Abstract
Cells throughout the body contain robust circadian rhythms important for their function. Circadian cycling of genes has been well characterized in many organs as well as in the suprachiasmatic nucleus, or SCN, which is the master circadian pacemaker in the brain. However, previous research on circadian cycling in the cerebral cortex has produced conflicting results and, for the most part, lacked cell type-specificity. Our lab has found canonical clock genes that are pivotal to the maintenance of cycling to be involved in homeostatic plasticity in excitatory neurons in the cerebral cortex. Homeostatic plasticity is a set of cellular mechanisms that bring neuronal firing rates back to baseline after large deviations in activity. Therefore, it is important to investigate if there is cyclical expression of canonical clock genes in excitatory cortical neurons. If there is cycling, this could indicate an interplay between circadian rhythms and homeostatic plasticity. If not, this suggests non-circadian functions for core clock genes in excitatory cortical neurons. We used two approaches to quantify circadian cycling in a cell-type specific manner in the cerebral cortex, quantitative polymerase chain reaction of neurons sorted by fluorescence and in situ hybridization in fluorescently labeled neurons. Currently, our results indicate that there is weak or no cycling of Bmal1 and out of phase cycling of the negative end of the feedback loop, particularly Per2, in excitatory cortical neurons.