Noradrenergic regulation of glial activation: molecular mechanisms and therapeutic implications.

摘要: It has been known for many years that the endogenous neurotransmitter noradrenaline (NA) exerts anti-inflammatory and neuroprotective effects both in vitro vivo. In cases site of action NA are beta-adrenergic receptors (βARs), causing an increase intracellular levels cAMP which initiates a broad cascade events including suppression inflammatory transcription factor activities, alterations nuclear localization proteins, induction patterns gene expression mediated through activity CREB factor. These changes lead not only to reduced events, but also contribute actions by increasing neurotrophic substances BDNF, GDNF, NGF. properties have prompted studies determine if treatments with drugs raise CNS could provide benefit various neurological conditions diseases having component. Moreover, evidence shows disruptions occurs several Alzheimer’s disease (AD), Parkinson’s (PD), Down’s syndrome, posttraumatic stress disorder (PTSD), multiple sclerosis (MS), suggesting damage producing neurons is common contributes initiation or progression neuropathology. Methods levels, reduce noradrenergic neurons, therefore represent potential preventative as well therapeutic approaches disease.