Type Diabetes

The two rodent models most commonly used for this kind of study include streptozotocin-induced diabetes in rodents and the spontaneously diabetic BB/Wor-rat. The first model develops incomplete insulin deficiency and severe hyperglycemia and is sustained without insulin supplementation. The second model develops acutely an immune-mediated ^-cell destruction with complete insulin (and C-peptide) deficiency and requires daily insulin supplementation for its survival (see Chapter 16) (36). Hence, the overriding metabolic abnormalities in these type 1 diabetic models are hyperglycemia and insulin deficiency.

Cerebral-Evoked Potentials

Electrophysiological changes arising from various brain regions, reflected by somatosensory-, visual- and auditory-evoked potentials occur in spontaneously diabetic BB/Wor-rats and the streptozotocin (STZ)-induced diabetic rats (3, 37). Like peripheral neuropathies occurring in these models, they are followed by progressive axonal degenerative changes and eventually axonal loss in the spinal cord dorsal columns and in the optic nerve (38, 39). Interestingly, such changes can be modified by insulin treatment and by aldose reductase inhibition (3, 40), paralleling the effects on peripheral neuropathy.

Cognitive Deficits

Several studies examining behavioral learning have shown progressive deficits in diabetic rodents, whereas simple avoidance tasks are preserved. Impaired spatial learning and memory as assessed by the Morris water maze paradigm occur progressively in both the spontaneously diabetic BB/Wor-rat and STZ-induced diabetic rodents (1, 11, 12, 22, 41, 42). The cognitive components reflected by impaired Morris water maze performances involve problem-solving, enhanced attention and storage, and retrieval of information (43). In the BB/Wor-rat significant deficits in latencies start to evolve after 4 months diabetes duration and progress to significant deficits in 8-month diabetic rats (Fig. 1) (1, 3,12,13).

Assessments using the radial-arm maze paradigm have shown that the cognitive sphere affected early, already at 3 months of diabetes in the BB/Wor-rat, involves memory retention (44). Insulin treatment of STZ-rats demonstrates significant prevention of Morris water maze deficits and intervention with insulin prevents further progression of cognitive function (11).

These beneficial effects are in part likely to be due to replacement of insulin -►

Fig. 1. Latencies in seconds to reach the submersed platform from the four quadrants of the Morris water maze (13) in control and type 1 diabetic BB/Wor-rats, after 2, 4, 6, and 8 months (A-D) of diabetes. The animals were placed in a circular pool of water with a constant temperature of 28° C. A platform was submerged 3 cm below the water 10 cm from the edge of the pool. The pool was divided into four quadrants and the time to reach the platform (latencies from each quadrant) was measured. Animals were trained

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