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Reactive astrocytosis is a well-known phenomenon that occurs rapidly after physical or metabolic injury to the brain. One of the important events during astrocyte differentiation is the increased expression of glial fibrillary acidic protein (GFAP), a member of the family of intermediate filament structural proteins. Free radicals are neurotoxic and free radical scavengers have been shown to protect the brain against neurotoxic damage. In the present study, we examined the effect of melatonin on astrocytic reactivity by determining the expression of the glial marker, GFAP, in different brain regions. Rats were exposed to constant light to reduce endogenous melatonin production; half of the animals were injected with melatonin during the exposure to constant light for 7 days. Western blots showed increases in total and degraded GFAP content in the brain of rats exposed to constant light. Melatonin administration caused a reduction of degraded GFAP content. In addition, melatonin significantly reduced neural tissue lipid peroxidation while constant light significantly enhanced the breakdown of lipids in the brain. Brain glutathione levels decreased significantly as a result of constant light exposure; this reduction was reversed by melatonin administration. These results suggest that melatonin potentially protects both neurons and glial cells from free radicals; melatonin's protective actions are probably related to the antioxidant properties of the indole.

We examined, using a Western blot technique, the contents and compositions of a specific neuronal protein, NCAM, and of an astrocyte marker, GFAP, in the hippocampus and cortex of rats with streptozotocin (STZ)-induced diabetes and compared these indices with those in control (intact) animals and STZ-diabetic rats treated with melatonin. Behavioral cognitive indices manifested in the passive avoidance test (PAT) and Morris water maze (MWM) learning performance were also estimated in the above groups of animals. As was found, STZ-diabetic rats demonstrated clear cognitive deficits according to the values of the retention latency in the PAT and time of reaching the escape platform in the MWM performance. In these animals, the GFAP content was elevated, and the amount of degraded products of this protein increased, as compared with the control. Simultaneously, considerable down-regulation of the NCAM expression and modifications of NCAM isoform composition were found in diabetic animals. In addition, significantly increased levels of lipid peroxidation (according to the amounts of malondialdehyde + 4-hydroxyalkenals) were measured in the cortex and hippocampus of rats with stable diabetic hyperglycemia. All the above-mentioned shifts were significantly smoothed or even nearly completely compensated in the case of treatment of STZ-diabetic rats with melatonin (10 mg/kg per day). The role of diabetes-related changes in the amount and composition of specific neural and glial proteins in the development of cognitive deficits, the involvement of oxidative stress in the mechanisms of the respective shifts, and possible mechanisms of the neuroprotective effect of melatonin with respect to diabetes-related pathological biochemical and behavioral shifts are discussed.

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