Odor increases [3H]phorbol dibutyrate binding to protein kinase C in olfactory structures of the brain. Effect of entorhinal cortex lesion

FAILLACE M.P., ZWILLER, J., DI SCALA, G. AND BERNABEU, R.

MOLECULAR BRAIN RESEARCH

ELSEVIER

Año: 2006 vol. 1068 p. 16 - 22

0169-328X

Since protein kinase C (PKC) is known to be activated in the olfactory bulb and inseveral limbic areas related to odor processing, we determined whether an olfactorystimulus was able to modulate the activity of PKC in animals with bilateral entorhinalcortex lesion. The translocation of PKC from the cytosol to the membrane was studiedusing the phorbol ester 12,13-dibutyrate ([3H]PDBu) binding in control and bilateralentorhinal cortex (EC) lesioned rats. The lesion of EC per se did not significantly affect[3H]PDBu binding in any of the brain structures analyzed, while odor stimulationinduced it in both control and EC-lesioned groups in the external plexiform layer of theolfactory bulb. In contrast, an odor-induced increase of [3H]PDBu binding in internalglomerular layer of the olfactory bulb was only observed in EC lesioned animals. Similarresults were obtained in the piriform cortex. In both CA1 and CA3 hippocampalsubfields, odor stimulation induced an increase of [3H]PDBu binding in both control andEC-lesioned animals, the increase being potentiated only in CA1 of lesioned rats. Thedentate gyrus and the amygdala exhibited a similar pattern of [3H]PDBu binding,showing a significant increase exclusively in EC-lesioned animals after odor stimulation.The results strongly suggest that the EC plays a key role in odor processing. PKC appearsto play an important role in responding to the activation of lipid second messengers,which have been described to be involved in the processing of odor stimuli in severalstructures of the olfactory pathway.