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

Regulation of Food Intake01:30

Regulation of Food Intake

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...
Drugs Affecting Neurotransmitter Synthesis01:29

Drugs Affecting Neurotransmitter Synthesis

Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase, which converts...
Adrenergic Agonists: Indirect-Acting Agents01:25

Adrenergic Agonists: Indirect-Acting Agents

Indirect-acting adrenergic agonists potentiate the effects of endogenous catecholamines through different mechanisms without directly binding to adrenoceptors.
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral bioavailability, and...
Attention-Deficit/Hyperactivity Disorder01:30

Attention-Deficit/Hyperactivity Disorder

Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by persistent inattention, hyperactivity, and impulsivity. It affects approximately 5-8% of children globally, with around 60-70% of cases persisting into adulthood. ADHD has significant implications for educational attainment, social interactions, and occupational success.
Diagnostic Criteria and Symptoms
To diagnose ADHD, symptoms must manifest before age 12 and be evident across multiple settings.
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
Drugs Affecting Neurotransmitter Release or Uptake01:21

Drugs Affecting Neurotransmitter Release or Uptake

Certain drugs can affect how neurotransmitters called catecholamines, are released or taken back up in the adrenergic neuron. They can have different effects on the body's sympathetic transmission. Reserpine, a natural compound found in the Rauwolfia shrub, blocks a transporter called vesicular monoamine transporter (VMAT), which leads to a buildup of catecholamines in the cell and reduces sympathetic transmission. Another drug called guanethidine works in multiple ways, including blocking...

You might also read

Related Articles

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

Sort by
Same author

Alexithymia in Anorexia Nervosa, More State Than Trait? A Multi-Dimensional Assessment of Emotion Processing in Patients With Anorexia Nervosa, Recovered Patients and Healthy Controls.

European eating disorders review : the journal of the Eating Disorders Association·2026
Same author

A prefrontal cortex-lateral hypothalamus circuit controls stress-driven increased food intake.

Nature communications·2026
Same author

Validation of the caregiver skills (CASK) scale in a Dutch sample of carers for adolescents with eating disorders.

Journal of eating disorders·2026
Same author

Therapists' Attitudes and Exclusion Criteria for Prolonged Exposure and EMDR in Patients With Eating Disorders and PTSD.

European eating disorders review : the journal of the Eating Disorders Association·2025
Same author

The Efficacy of Pharmacological Treatment of Depression in Anorexia Nervosa and Underweight Patients: A Systematic Review.

European eating disorders review : the journal of the Eating Disorders Association·2025
Same author

Electrophysiological effects of deep brain stimulation in anorexia nervosa.

Journal of psychiatric research·2025

Related Experiment Video

Updated: Jul 5, 2026

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing
05:45

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing

Published on: October 25, 2019

Leptin's effect on hyperactivity: potential downstream effector mechanisms.

J J G Hillebrand1, M J H Kas, A A van Elburg

  • 1Rudolf Magnus Institute of Neuroscience, Department of Pharmacology and Anatomy, University Medical Centre, Utrecht, The Netherlands. jacquelien-hillebrand@ethz.ch

Physiology & Behavior
|May 23, 2008
PubMed
Summary
This summary is machine-generated.

Hyperactivity is common in Anorexia Nervosa (AN) and hinders recovery. This study investigates the neurobiological mechanisms behind AN hyperactivity using an animal model, exploring how leptin treatment reduces this behavior.

More Related Videos

Comprehensive Profiling of Dopamine Regulation in Substantia Nigra and Ventral Tegmental Area
09:54

Comprehensive Profiling of Dopamine Regulation in Substantia Nigra and Ventral Tegmental Area

Published on: August 10, 2012

A RAPID Method for Blood Processing to Increase the Yield of Plasma Peptide Levels in Human Blood
11:36

A RAPID Method for Blood Processing to Increase the Yield of Plasma Peptide Levels in Human Blood

Published on: April 28, 2016

Related Experiment Videos

Last Updated: Jul 5, 2026

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing
05:45

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing

Published on: October 25, 2019

Comprehensive Profiling of Dopamine Regulation in Substantia Nigra and Ventral Tegmental Area
09:54

Comprehensive Profiling of Dopamine Regulation in Substantia Nigra and Ventral Tegmental Area

Published on: August 10, 2012

A RAPID Method for Blood Processing to Increase the Yield of Plasma Peptide Levels in Human Blood
11:36

A RAPID Method for Blood Processing to Increase the Yield of Plasma Peptide Levels in Human Blood

Published on: April 28, 2016

Area of Science:

  • Neurobiology
  • Behavioral Science
  • Endocrinology

Background:

  • Anorexia Nervosa (AN) frequently involves hyperactivity, impeding weight gain and treatment success.
  • Hyperactivity in AN is linked to poor clinical outcomes and suggests an underlying neurobiological basis.
  • Leptin treatment has previously shown efficacy in reducing hyperactivity in the activity-based anorexia (ABA) rat model.

Purpose of the Study:

  • To elucidate the downstream effector mechanisms responsible for leptin's attenuation of hyperactivity in the ABA rat model.
  • To gain insight into the neurobiological underpinnings of hyperactivity in Anorexia Nervosa.

Main Methods:

  • Utilized the activity-based anorexia (ABA) rat model, an established translational model for AN-related hyperactivity.
  • Investigated potential downstream molecular and neural pathways affected by leptin treatment in ABA rats.

Main Results:

  • Identified specific downstream effector mechanisms through which leptin exerts its anti-hyperactivity effects in the ABA model.
  • Provided novel insights into the neurobiological basis of hyperactivity in Anorexia Nervosa.

Conclusions:

  • Leptin's anti-hyperactivity effects in AN are mediated by specific downstream pathways.
  • Understanding these mechanisms may lead to targeted therapeutic strategies for managing hyperactivity in Anorexia Nervosa patients.