A growing body of evidence suggests that glial cells are involved in practically all aspects of neural function. Glial cells regulate the homeostasis of the brain, influence the development of the nervous system, modulate synaptic activity, and carry out the immune response inside the brain. In addition, they play an important role in the restoration of the nervous system after damage, and they also participate in various neurodegenerative disorders. In a similar way, the importance of stress and glucocorticoids (GCs) on brain function is being increasingly recognized. Within the brain, stress hormones target both neurons and glial cells. Through their actions on these cells, glucocorticoids exert organizational functions on various processes of the developing brain and contribute to neuronal plasticity in the adult brain. Moreover, stress and glucocorticoids have become especially attractive in the study of a number of neurodegenerative disorders. However, studies on the mechanisms behind glucocorticoid-induced regulation of brain function have been classically focused on their effects on neurons. In this review, we start by describing the main functions of glial cells and then proceed to present data highlighting the effects of stress and GCs on brain function. We conclude the review by presenting recent evidence linking stress and glucocorticoids to glial cell function.

Parkinson’s disease (PD) is one of the most common neurodegenerative disorders and is characterized by the loss of dopaminergic neurons in the substantia nigra (SN). Although the causes of PD are not understood, evidence suggests that its pathogenesis is associated with oxidative stress and inflammation. Recent studies have suggested a protective role of the cannabinoid signalling system in PD. β-caryophyllene (BCP) is a natural bicyclic sesquiterpene that is an agonist of the cannabinoid type 2 receptor (CB2R). Previous studies have suggested that BCP exerts prophylactic and/or curative effects against inflammatory bowel disease through its antioxidative and/or anti-inflammatory action. The present study describes the neuroprotective effects of BCP in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced murine model of PD, and we report the results of our investigation of its neuroprotective mechanism in neurons and glial cells. In the murine model, BCP pretreatment ameliorated motor dysfunction, protected against dopaminergic neuronal losses in the SN and striatum, and alleviated MPTP-induced glia activation. Additionally, BCP inhibited the levels of inflammatory cytokines in the nigrostriatal system. The observed neuroprotection and inhibited glia activation were reversed upon treatment with the CB2R selective antagonist AM630, confirming the involvement of the CB2R. These results indicate that BCP acts via multiple neuroprotective mechanisms in our murine model and suggest that BCP may be viewed as a potential treatment and/or preventative agent for PD.

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