BRAIN-STEM DYSFUNCTION IS PROVOKED BY A LESS PRONOUNCED HYPOGLYCEMIC STIMULUS IN DIABETIC BB RATS

Recent studies suggest that moderate hypoglycemia impairs brainstem fu nction in normal humans and rats. To examine whether diabetes alters t his response, simultaneous auditory-evoked potentials were recorded di rectly 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 eith er during hyper-insulinemic euglycemia (5.6 mmol/l, n = 4) or mild hyp oglycemia (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 wa s not affected during euglycemia in diabetic rats. However, when plasm a glucose was lowered to 3.5 mmol/l, the diabetic rats showed a 10% de lay 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 gl ucose levels were lowered to 2.8 mmol/l, however, brain function was i mpaired in nondiabetic rats as well. Again the defect was restricted t o 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 non diabetic and diabetic rats. However, in the diabetic rats, this altera tion occurs after a less pronounced hypoglycemic stimulus. Our finding s suggest that chronic hyperglycemia leads to metabolic adaptions that render the diabetic brain more susceptible to mild hypoglycemia.