Project Summary
Neuromodulatory systems, including the locus coeruleus – norepinephrine (LC-NE) system (i.e. noradrenergic
system), exert heavy influences on sensory perception and perceptual behavior. In sensory pathways, the
thalamus is strategically positioned to dynamically gate information flow to the cortex. Previous work has
demonstrated that the timing across population thalamic neurons switched the nature of information flow to the
cortex and the switch was manifested in perceptual behavior. More recent work showed that LC activation
increased the feature selectivity of individual thalamic relay neurons, and this improvement was due to LC
regulation of the interplay between the thalamic relay nucleus and thalamic reticular nucleus. However, how
the population coding of sensory information by thalamic neurons is modulated by the LC-NE system remains
mostly unknown. The LC is the primary source of norepinephrine to the forebrain, and the malfunction of the
LC-NE system has been implicated in major clinical disorders, including schizophrenia, Parkinson’s disease
(PD), Alzheimer’s disease, attention deficit hyper-activity disorder (ADHD), and depression. Moreover,
abnormal activity in the thalamus has been implicated in brain disorders, including PD, central pain syndrome,
and depression. The diversity supplement project will examine the influence of the LC – NE system on
thalamic population coding of tactile signals. More specifically, using neuropixels recording in awake thalamus
in concert with chemogenetic stimulation of the LC, we will 1) characterize the population coding of a variety of
properties of tactile signals, including amplitude, velocity, and direction etc., for neurons in the thalamic relay
nucleus and thalamic reticular nucleus with and without LC stimulation, and 2) examine the contribution of
thalamic population response to tactile detection performance with and without LC stimulation. This project will
provide much-needed insight about how the LC-NE systems modulates thalamic sensory processing. Such
information is essential to better understand neurological disorders in which abnormal thalamic activity and
noradrenergic activity have been reported.
