Neuronal Plasticity and Antidepressants in the Diabetic Brain.

BEAUQUIS J; ROIG P; DE NICOLA AF; SARAVIA F

Río de Janeiro, Brasil

Congreso; VII Congress of the International Society for NeuroImmunoModulation.; 2008

International Society for NeuroImmunoModulation

Diabetes correlates with several brain alterations, being the hippocampus one of the more affected structures. Type 1 Diabetes patients present elevated risk of cognitive impairment, stroke, dementia and Alzheimer disease. Moreover, depression is strongly associated with this autoimmune disease. Some authors proposed a link between depression and low hippocampal neurogenesis. In this line, we reported a marked reduction in neurogenic ability in spontaneous and streptozotocin-induced diabetic mice, where the antidepressant fluoxetine (FXT) was able to prevent it. Remarkably FXT had no effect on control mice. In order to explore other potential consequences of antidepressant treatment on limbic structures, we performed a morphological study of the dendritic tree associated to pyramidal neurons in the hippocampus of diabetic mice treated with FXT. With this purpose, a modified silver impregnation Golgi technique was used. The total dendritic length of CA1 and CA3 neurons measured by computerized analysis showed a clear decrease in diabetic mice group compared to controls. The Sholl analysis- that allows the neuron image reconstruction integrating different focuses- undoubtedly revealed less branching of basal dendrites in diabetic animals. Diabetic mice treated with FXT during 10 days exhibited a strong reversion in these parameters, with values similar to controls. Diabetic mice displayed a decreased spine density in CA3 neurons compared with control animals; but FXT treatment restored spine density to control levels. Our results are firstly, an additional evidence for the deleterious effects of diabetes on brain hippocampal plasticity that could be related to depression incidence, and secondly, a new support of the positive effect that antidepressant treatment exerts on dendritic tree plasticity and consecutively on synaptic connectivity.