Lesions of the glutamatergic cortico-striatal projections in the rat ameliorate hypoglycemic brain damage in the striatum.
Unilateral ablations of the motor cortex were performed on rats. One to two weeks following the ablation they were subjected to 30 min of reversible insulin-induced hypoglycemic coma. The levels of glutamate, aspartate, gamma-aminobutyric acid (GABA), taurine, adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP) and phosphocreatine (PCr) were determined in frozen tissue sections from the superior half of the caudate nucleus. The lesions induced a specific reduction in the levels of glutamate by approx. 10% in the dorsal caudate nucleus ipsilateral to the lesion, while no significant differences in the levels of aspartate, GABA, taurine, ATP, ADP, AMP or PCr were noted. Neuronal necrosis in the caudate nucleus in animals subjected to 30 min of insulin-induced hypoglycemic coma and one week recovery was assessed by light microscopy. Contralateral to the lesion, extensive neuronal necrosis, mainly affecting small and medium-sized neurons, was observed in the dorsal and lateral caudate nucleus. In the caudate ipsilateral to the lesion a complete amelioration of necrosis was noted in areas subjacent to the lesion. The data suggest that hypoglycemic brain damage is induced by excitotoxins such as glutamate or related compounds.
Wieloch
T
T
Engelsen
B
B
Westerberg
E
E
Auer
R
R
D000818:Animals; D001925:Brain Damage, Chronic / Q000209:etiology* / Q000473:pathology; D002421:Caudate Nucleus / Q000378:metabolism / Q000473:pathology; D002540:Cerebral Cortex / Q000502:physiology*; D003342:Corpus Striatum / Q000502:physiology*; D005971:Glutamates / Q000378:metabolism / Q000502:physiology*; D018698:Glutamic Acid; D007003:Hypoglycemia / Q000150:complications*; D051381:Rats; D011919:Rats, Inbred Strains; D009435:Synaptic Transmission
D005971:Glutamates; D018698:Glutamic Acid