Molecular Plasticity
Why do we need to sleep and what are the regulating mechanisms behind the sleep-wakefulness cycle? Which factors influence synaptic plasticity and how is neuroreceptor expression influenced? These questions describe the main research interests of the team.
Current projects investigate:
The effects of chronic sleep restriction on the adenosine receptor availability in healthy human volunteers.
The effects of optogenetic and chemogenetic stimulation on neuroreceptor expression or neurotransmitter binding. The goal of this research is to determine the role of specific wake promoting neuronal populations on neurotransmitter availability and metabolism in cortical regions. The overarching hypothesis is:
“Cortically projecting cholinergic neurons of the basal forebrain area are an essential mediator of cortical activation and neuromodulator release during sleep deprivation”.
The objectives include a setup of a sleep deprivation model by selective optogenetic stimulation of the nucleus basalis Meynert and determination of the metabolic changes that occur during optogenetic stimulation of the nuclei with glucose PET.
These changes will be compared with neuroreceptor availability changes that occur during optogenetic stimulation of the nuclei with glutamate receptor PET and adenosine receptor.
Information on the depiction of synaptic plasticity during therapeutic sleep deprivation can be found at Sleepless.
Information on the influence of daily coffee consumption on cognitive performance compared to chronic sleep deprivation can be found at PET Kaffee.
An overview of all INM-2 publications can be found here.