Neural Regeneration Research ›› 2020, Vol. 15 ›› Issue (11): 2035-2036.doi: 10.4103/1673-5374.282255

Previous Articles     Next Articles

Regulation of β2-adrenoceptors in brain glia: implications for neuroinflammatory and degenerative disorders

Karen M. Ryan1, Andrew Harkin2   

  1. 1 Trinity College Institute of Neuroscience, Trinity College Dublin; Department of Psychiatry, St. Patrick’s University Hospital, Trinity College Dublin, Dublin, Ireland   2 Neuropsychopharmacology Research Group, School of Pharmacy and Pharmaceutical Sciences & Trinity College Institute of Neuroscience, Trinity College Dublin, Dublin, Ireland
  • Online:2020-11-15 Published:2020-08-06
  • Contact: Andrew Harkin, PhD, aharkin@tcd.ie.

Abstract: Within the central nervous system (CNS), the primary source of the catecholamine neurotransmitter noradrenaline is the locus coeruleus (LC) in the pontine tegmentum, with LC neurons projecting to almost all regions of the brain and spinal cord. Following its release from LC neurons, noradrenaline has wide ranging effects. For example, noradrenaline is the endogenous agonist for G-coupled α- and β-adrenoceptors that are expressed on many cell types, including neurons and glia, in both the peripheral nervous system and CNS. It is via these receptors that noradrenaline exerts its anti-inflammatory and neurotrophic effects in the brain. Noradrenaline additionally has adrenoceptor-independent neuroprotective actions, and as such plays a role in free radical scavenging and reducing oxidative stress (Feinstein et al., 2016).