The basal forebrain (BF) constitutes a major neuromodulatory center, providing extensive projections to the entire forebrain, including all of cortex. Mounting evidence demonstrates that these projections play a key role in cognitive functions, including learning and attention. Damage or deterioration of BF in humans leads to severe cognitive impairments, such as dementia and executive dysfunction. Given the association of BF with higher cognitive functions and a host of disease states, surprisingly little is known about how it accomplishes these intricate tasks. This is largely due to technical challenges because BF neurons expressing the neuromodulatory transmitter acetylcholine are intermingled with a parallel inhibitory (GABAergic) projection system within a confined anatomical area and traditional techniques do not allow separating these two projection systems in behaving animals.The Kepecs group at CSHL have two techniques that are uniquely suitable to tackle this challenge. First, they successfully adapted the quantitative psychophysical methods of primate neuroscience—the current gold standard in research on the neural mechanisms of cognition—for use in mice, enabling us to employ molecular-genetic tools. Second, they developed an “optogenetic tagging” technique to selectively record from and control genetically identified neurons.With these methods I propose to study how different BF subsystems support sustained attention and spatial learning. I will record from identified BF neurons to establish the moment-to-moment correlation between neural activity and behavioral measures (e.g. reaction time). Gaining control over identified neurons at high temporal precision will also enable me to establish their necessity and sufficiency for behavioral functions on a trial-to-trial basis.Learning and transferring these cutting-edge techniques to Hungary will benefit both my return host laboratory and enable me to transition to an independent researcher position.