Quercetin improves cerebral ischemia/reperfusion injury by promoting microglia/macrophages M2 polarization via regulating PI3K/Akt/NF-κB signaling pathway.

The modulation of microglial polarization from the pro-inflammatory M1 to the anti-inflammatory M2 phenotype shows promise as a therapeutic strategy for ischemic stroke. Quercetin, a natural flavonoid abundant in various plants, possesses anti-inflammatory, anti-apoptotic, and antioxidant properties. Nevertheless, its effect and underlying mechanism on microglia/macrophages M1/M2 polarization in the treatment of cerebral ischemia/reperfusion injury (CI/RI) remain poorly explored.

Chronic cocaine administration switches corticotropin-releasing factor2 receptor-mediated depression to facilitation of glutamatergic transmission in the lateral septum.

Corticotropin-releasing factor (CRF) and urocortin (Ucn I) are endogenous members among a family of CRF-related peptides that activate two different and synaptically localized G-protein-coupled receptors, CRF1 and CRF2. These peptides and their receptors have been implicated in stress responses and stress with cocaine abuse. In this study, we observed significant alterations in excitatory transmission and CRF-related peptide regulation of excitatory transmission in the lateral septum mediolateral nucleus (LSMLN) after chronic cocaine administration.

Corticotropin-releasing factor and Urocortin I modulate excitatory glutamatergic synaptic transmission.

Corticotropin-releasing factor (CRF)-related peptides serve as hormones and neuromodulators of the stress response and play a role in affective disorders. These peptides are known to alter complex behaviors and neuronal properties, but their receptor-mediated effects at CNS synapses are not well described. Here we show that excitatory glutamatergic transmission is modulated by two endogenous CRF-related peptide ligands, corticotropin-releasing factor [CRF rat/human (r/h)] and Urocortin I (Ucn I), within the central nucleus of the amygdala (CeA) and the lateral septum mediolateral nucleus (LSMLN).

Serotonin produces an enhanced outward current recorded at rat dorsal lateral septal neurons from the Flinders Sensitive Line of rats, a genetically-selected animal model of depression.

Abnormalities in serotonin (5-HT), serotonin receptors, and serotonergic neurons have been reported in studies of brains from patients diagnosed clinically with depression. In this study, we examined a known cellular function of 5-HT(1A) receptor activation in dorsolateral septal nucleus (DLSN) neurons, namely, a concentration dependent 5-HT-induced outward current, and compared basic neuronal membrane properties and activities of DLSN neurons from two known genetic lines of rats. As compared to "control" rats (Flinders Resistant Line, FRL), DLSN neurons from Flinders Sensitive Line of rats (FSL) did not exhibit significant differences in resting membrane potential, membrane input resistance, or changes in typical spontaneous inhibitory or excitatory post-synaptic currents.