Journal
NEURON
Volume 96, Issue 6, Pages 1272-+Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2017.11.041
Keywords
-
Categories
Funding
- ARCS Foundation Scholarship
- UCSF Discovery Fellowship
- NIH NRSA Predoctoral Fellowship [F31-HL131463, F31-HL137383]
- Genentech Foundation Predoctoral Fellowship
- NSF Graduate Research Fellowship [1144247]
- New York Stem Cell Foundation
- American Diabetes Association Pathway Program
- Rita Allen Foundation
- McKnight Foundation
- Alfred P. Sloan Foundation
- Brain and Behavior Research Foundation
- Esther A. & Joseph Klingenstein Foundation
- Program for Breakthrough Biological Research
- UCSF DERC [P30-DK06372]
- NORC [P30-DK098722]
- NIH New Innovator Award [DP2-DK109533, R01-NS094781, R01-DK106399]
Ask authors/readers for more resources
The brain transforms the need for water into the desire to drink, but how this transformation is performed remains unknown. Here we describe the motivational mechanism by which the forebrain thirst circuit drives drinking. We show that thirst-promoting subfornical organ neurons are negatively reinforcing and that this negative-valence signal is transmitted along projections to the organum vasculosum of the lamina terminalis (OVLT) and median preoptic nucleus (MnPO). We then identify molecularly defined cell types within the OVLT and MnPO that are activated by fluid imbalance and show that stimulation of these neurons is sufficient to drive drinking, cardiovascular responses, and negative reinforcement. Finally, we demonstrate that the thirst signal exits these regions through at least three parallel pathways and show that these projections dissociate the cardiovascular and behavioral responses to fluid imbalance. These findings reveal a distributed thirst circuit that motivates drinking by the common mechanism of drive reduction.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available