Blood flow and metabolism in heterotopic cerebellar grafts during hypoglycemia.

Published

Journal Article

Hypoglycemia-induced disturbances of brain metabolism and neuronal injury exhibit a distinct predilection for forebrain structures, in particular the caudate-putamen, hippocampus and cerebral cortex, whereas the cerebellum is remarkably resistant. In an attempt to assess the biological basis of this differential regional vulnerability, we have used a neural transplantation technique to compare hemodynamic and metabolic changes in cerebellum during severe hypoglycemia with those in heterotopic cerebellar grafts. To this end, the cerebellar anlage of fetal rat brain (day 15 of gestation) was stereotactically transplanted into the vulnerable caudate-putamen. Following a differentiation period of 8 weeks the grafts had developed into an organotypic population of mature cells with laminar histoarchitecture. Host animals were then subjected to insulin-induced hypoglycemia. After 15 min of isoelectric EEG, blood flow was increased throughout the brain but residual glucose consumption was significantly higher in cerebellum (0.29 mumol/g per min) and cerebellar grafts (0.22 mumol/g per min) as a result of increased glucose extraction. Hypoglycemia caused a depletion of ATP in all brain structures except cerebellum where normal levels were maintained. Correlation of local ATP content and glucose utilization revealed a threshold-like decline of ATP at a glucose utilization rate of 0.27 mumol/g per min. ATP, in consequence, was normal in cerebellum but partially depleted in cerebellar grafts. It is concluded that the resistance of cerebellum to hypoglycemia is due to its capacity for higher glucose extraction at low blood glucose levels, and that this unique intrinsic property is preserved after heterotopic transplantation.

Full Text

Cited Authors

  • Kiessling, M; Mies, G; Paschen, W; Thilmann, R; Detmar, M; Hossmann, KA

Published Date

  • January 1988

Published In

Volume / Issue

  • 77 / 2

Start / End Page

  • 142 - 151

PubMed ID

  • 3227812

Pubmed Central ID

  • 3227812

Electronic International Standard Serial Number (EISSN)

  • 1432-0533

International Standard Serial Number (ISSN)

  • 0001-6322

Language

  • eng