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

Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists01:30

Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists

869
Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function.
869
Exercise and Muscle Performance01:27

Exercise and Muscle Performance

5.1K
Exercise induces a range of adaptations in muscle tissue, depending on the type and duration of activity. Such physical training can be broadly categorized into two types: endurance exercises and resistance exercises.
Endurance exercises
Endurance exercises involve running, swimming, or cycling, which require repetitive movements with low force output. When a person engages in endurance exercise, a few noticeable changes occur in their skeletal muscles. For instance, the number of capillaries...
5.1K
Drugs Acting on Autonomic Ganglia: Stimulants01:23

Drugs Acting on Autonomic Ganglia: Stimulants

2.3K

Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating...
2.3K
Adrenergic Agonists: Indirect-Acting Agents01:25

Adrenergic Agonists: Indirect-Acting Agents

3.0K
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...
3.0K
Direct-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship01:22

Direct-Acting Cholinergic Agonists: Chemistry and Structure-Activity Relationship

2.5K
Cholinergic agonists or cholinomimetics mimic the action of acetylcholine to stimulate the parasympathetic nervous system. They are categorized into direct-acting and indirect-acting agents. The direct-acting cholinergic drugs induce the parasympathetic response by directly binding to the muscarinic or nicotine receptors. In comparison, the indirect-acting cholinergic drugs prevent acetylcholine hydrolysis, indirectly contributing to the extended parasympathetic response.
The direct-acting...
2.5K

You might also read

Related Articles

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

Sort by
Same author

Supraphysiological androgen administration does not exert any additive benefits on hippocampal plasticity-related markers and behavior in previously untrained male mice.

Hormones and behavior·2026
Same author

Comparison of treatment with GP2017 (an adalimumab biosimilar) and reference adalimumab in people with plaque psoriasis: a plain language summary of the ADACCESS trial.

Immunotherapy·2026
Same author

Substantial Comparability of Singlicate Versus Duplicate Analysis-A Retrospective Evaluation of Clinical Immunogenicity in a Biosimilar PK Study.

The AAPS journal·2025
Same author

Muscle Cathepsin B Treatment Improves Behavioral and Neurogenic Deficits in a Mouse Model of Alzheimer's Disease.

Aging cell·2025
Same author

Potential Role of Extracellular Vesicles in Mediating Effects of Exercise on Brain Function.

Advances in neurobiology·2025
Same author

Sella Turcica and Cranial Base Symmetry in Anterior Synostotic Plagiocephaly Patients: A Retrospective Case-Control Study.

Diagnostics (Basel, Switzerland)·2025
Same journal

Retraction: Long noncoding RNA XIST is a prognostic factor in colorectal cancer and inhibits 5-fluorouracil-induced cell cytotoxicity through promoting thymidylate synthase expression.

Oncotarget·2026
Same journal

TRAIL-R2 in the shadows: Epigenetic silencing and clinical implications in breast cancer.

Oncotarget·2026
Same journal

Retraction: MALAT1 predicts poor survival in osteosarcoma patients and promotes cell metastasis through associating with EZH2.

Oncotarget·2026
Same journal

Laryngeal leiomyosarcoma: A rare case report and literature review.

Oncotarget·2026
Same journal

Correction: Postsurgery fluids promote transition of cancer stem cell toendothelial and AKT/mTOR activity contributing to relapse of giant cell tumors of bone.

Oncotarget·2026
Same journal

DHHC3 interferes with antitumor immunity in melanoma cells.

Oncotarget·2026
See all related articles

Related Experiment Video

Updated: Apr 5, 2026

Application of Passive Head Motion to Generate Defined Accelerations at the Heads of Rodents
05:04

Application of Passive Head Motion to Generate Defined Accelerations at the Heads of Rodents

Published on: July 21, 2022

2.3K

Exercise-mimetic AICAR transiently benefits brain function.

Davide Guerrieri1, Henriette van Praag1

  • 1Neuroplasticity and Behavior Unit, Laboratory of Neurosciences, National Institute on Aging, Baltimore, MD, USA.

Oncotarget
|August 20, 2015
PubMed
Summary
This summary is machine-generated.

Running benefits brain plasticity, but the drug AICAR, which activates muscle AMP-kinase (AMPK), does not provide sustained brain benefits. Exercise mimetics may not replicate long-term positive effects of physical activity on the brain.

Keywords:
AICARAMPKGerotargethippocampusmusclerunning

More Related Videos

Orienteering as a Tool for Cognitive Research: An Implementation Guide
07:13

Orienteering as a Tool for Cognitive Research: An Implementation Guide

Published on: November 29, 2024

1.7K
Activating Autophagy by Aerobic Exercise in Mice
08:44

Activating Autophagy by Aerobic Exercise in Mice

Published on: February 3, 2017

12.9K

Related Experiment Videos

Last Updated: Apr 5, 2026

Application of Passive Head Motion to Generate Defined Accelerations at the Heads of Rodents
05:04

Application of Passive Head Motion to Generate Defined Accelerations at the Heads of Rodents

Published on: July 21, 2022

2.3K
Orienteering as a Tool for Cognitive Research: An Implementation Guide
07:13

Orienteering as a Tool for Cognitive Research: An Implementation Guide

Published on: November 29, 2024

1.7K
Activating Autophagy by Aerobic Exercise in Mice
08:44

Activating Autophagy by Aerobic Exercise in Mice

Published on: February 3, 2017

12.9K

Area of Science:

  • Neuroscience
  • Exercise Physiology
  • Molecular Biology

Background:

  • Exercise, particularly running, is known to enhance cognitive functions like learning and memory.
  • The specific peripheral factors, such as muscle AMP-kinase (AMPK) activation, that mediate these exercise-induced brain benefits are not fully understood.
  • Investigating whether muscle AMPK activation can predict improvements in brain plasticity is crucial for understanding exercise's impact on the brain.

Purpose of the Study:

  • To compare the effects of running versus administering an AMPK agonist (AICAR) on muscle and brain function in mice.
  • To determine if muscle AMPK activation by AICAR can mimic the beneficial effects of running on brain plasticity and gene expression.
  • To assess the long-term sustainability of exercise- and AICAR-induced changes in the brain.

Main Methods:

  • Male C57BL/6J mice were treated with either running or AICAR (500 mg/kg) for 3, 7, or 14 days.
  • Muscle AMPK signaling (pAMPK levels) was measured to ensure equivalent activation between running and AICAR groups at 7 and 14 days.
  • Brain plasticity markers, cell proliferation, gene expression (microarray), oxidative stress, and inflammation were evaluated in the hippocampus (DG) and lateral entorhinal cortex (LEC).

Main Results:

  • At 7 days, both running and AICAR increased new cell proliferation and brain-derived neurotrophic factor (BDNF) levels in the DG.
  • Gene expression analysis revealed significant overlap between running and AICAR in regulating neuronal, mitochondrial, and metabolism-related genes in the DG and LEC.
  • At 14 days, while muscle effects remained similar, AICAR's brain effects reversed: it no longer boosted cell proliferation or neurotrophin levels but increased apoptotic and inflammatory gene expression (interleukin-1β).

Conclusions:

  • Muscle AMPK activation by AICAR can transiently mimic some positive effects of running on brain plasticity and gene expression.
  • However, the beneficial effects of AICAR on the brain are not sustainable and can even become detrimental over time.
  • Consistent running provides sustained benefits to brain function, suggesting that peripheral AMPK activation alone is insufficient to replicate the long-term positive impact of exercise.