated by prostatin E2 can cause disgust and reduce excitability.
overall, the study identified small glial cell activity as a mechanism that induces negative emotions through IL-6 and prostetin-mediated mechanisms.
targeting IL-6 subjects or prostetin signaling methods can provide new therapeutic directions for inflammation, nerve and mental illness associated with small glial cell activity, and emotional and emotional changes.
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