An In Vivo And In Vitro Comparative Study On The Mechanism Of The Selective Vulnerability Of The Inferior Colliculus In Experimental Thiamine-Deficient Encephalopathy

We analyzed the mechanism of the selective vulnerability in the midbrain which results in time inferior colliculus being affected, but the adjacent superior colliculus usually being spared, in thiamine-deficient encephalopathy. After first confirming in an in vivo, experiment that the same selective vulnerability occurs in weanling rats, fragments of the superior and inferior colliculi of embryonic day 18 of fetal rats were cultured in nutrient medium for three weeks and then cultured in a thiamine-free medium with or without the addition of pyrithiamine in concentrations of 10(-7) mol/L, 10(-5) mol/L, and 10(-4) mol/L, for a maximum of two additional weeks, In vitro, as early as the third day of thiamine deficiency, ultrastructural examination showed hydropic swelling of the neuronal processes and then of the perikarya that later resulted in cell death in the superior and inferior colliculi. In contrast to the in vivo findings, the astrocytes and oligodendrocytes were relatively preserved, These changes occurred equally in both cultured tissue of the inferior colliculus and of the superior colliculus. It was confirmed in arm in vitro recovery experiment that these changes were attributable to thiamine deficiency not pyrithiamine-toxicity, and that their severity paralleled the concentration of pyrithiamine. On the basis of these findings, two possible mechanisms ape proposed to explain the selective vulnerability of the inferior colliculus in thiamine-deficient encephalopathy: (i) functional and/or structural specificity of the blood vessels in the inferior colliculus; or (ii) peculiarities of the neuronal inputs into it.