Cadre stéréotaxique portable (design allégé) pour Rat

Publications

GABAergic ventrolateral pre‑optic nucleus neurons are involved in the mediation of the anesthetic hypnosis induced by propofol

Jie Yuan et al. Molecular Medicine Reports 2017

Intravenous anesthetics have been used clinically to induce unconsciousness for seventeen decades, however the mechanism of anesthetic‑induced unconsciousness remains to be fully elucidated. It has previously been demonstrated that anesthetics exert sedative effects by acting on endoge­nous sleep‑arousal circuits. However, few studies focus on the ventrolateral pre‑optic (VLPO) to locus coeruleus (LC) sleep‑arousal pathway. The present study aimed to investigate if VLPO is involved in unconsciousness induced by propofol. The present study additionally investigated if the inhibitory effect of propofol on LC neurons was mediated by activating VLPO neurons. Microinjection, target lesion and extracellular single‑unit recordings were used to study the role of the VLPO‑LC pathway in propofol anesthesia. The results demonstrated that GABAA agonist (THIP) or GABAA antagonist (gabazine) microinjections into VLPO altered the time of loss of righting reflex and the time of recovery of righting reflex. Furthermore, propofol suppressed the spontaneous firing activity of LC noradrenergic neurons. There was no significant difference observed in firing activity between VLPO sham lesion and VLPO lesion rats. The findings indicate that VLPO neurons are important in propofol‑induced unconsciousness, however are unlikely to contribute to the inhibitory effect of propofol on LC spontaneous firing activity.

Neural repair by NT3-chitosan via enhancement of endogenous neurogenesis after adult focal aspiration brain injury

PengHao et al.  Biomaterials 2017

The latent regenerative potential of endogenous neural stem/progenitor cells (NSCs) in the adult mammalian brain has been postulated as a likely source for neural repair. However, the inflammatory and inhibitory microenvironment after traumatic brain injury (TBI) prohibits NSCs from generating new functional neurons to restore brain function. Here we report a biodegradable material, chitosan, which, when loaded with neurotrophin-3 (NT3) and injected into the lesion site after TBI, effectively engaged endogenous NSCs to proliferate and migrate to the injury area. NSCs differentiate and mature into functional neurons, forming nascent neural networks that further integrate into existing neural circuits to restore brain function. Three main actions of NT3-chitosan, i.e., pro-neurogenesis, anti-inflammation, and pro-revascularization, elicit significant regeneration after TBI. Our study suggests that through creating an optimal microenvironment, endogenous NSCs are capable of executing neural repair, thus widening the therapeutic strategies to treat TBI and perhaps stroke or other neurological conditions.