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

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.
Desensitization and Tachyphylaxis01:20

Desensitization and Tachyphylaxis

Tachyphylaxis is described as a rapid decrease in response to a drug after repeated or continuous administration of the same drug dose. It is a phenomenon where the body becomes less responsive to a particular substance or intervention over time, requiring higher doses or stronger interventions to achieve the same effect. It results from adaptive changes in the body's receptors, signaling pathways, or physiological processes that occur in response to prolonged exposure to a stimulus.
Several...
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...
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...
Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists01:30

Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists

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. They...
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

High-order brain interactions during ketamine-induced state changes: A functional marker of response in late-life treatment-resistant depression?

Translational psychiatry·2026
Same author

Short-term lithium treatment modulates excitation/inhibition balance in resting-state electroencephalography (EEG) among survivors of medically severe suicide attempts.

Experimental and clinical psychopharmacology·2026
Same author

Mitigating Post-Traumatic Stress Disorder Risk Through Gender-Sensitive Trauma-Informed Care in the Emergency Department-A Narrative Review.

The Journal of emergency medicine·2025
Same author

Interacting immediate and long-term action regulation in suicidal behavior.

Journal of mood and anxiety disorders·2025
Same author

Differential Impact of Serotonin Signaling Methylphenidate on Young versus Adult: Insights from Behavioral and Dorsal Raphe Nucleus Neuronal Recordings from Freely Behaving Rats.

International journal of molecular sciences·2024
Same author

Use of Cigarettes and E-Cigarettes, Impulsivity, and Anxiety: Influences on Suicidal Ideation Among Youth and Young Adults in Texas.

Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco·2024
Same journal

Expression of concern: "Effect of perioperative preemptive analgesia on hippocampal GABAA receptor α1/α5 balance in aged mild cognitive impairment rats" [Brain Res. Bull. 237 (2026) 111811].

Brain research bulletin·2026
Same journal

Ubiquitination in ischemic stroke: Molecular mechanisms and therapeutic implications.

Brain research bulletin·2026
Same journal

Corrigendum to "Peripheral to central: Exploring the neural, endocrine, and immune pathways of the gut-brain axis in postoperative neurocognitive dysfunction" [Brain Res. Bull. 242 (2026) 111975].

Brain research bulletin·2026
Same journal

GLUT1-driven glycolytic reprogramming in microglia promotes neuroinflammation and cognitive deficits in sepsis-associated encephalopathy.

Brain research bulletin·2026
Same journal

Spinal astrocytes hardly proliferate following peripheral nerve injury: Evidence from adult Aldh1l1-GFP reporter mice.

Brain research bulletin·2026
Same journal

Shared neural mechanisms of trait mindfulness and hypnotic susceptibility: A scoping review toward a unifying predictive coding framework.

Brain research bulletin·2026
See all related articles

Related Experiment Video

Updated: Jul 6, 2026

Assessment of Cocaine-induced Behavioral Sensitization and Conditioned Place Preference in Mice
10:28

Assessment of Cocaine-induced Behavioral Sensitization and Conditioned Place Preference in Mice

Published on: February 18, 2016

Methylphenidate sensitization is prevented by prefrontal cortex lesion.

Min J Lee1, Alan C Swann, Nachum Dafny

  • 1Department of Neurobiology and Anatomy, The University of Texas-Medical School at Houston, P.O. Box 20708, Houston, TX 77225, United States.

Brain Research Bulletin
|April 9, 2008
PubMed
Summary
This summary is machine-generated.

The prefrontal cortex (PFC) is essential for developing behavioral sensitization to methylphenidate (MPD), a medication for Attention Deficit Hyperactivity Disorder. While MPD affects activity acutely, PFC lesions prevent long-term changes in response to the drug.

More Related Videos

High-definition Transcranial Direct Current Stimulation over Right Dorsolateral Prefrontal Cortex to Enhance Metacognitive Sensitivity
06:11

High-definition Transcranial Direct Current Stimulation over Right Dorsolateral Prefrontal Cortex to Enhance Metacognitive Sensitivity

Published on: September 26, 2025

A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration
09:16

A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration

Published on: January 22, 2016

Related Experiment Videos

Last Updated: Jul 6, 2026

Assessment of Cocaine-induced Behavioral Sensitization and Conditioned Place Preference in Mice
10:28

Assessment of Cocaine-induced Behavioral Sensitization and Conditioned Place Preference in Mice

Published on: February 18, 2016

High-definition Transcranial Direct Current Stimulation over Right Dorsolateral Prefrontal Cortex to Enhance Metacognitive Sensitivity
06:11

High-definition Transcranial Direct Current Stimulation over Right Dorsolateral Prefrontal Cortex to Enhance Metacognitive Sensitivity

Published on: September 26, 2025

A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration
09:16

A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration

Published on: January 22, 2016

Area of Science:

  • Neuroscience
  • Pharmacology
  • Behavioral Science

Background:

  • Methylphenidate (MPD), or Ritalin, treats Attention Deficit Hyperactivity Disorder (ADHD).
  • Repeated MPD administration leads to dose-dependent sensitization.
  • MPD's mechanism involves dopamine transporter binding, increasing synaptic dopamine and acting as an indirect agonist.

Purpose of the Study:

  • To investigate the prefrontal cortex's (PFC) role in the acute and chronic effects of MPD.
  • To determine if the PFC is necessary for MPD-induced behavioral sensitization.

Main Methods:

  • Utilized the open field assay in male Sprague-Dawley rats.
  • Created bilateral electrolytic lesions of the PFC in a subset of animals.
  • Administered saline, followed by MPD (2.5mg/kg) daily for six days, with washout and re-challenge phases.

Main Results:

  • Acute MPD administration increased locomotor activity in both sham and PFC-lesioned groups.
  • Behavioral sensitization to MPD was observed in the sham group.
  • The PFC-lesioned group failed to exhibit behavioral sensitization to MPD.

Conclusions:

  • The PFC is not required for the acute locomotor effects of MPD.
  • The PFC is crucial for the development of behavioral sensitization to MPD.
  • These findings highlight the PFC's role in mediating long-term adaptive changes to chronic stimulant exposure.