Activity-dependent constraints on catecholamine signaling
Li Li,
Akshay N. Rana,
Esther M. Li,
Jiesi Feng,
Yulong Li,
Michael R. Bruchas
Affiliations
Li Li
Department of Anesthesiology & Pain Medicine, University of Washington, Seattle, WA 98195, USA; Center for Neurobiology of Addiction, Pain, and Emotion, University of Washington, Seattle, WA 98195, USA; Seattle Children’s Research Institute, Seattle, WA 98101, USA; Corresponding author
Akshay N. Rana
Department of Anesthesiology & Pain Medicine, University of Washington, Seattle, WA 98195, USA; Center for Neurobiology of Addiction, Pain, and Emotion, University of Washington, Seattle, WA 98195, USA
Esther M. Li
Department of Anesthesiology & Pain Medicine, University of Washington, Seattle, WA 98195, USA; Center for Neurobiology of Addiction, Pain, and Emotion, University of Washington, Seattle, WA 98195, USA; Department of Psychology, University of Washington, Seattle, WA 98105, USA
Jiesi Feng
State Key Laboratory of Membrane Biology, School of Life Sciences, Peking University, Beijing 100871, China
Yulong Li
State Key Laboratory of Membrane Biology, School of Life Sciences, Peking University, Beijing 100871, China; PKU-IDG/McGovern Institute for Brain Research, Beijing 100871, China; Peking-Tsinghua Center for Life Sciences, New Cornerstone Science Laboratory, Academy for Advanced Interdisciplinary Studies, Peking University, Beijing 100871, China
Michael R. Bruchas
Department of Anesthesiology & Pain Medicine, University of Washington, Seattle, WA 98195, USA; Center for Neurobiology of Addiction, Pain, and Emotion, University of Washington, Seattle, WA 98195, USA; Department of Bioengineering, University of Washington, Seattle, WA 98105, USA; Department of Pharmacology, University of Washington, Seattle, WA 98195, USA; Corresponding author
Summary: Catecholamine signaling is thought to modulate cognition in an inverted-U relationship, but the mechanisms are unclear. We measured norepinephrine and dopamine release, postsynaptic calcium responses, and interactions between tonic and phasic firing modes under various stimuli and conditions. High tonic activity in vivo depleted catecholamine stores, desensitized postsynaptic responses, and decreased phasic transmission. Together, these findings provide a more complete understanding of the inverted-U relationship, offering insights into psychiatric disorders and neurodegenerative diseases with impaired catecholamine signaling.
