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Up-regulation of ?2AR after brain damage in vivo induces neurotrophic growth factors release, activates astrocytes, and regulates microglial activation mediating neuroprotection in several models of neuronal damage 1. Microglia, the innate immunity cells in the brain, express high levels of ?2AR at their cell surface. Many studies have found that depletion of norepinephrine (NE), the endogenous ?2AR agonist, increased the microglial-induced neuroinflammation and administration of NE protects the neurons from microglial-induced cell death 2,3. NE administration causes dose-dependent blockage of microglial expression of the inflammatory mediators such as tumor necrosis factor ? (TNF ?), interleukin-1 ? (IL-1 ?), interleukin-6 (IL-6), reactive oxygen species (ROS), and nitric oxide 4.

In a rat model of traumatic brain injury (TBI), Zlotnik et al. have showed that ?2AR agonists decreased blood glutamate levels which are typically increased in response to injury and are generally neurotoxic and those agonists induced neuroprotection after TBI, decreased brain function impairment and improved recovery after

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injury 5.


Also, ?2AR antagonists were found to block interleukin -6 production and acute inflammatory response providing neuroprotection in a rat model of hemorrhagic stroke 6. In contrast, the same antagonist did not cause any neuroprotective effect in a model of focal cerebral ischemia. In this model, the antagonist abrogated the

neuroprotection achieved by treatment with ?2AR agonists 7.

These diverse results could be due to the differences between

the two models of stroke brain-damage and the mechanisms responsible for the damage.


In all these studies, the models required pretreatment with the ?2AR agonists (or antagonist) for neuroprotection. In contrast, treating an LPS-stimulated rodent model of Parkinson’s disease with the long-acting agonist after initiation of the disease inhibited microglial activation and prevented neurotoxicity 8.


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