997 Int. J. Morphol., 27(4):997-1001, 2009. Resistance of CA1 Pyramidal Cells to STZ-Induced Diabetes in Young Rats Resistencia de las Células Piramidales CA1 a Diabetes Inducida por STZ en Ratas Jóvenes * Seyyed Amirhossein Fazeli; * Anneh Mohammad Gharravi; ** Mehrdad Jahanshahi; * Soraya Ghafari; *** Naser Behnampour & **** Mohammad Jafar Golalipour FAZELI, S. A.; GHARRAVI, A. M.; JAHANSHAHI, M.; GHAFARI, S.; BEHNAMPOUR, N. & GOLALIPOUR, M. J. Resistance of CA1 pyramidal cells to STZ-induced diabetes in young rats. Int. J. Morphol., 27(4):997-1001, 2009. SUMMARY: The pyramidal cell density of CA1 hippocampal subfield following STZ-induced diabetes in young rats were studied. 12 male albino 6-week Wistar rats were allocated equally in groups of normal and diabetic. Hyperglycemia induced by Streptozotocin (80 mg/kg) in animals of diabetic group. After 5 weeks of study, all the rats were sacrificed and coronal sections were taken from dorsal hippocampal formation of the right cerebral hemispheres and stained with crysel violet. The area densities of the CA1 pyramidal cells were measured and compared among two groups. No significant difference between the densities of two experimental groups was found. The results can arise from the short period of diabetes and also the possible regenerative processes in developing brain of the young diabetic rats which compensated significant diabetes-induced neuronal loss. KEY WORDS: Pyramidal cell density; CA1; Hippocampus; Diabetes; Rat. INTRODUCTION It has been shown that diabetes predisposes the patient for neuropsychiatric deficits as stroke, cerebrovascular diseases, diabetic encephalopathy, depression and anxiety (Kuhad & Chopra, 2007). Diabetic encephalopathy, characterized by impaired cognitive functions and neurochemical and structural abnormalities, involves direct neuronal damage caused by intracellular glucose (Kuhad & Chopra). Primary diabetic encephalopathy may cause by hyperglycemia and impaired insulin action diabetes. In contrast, secondary diabetic encephalopathy appears to arise from hypoxic–ischemic insults due to underlying microvascular disease or as a consequence of hypoglycemia (Sima et al., 2004). The hippocampal formation plays an important role in spatial navigation and the formation of certain types of memories (Sneider et al., 2006). Subregional models of hippocampal function suggest that CA1 function is critical in correctly identifying novel relationships among objects within a particular spatial context. Furthermore, it is proposed that CA1 is not necessary for short-term (<5 min), but is specifically invested in intermediate-term (5 min to 24 h) maintenance and retrieval of the familiar spatial context (Vago & Kesner, 2008). The impairment of CA1 hippocampal subfield has been reported by previous studies. Biessels et al. who demonstrated either a lack of inducible long-term potentiation of CA1 or a decreased slope of excitory postsynaptic potentials from the same field, suggested both pre- and postsynaptic impairments of CA1 (Biessels et al.,1996). The morphologic changes of CA1 following type 1 diabetes have shown some discrepancies. Some data suggested an apoptosis-induced neuronal loss in type 1 diabetes (Li et al., 2002). The findings indicate that neuronal apoptosis occurs only after a prolonged duration of diabetes and that it may be duration-related (Li et al.). In contrast, it has been shown that a short period of type 1 diabetes can be associated with an increase in small neurons in CA1 hippocampal subfield of the young rats (Malone et al., 2006). * Department of Embryology and Histology, Gorgan University of Medical Sciences, Gorgan, Iran. ** Assistant professor, Department of Anatomy, Gorgan University of Medical Sciences, Gorgan, Iran. *** Department of Health, Gorgan University of Medical Sciences, Gorgan, Iran. **** Professor, Department of Anatomical Sciences (Embryology and Histology), Gorgan University of Medical Sciences, Gorgan, Iran.