Recent studies suggest that moderate hypoglycemia impairs brainstem function in normal humans and rats. To examine whether diabetes alters this response, simultaneous auditory-evoked potentials were recorded directly from the inferior colliculus (IC) and from the brainstem before and after controlled hypoglycemia (clamp) in awake insulin-dependent diabetic BB/Wor rats. Hyperglycemic diabetic animals were studied either during hyperinsulinemic euglycemia (5.6 mmol/l, n = 4) or mild hypoglycemia (3.5 mmol/l, n = 9). Nondiabetic controls were also studied at 3.5 mmol/l (n = 7) and at 2.8 mmol/l (n = 6). Brainstem function was not affected during euglycemia in diabetic rats. However, when plasma glucose was lowered to 3.5 mmol/l, the diabetic rats showed a 10% delay in IC evoked potential (ICEP) latency, whereas nondiabetic animals did not. This occurred despite similar counterregulatory hormones in both groups. The brainstem auditory-evoked potential (BAEP) localized the defect in the diabetic group to an area in or near the IC. When glucose levels were lowered to 2.8 mmol/l, however, brain function was impaired in nondiabetic rats as well. Again the defect was restricted to an area in or near the IC. We conclude that mild hypoglycemia causes a functional impairment in the IC region of the brainstem in both nondiabetic and diabetic rats. However, in the diabetic rats, this alteration occurs after a less pronounced hypoglycemic stimulus. Our findings suggest that chronic hyperglycemia leads to metabolic adaptions that render the diabetic brain more susceptible to mild hypoglycemia.

This content is only available via PDF.