Water maze learning and hippocampal synaptic plasticity in streptozotocin-diabetic rats: effects of insulin treatment

• Published in: Brain research Vol. 800; no. 1; pp. 125 - 135
• Main Authors: Biessels, Geert-Jan, Kamal, Amer, Urban, Ivan J.A, Spruijt, Berrie M, Erkelens, D.Willem, Gispen, Willem Hendrik
• Format: Journal Article
• Language: English
• Published: London Elsevier B.V 27.07.1998; Amsterdam Elsevier; New York, NY
• Subjects: Animals; Biological and medical sciences; Diabetes; Diabetes Mellitus, Experimental - drug therapy; Diabetes Mellitus, Experimental - physiopathology; Diabetes Mellitus, Experimental - psychology; Diabetes. Impaired glucose tolerance; Endocrine pancreas. Apud cells (diseases); Endocrinopathies; Etiopathogenesis. Screening. Investigations. Target tissue resistance; Hippocampus; Hippocampus - drug effects; Hippocampus - physiology; Hippocampus - physiopathology; Insulin; Insulin - therapeutic use; Learning; Long-term potentiation; Male; Maze Learning - drug effects; Medical sciences; Motor Neurons - physiology; Neural Conduction; Neuronal Plasticity - drug effects; Neuronal Plasticity - physiology; Neurons, Afferent - physiology; Rats; Rats, Wistar; Reference Values; Sciatic Nerve - drug effects; Sciatic Nerve - physiology; Sciatic Nerve - physiopathology; Space Perception - drug effects; Space Perception - physiology; Synapses - drug effects; Synapses - physiology; Time Factors; Water maze; Learning; Diabetes; Insulin; Long-term potentiation; Hippocampus; Water maze; Endocrinopathy; Potentiation; Pancreatic hormone; Rat; Diabetes mellitus; Rodentia; Central nervous system; Spatial orientation; Space perception; Long term; Vertebrata; Mammalia; Acquisition process; Animal; Synaptic plasticity; Perception; Perceptive learning; Brain (vertebrata)
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(98)00510-1

Streptozotocin-diabetic rats express deficits in water maze learning and hippocampal synaptic plasticity. The present study examined whether these deficits could be prevented and/or reversed with insulin treatment. In addition, the water maze learning deficit in diabetic rats was further characterized. Insulin treatment was commenced at the onset of diabetes in a prevention experiment, and 10 weeks after diabetes induction in a reversal experiment. After 10 weeks of treatment, insulin-treated diabetic rats, untreated diabetic rats and non-diabetic controls were tested in a spatial version of the Morris water maze. Next, hippocampal long-term potentiation (LTP) was measured in vitro. To further characterize the effects of diabetes on water maze learning, a separate group of rats was pre-trained in a non-spatial version of the maze, prior to exposure to the spatial version. Both water maze learning and hippocampal LTP were impaired in diabetic rats. Insulin treatment commenced at the onset of diabetes prevented these impairments. In the reversal experiment, insulin treatment failed to reverse established deficits in maze learning and restored LTP only partially. Non-spatial pre-training abolished the performance deficit of diabetic rats in the spatial version of the maze. It is concluded that insulin treatment may prevent but not reverse deficits in water maze learning and LTP in streptozotocin-diabetic rats. The pre-training experiment suggests that the performance deficit of diabetic rats in the spatial version of the water maze is related to difficulties in learning the procedures of the maze rather than to impairments of spatial learning.