Differential alterations of second messenger systems and cerebral glucose use following excitotoxic lesion of rat cerebral cortex.

Quantitative autoradiography of [3H]forskolin and [3H]phorbol 12,13 dibutyrate (PDBu) binding was examined 21 days after unilateral lesioning of the rat visual cortex using ibotenic acid. In the same animals, the functional deficit was assessed using quantitative [14C]-2-deoxyglucose autoradiography. [3H]Forskolin binding was significantly reduced in each layer of the lesioned visual cortex by at least 40% compared to the contralateral hemisphere. Significant reductions in [3H]forskolin binding were observed in the superior colliculus (-15%) and dorsal lateral geniculate body (-12%) ipsilateral to the lesioned cortex. [3H]PDBu binding was significantly reduced in the lesioned visual cortex (layers V-VI) by 34%, compared with the control hemisphere. There were no significant alterations in [3H]DPBu binding in any other brain regions. Following ibotenate-induced lesioning of the visual cortex, glucose use was significantly reduced throughout the lesioned cortex by at least 25% with minor alterations in glucose use in the ipsilateral dorsal lateral geniculate body and superior colliculus. The present study highlights the relative robustness of [3H]PDBu binding compared to [3H]forskolin binding after excitotoxic damage to the cerebral cortex and suggests that [3H]forskolin binding sites are present on cortical efferent fibres.