Animals must modify their behavior with appropriate timing to respond to environmental changes. Yet, the molecular and neural mechanisms regulating the timing of behavioral transition remain largely unknown. By performing forward genetics to reveal mechanisms that underlie the plasticity of thermotaxis behavior in , we demonstrated that SLO potassium channels and a cyclic nucleotide-gated channel, CNG-3, determine the timing of transition of temperature preference after a shift in cultivation temperature. We further revealed that SLO and CNG-3 channels act in thermosensory neurons and decelerate alteration in the responsiveness of these neurons, which occurs prior to the preference transition after a temperature shift. Our results suggest that regulation of sensory adaptation is a major determinant of latency before animals make decisions to change their behavior.
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http://dx.doi.org/10.1038/s42003-018-0124-5 | DOI Listing |
Molecules
November 2024
Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
Epilepsy of infancy with migrating focal seizures (EIMFS) is a rare, serious, and pharmacoresistant epileptic disorder often linked to gain-of-function mutations in the gene. encodes the sodium-activated potassium channel known as SLACK, making small molecule inhibitors of SLACK channels a compelling approach to the treatment of EIMFS and other epilepsies associated with mutations. In this manuscript, we describe a hit optimization effort executed within a series of 2-aryloxy--(pyrimidin-5-yl)acetamides that were identified via a high-throughput screen.
View Article and Find Full Text PDFMolecules
September 2024
College of Pharmacy, Woosuk University, Wanju 55338, Republic of Korea.
Alcohol use disorder (AUD) is the most common substance use disorder and poses a significant global health challenge. Despite pharmacological advances, no single drug effectively treats all AUD patients. This study explores the protective potential of hispidol, a 6,4'-dihydroxyaurone, for AUD using the model system.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
September 2024
Physiopathologie et Génétique du Neurone et du Muscle, Université de Lyon, Université Claude Bernard Lyon 1, CNRS UMR 5261, INSERM U1315, Faculté de Médecine Rockefeller, Lyon 69008, France.
Proc Natl Acad Sci U S A
May 2024
Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114.
Type 1 voltage-activated calcium channels (CaV1) in the plasma membrane trigger calcium release from the sarcoplasmic reticulum (SR) by two mechanisms. In voltage-induced calcium release (VICR), CaV1 voltage sensing domains are directly coupled to ryanodine receptors (RYRs), an SR calcium channel. In calcium-induced calcium release (CICR), calcium ions flowing through activated CaV1 channels bind and activate RYR channels.
View Article and Find Full Text PDFBiophys J
July 2024
Department of Anesthesiology and Perioperative Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas; Molecular & Translational Biology and Neuroscience Programs, MD Anderson UT Health Graduate School of Biomedical Sciences, Houston, Texas. Electronic address:
Voltage-gated potassium channels are critical in modulating cellular excitability, with Slo (slowpoke) channels forming a unique family characterized by their large conductance and dual regulation by electrical signals and intracellular messengers. Despite their structural and evolutionary similarities, Slo1 and Slo3 channels exhibit significant differences in their voltage-gating properties. This study investigates the molecular determinants that differentiate the voltage-gating properties of human Slo1 and mouse Slo3 channels.
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