Behavioral Neuroscience Projects

Contacts: Valter Tucci (Team Leader), Glenda Lassi (Research fellow).

In mammals the identification of the three main states, wakefulness, NREM and REM sleep, has been widely documented.

However, no clear explanation has been offered as to why we have different sleep states. Data from experimental and clinical studies suggest that both NREM and REM sleep may be regulated by separate sets of genes. Some of these genes may be imprinted. For example, Prader-Willi syndrome and Angelman syndrome are neurodevelopmental syndromes that exhibit opposite imprinting profiles and, interestingly, opposite sleep disturbances.

Other evidence implies that maternally-expressed 5HT2A receptors mediate aminergic inhibition of REM-on cells in the parabrachialis lateralis region, but that paternally expressed GABA B receptors may mediate inhibition of these aminergic inhibitory effects on REM, thus facilitating REM expression. These data are consistent with a conflict model wherein NREM expression is aligned with matriline genes, while REM is aligned with patriline genes. We will test the hypothesis that maternal and paternal line genes regulate different states of sleep (NREM vs. REM sleep) and modulate cognitive processing during sleep.

If it could be demonstrated that imprinted genes influence sleep and cognitive expression, this would open up new theoretical and clinical perspectives on sleep and cognition.