• M E Brocca, L Pietranera, P Roig, A Lima, and A F De Nicola.
• Laboratory of Neuroendocrine Biochemistry, Instituto de Biología y Medicina Experimental, Buenos Aires, Argentina.
• Neuroscience. 2014 Nov 7;280:243-53.

AbstractPrevious work has shown a reduction of apical dendritic length and spine density in neurons from the CA1 hippocampus subfield of spontaneously hypertensive rats (SHRs). These abnormalities are prevented by treatment for 2 weeks with 17β-estradiol. In view of the fact that diabetes and hypertension are comorbid diseases, we have now studied the effect of Streptozotocin-induced diabetes on the dendritic tree and spines of CA1 hippocampus neurons, and also compared the regulation of these parameters by 17β-estradiol in diabetic and normoglycemic SHR. Twenty-week-old male SHR received i.v. 40-mg/kg Streptozotocin or vehicle and studied 1 month afterward. A group of normoglycemic and hyperglycemic SHR also received s.c. a single 17β-estradiol pellet or vehicle for 2weeks. Hippocampus sections were impregnated with silver nitrate following a modified Golgi's method and the arbor of CA1 pyramidal neurons analyzed by Sholl's method. 17β-Estradiol treatment of normoglycemic SHR reversed the reduced length of apical dendrites, the low spine density and additionally decreased blood pressure (BP). Diabetic SHR showed increased length of apical and basal dendrites but reduced spine density compared to normoglycemic SHR. Diabetes also decreased BP of SHR. Treatment with 17β-estradiol of diabetic SHR enhanced dendritic length, increased dendritic spine density and further decreased BP. Thus, changes of cytoarchitecture of CA1 neurons due to 17β-estradiol treatment of normoglycemic SHR persisted after diabetes induction. A decrease of BP may also contribute to the central effects of 17β-estradiol in SHR diabetic rats.Copyright © 2014 IBRO. Published by Elsevier Ltd. All rights reserved.

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