Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

8.3K
Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
8.3K
Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

3.2K
Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
3.2K
Transducer Mechanism: G Protein–Coupled Receptors01:30

Transducer Mechanism: G Protein–Coupled Receptors

8.2K
G Protein–Coupled Receptors (GPCRs) are membrane-bound receptors that transiently associate with heterotrimeric G proteins and induce an appropriate response to various stimuli. GPCRs regulate critical physiological pathways and are excellent drug targets for treating diseases such as diabetes, cancer, obesity, depression, or Alzheimer's. Nearly 35% of approved drugs implement their therapeutic effects by selectively interacting with specific GPCRs.
GPCRs are also called heptahelical,...
8.2K
Regulation of Food Intake01:30

Regulation of Food Intake

3.2K
Short-term regulation of food intake primarily involves neural signals from the gastrointestinal (GI) tract, blood nutrient levels, and GI tract hormones. Communication between the gut and brain via vagal nerve fibers plays a significant role in evaluating the contents of the gut. Clinical studies have shown that protein ingestion produces a more prolonged response in these nerve fibers compared to an equivalent amount of glucose. Additionally, the activation of stretch receptors caused by GI...
3.2K
Physiology of Emotion01:20

Physiology of Emotion

4.4K
The physiology of emotions is a multifaceted process involving the autonomic nervous system, brain structures, hormones, and neurotransmitters. This intricate interplay dictates how emotions manifest in the body and influence behavior.
Autonomic Nervous System
The autonomic nervous system (ANS) plays a critical role in emotional responses by regulating involuntary physiological functions. It consists of two main components: the sympathetic and parasympathetic systems. The sympathetic system...
4.4K
G-protein Coupled Receptors01:21

G-protein Coupled Receptors

134.4K
G-protein coupled receptors are ligand binding receptors that indirectly affect changes in the cell. The actual receptor is a single polypeptide that transverses the cell membrane seven times creating intracellular and extracellular loops. The extracellular loops create a ligand specific pocket which binds to neurotransmitters or hormones. The intracellular loops holds onto the G-protein.
134.4K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Co-expression-based models improve eQTL predictions for transcriptome-wide association studies and highlight new schizophrenia-associated genes.

Nature genetics·2026
Same author

Genetic Risk and Resilience for Schizophrenia Stratified by Perinatal Gene Expression Predict Adult Cognitive Performance.

bioRxiv : the preprint server for biology·2026
Same author

Magnetoencephalographic Microstates Reveal Disrupted Brain Activity Patterns in Schizophrenia Controlling for Treatment-Related Modulations.

Schizophrenia bulletin·2026
Same author

Behavioral and Personality Changes as the First Manifestation of Spinocerebellar Ataxia Type 2.

Cerebellum (London, England)·2026
Same author

Neurobiological Signatures of Trauma, Personality, and Depressivity: A Transdiagnostic Machine Learning Study in Adolescents and Young Adults.

Biological psychiatry·2026
Same author

Biosignatures of cognitive basic symptoms mark a distinct neurodevelopmental pathway to schizophrenia.

Brain : a journal of neurology·2026

Related Experiment Video

Updated: Apr 6, 2026

Dissecting Cell-Autonomous Function of Fragile X Mental Retardation Protein in an Auditory Circuit by In Ovo Electroporation
11:10

Dissecting Cell-Autonomous Function of Fragile X Mental Retardation Protein in an Auditory Circuit by In Ovo Electroporation

Published on: July 6, 2022

2.8K

FXR1P is a GSK3β substrate regulating mood and emotion processing.

Thomas Del'Guidice1, Camille Latapy1, Antonio Rampino2

  • 1Department of Psychiatry and Neuroscience, Faculty of Medicine, Université Laval, Québec-City, QC, Canada G1J 2G3;

Proceedings of the National Academy of Sciences of the United States of America
|August 5, 2015
PubMed
Summary

Researchers discovered a new signaling pathway involving GSK3β and FXR1P that regulates mood and emotion. This finding may explain how certain medications impact mental health conditions like bipolar disorder.

Keywords:
FXR1Pbipolar disorderemotion processingglycogen synthase kinase 3mood

More Related Videos

Developing a Rat Model for Bipolar Disorder
04:42

Developing a Rat Model for Bipolar Disorder

Published on: May 2, 2025

1.7K
Generation and Characterization of Human Induced Pluripotent Stem Cell-derived Astrocytes Lacking Fragile X Messenger Ribonucleoprotein
10:59

Generation and Characterization of Human Induced Pluripotent Stem Cell-derived Astrocytes Lacking Fragile X Messenger Ribonucleoprotein

Published on: June 6, 2025

1.2K

Related Experiment Videos

Last Updated: Apr 6, 2026

Dissecting Cell-Autonomous Function of Fragile X Mental Retardation Protein in an Auditory Circuit by In Ovo Electroporation
11:10

Dissecting Cell-Autonomous Function of Fragile X Mental Retardation Protein in an Auditory Circuit by In Ovo Electroporation

Published on: July 6, 2022

2.8K
Developing a Rat Model for Bipolar Disorder
04:42

Developing a Rat Model for Bipolar Disorder

Published on: May 2, 2025

1.7K
Generation and Characterization of Human Induced Pluripotent Stem Cell-derived Astrocytes Lacking Fragile X Messenger Ribonucleoprotein
10:59

Generation and Characterization of Human Induced Pluripotent Stem Cell-derived Astrocytes Lacking Fragile X Messenger Ribonucleoprotein

Published on: June 6, 2025

1.2K

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Psychiatry

Background:

  • Glycogen synthase kinase 3β (GSK3β) inhibition is a known mechanism of psychoactive drugs.
  • The specific substrates through which GSK3β influences behavior are not well understood.

Purpose of the Study:

  • To identify substrates of GSK3β involved in behavioral regulation.
  • To elucidate the role of a novel GSK3β/FXR1P signaling pathway in mood and emotion processing.

Main Methods:

  • Identified fragile X mental retardation-related protein 1 (FXR1P) as a GSK3β substrate.
  • Investigated the effects of GSK3β phosphorylation on FXR1P levels and function.
  • Examined the impact of FXR1P overexpression and genetic polymorphisms on mood-related behaviors in mice and humans.

Main Results:

  • GSK3β phosphorylates FXR1P, leading to its down-regulation.
  • Mood stabilizer treatments in mice inhibit GSK3β and increase FXR1P levels.
  • FXR1P overexpression in mice mimics mood-related responses, and genetic variations in FXR1P/GSK3β impact human emotional stability.

Conclusions:

  • A novel GSK3β/FXR1P signaling pathway regulates mood and emotion processing.
  • This pathway provides a mechanistic explanation for the mood-regulating effects of GSK3β inhibitors in mental illnesses.
  • The pathway may also be involved in inflammation and cell proliferation.