TY - JOUR
T1 - Remote control of glucose-sensing neurons to analyze glucose metabolism
AU - Alvarsson, Alexandra
AU - Stanley, Sarah A.
N1 - Funding Information:
A. Alvarsson is supported by a postdoctoral fellowship from the Swedish Society for Medical Research. Support for this work was also provided by National Institutes of Health Grants MH-105941 and 1R01 NS-097184, American Diabetes Association Grant 1-17-ACE-31, an Einstein-Mt. Sinai Diabetes Research Center Pilot and Feasibility Award (National Institute of Diabetes and Digestive and Kidney Diseases Grant P30 DK-020541), and an Alexander and Alexandrine Sinsheimer Scholar Award.
Publisher Copyright:
© 2018 American Physiological Society. All rights reserved.
PY - 2018/9
Y1 - 2018/9
N2 - The central nervous system relies on a continual supply of glucose, and must be able to detect glucose levels and regulate peripheral organ functions to ensure that its energy requirements are met. Specialized glucose-sensing neurons, first described half a century ago, use glucose as a signal and modulate their firing rates as glucose levels change. Glucose-excited neurons are activated by increasing glucose concentrations, while glucose-inhibited neurons increase their firing rate as glucose concentrations fall and decrease their firing rate as glucose concentrations rise. Glucose-sensing neurons are present in multiple brain regions and are highly expressed in hypothalamic regions, where they are involved in functions related to glucose homeostasis. However, the roles of glucose-sensing neurons in healthy and disease states remain poorly understood. Technologies that can rapidly and reversibly activate or inhibit defined neural populations provide invaluable tools to investigate how specific neural populations regulate metabolism and other physiological roles. Optogenetics has high temporal and spatial resolutions, requires implants for neural stimulation, and is suitable for modulating local neural populations. Chemogenetics, which requires injection of a synthetic ligand, can target both local and widespread populations. Radio-and magnetogenetics offer rapid neural activation in localized or widespread neural populations without the need for implants or injections. These tools will allow us to better understand glucose-sensing neurons and their metabolism-regulating circuits.
AB - The central nervous system relies on a continual supply of glucose, and must be able to detect glucose levels and regulate peripheral organ functions to ensure that its energy requirements are met. Specialized glucose-sensing neurons, first described half a century ago, use glucose as a signal and modulate their firing rates as glucose levels change. Glucose-excited neurons are activated by increasing glucose concentrations, while glucose-inhibited neurons increase their firing rate as glucose concentrations fall and decrease their firing rate as glucose concentrations rise. Glucose-sensing neurons are present in multiple brain regions and are highly expressed in hypothalamic regions, where they are involved in functions related to glucose homeostasis. However, the roles of glucose-sensing neurons in healthy and disease states remain poorly understood. Technologies that can rapidly and reversibly activate or inhibit defined neural populations provide invaluable tools to investigate how specific neural populations regulate metabolism and other physiological roles. Optogenetics has high temporal and spatial resolutions, requires implants for neural stimulation, and is suitable for modulating local neural populations. Chemogenetics, which requires injection of a synthetic ligand, can target both local and widespread populations. Radio-and magnetogenetics offer rapid neural activation in localized or widespread neural populations without the need for implants or injections. These tools will allow us to better understand glucose-sensing neurons and their metabolism-regulating circuits.
KW - Glucose
KW - Magnetogenetics
KW - Neuromodulation
KW - Radiogenetics
UR - http://www.scopus.com/inward/record.url?scp=85053753839&partnerID=8YFLogxK
U2 - 10.1152/ajpendo.00469.2017
DO - 10.1152/ajpendo.00469.2017
M3 - Review article
C2 - 29812985
AN - SCOPUS:85053753839
SN - 0193-1849
VL - 315
SP - E327-E339
JO - American Journal of Physiology - Endocrinology and Metabolism
JF - American Journal of Physiology - Endocrinology and Metabolism
IS - 3
ER -