All animals live in constantly changing environments and are, therefore, subjected to fluctuations in critical environmental cues such as temperature. Given that all biochemical reactions are temperature sensitive to a certain extent, it is particularly critical for animals to compensate for these temperature changes in order to maintain steady internal conditions. In order to do so, animals must be able to detect small temperature changes and then trigger the appropriate homeostatic compensatory mechanisms. To date, research into the molecular and neuronal basis of temperature detection and thermotransduction, and the physiological mechanisms of temperature adaptation and compensation, have largely been pursued as independent lines of investigation. To obtain a full understanding of how animals respond appropriately to temperature changes, these intellectual issues must be brought together and studied as a whole. In this Program Project grant we bring together researchers experienced in issues of temperature detection and temperature compensation to ask how animals detect temperature changes and translate this information to effect compensatory changes in neuron function to maintain behavioral robustness. A particular strength of this proposal is the synergy among investigators exploring these issues in multiple systems;this diversity will elucidate common underlying principles that can be generalized ID other species. The overall questions being asked here are: 1) What are the molecular mechanisms by which animals detect temperature changes? 2) What are the neuronal mechanisms that encode information about temperature changes? 3) How do motor programs compensate for temperature fluctuations? 4) What defines the limits of the range in which these homeostatic mechanisms operate? 5) What are the common principles of temperature detection and compensation among species?

Public Health Relevance

Like cold-blooded animals, warm-blooded animals are also susceptible to the effects of alterations in their ability to correctly sense and compensate for temperature changes. 'Crashes'of nervous system function occur when compensation mechanisms fail. Understanding the limits of compensatory mechanisms will inform our understanding of critical medical issues such as febrile seizures, Uhthoff's phenomenon in multiple sclerosis, psychomotor stimulant drug-induced hypothermia and familial episodic pain syndrome among others.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Research Program Projects (P01)
Project #
1P01GM103770-01
Application #
8416054
Study Section
Special Emphasis Panel (ZRG1-CB-P (40))
Program Officer
Sesma, Michael A
Project Start
2013-05-15
Project End
2018-04-30
Budget Start
2013-05-15
Budget End
2014-04-30
Support Year
1
Fiscal Year
2013
Total Cost
$1,308,258
Indirect Cost
$239,277
Name
Brandeis University
Department
Biology
Type
Schools of Arts and Sciences
DUNS #
616845814
City
Waltham
State
MA
Country
United States
Zip Code
02454
Luo, Linjiao; Cook, Nathan; Venkatachalam, Vivek et al. (2014) Bidirectional thermotaxis in Caenorhabditis elegans is mediated by distinct sensorimotor strategies driven by the AFD thermosensory neurons. Proc Natl Acad Sci U S A 111:2776-81
Luo, Linjiao; Wen, Quan; Ren, Jing et al. (2014) Dynamic encoding of perception, memory, and movement in a C. elegans chemotaxis circuit. Neuron 82:1115-28