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

Adrenergic Receptors: ɑ Subtype01:31

Adrenergic Receptors: ɑ Subtype

Adrenoceptors are classified into α and ꞵ classes based on their potencies to catecholamine agonists. α-adrenoceptors show the following order of catecholamine potency:
Adrenaline ≥ Noradrenaline >> Isoprenaline
α-adrenoceptors are further divided into α1 and α2-adrenoceptors.
α1-Adrenoceptors: These receptors are located postsynaptically on the effector organs and cause constriction of smooth muscle mediated by activation of phospholipase C—inositol-1,4,5-trisphosphate...
Adrenergic Receptors: β Subtype01:26

Adrenergic Receptors: β Subtype

β-adrenoceptors have varied sensitivities towards adrenaline, noradrenaline, and isoprenaline. The order of agonist potency is as follows:
Isoprenaline > Adrenaline > Noradrenaline
Neurotransmitter binding to these receptors causes activation of adenylyl cyclase resulting in increased concentrations of cAMP and modulation of calcium ion channels within the cell. They are further classified into β1, β2, and β3 subtypes.
β1-adrenoceptors: β1-adrenoceptors have equal affinities for...
Ligand-Gated Ion Channel Receptor: Gating Mechanism01:30

Ligand-Gated Ion Channel Receptor: Gating Mechanism

Ligand-gated ion channels are transmembrane proteins that play a vital role in intercellular communication and functions of the nervous system. They allow the influx of ions across the membrane once the neurotransmitter binds, allowing the subsequent transmission of electrical excitation across the neurons. Other ligand-gated ion channels, like the γ-aminobutyric acid (GABA) receptor, permit anions like chloride into the cells on the binding of the GABA molecule. Their entry into the cell...
Adrenergic Receptors (Adrenoceptors): Classification01:27

Adrenergic Receptors (Adrenoceptors): Classification

Adrenergic receptors, or adrenoceptors, respond to the autonomic neurotransmitter noradrenaline and other endogenous catecholamine agonists. They are classified into two main families, α and β, based on their pharmacological response and are further subdivided depending on their location, elicited response, and affinity to specific agonists or antagonists.
α-Adrenoceptors
α-Adrenoceptors are classified into two main subtypes: α1 and α2. The α1 adrenoceptors, which are found on postsynaptic...
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 Neurons: Neurotransmission01:27

Adrenergic Neurons: Neurotransmission

Postganglionic sympathetic fibers (except those supplying the sweat glands) releasing noradrenaline or norepinephrine are called noradrenergic or adrenergic neurons. Noradrenaline, dopamine, adrenaline, or epinephrine are collectively called "catecholamines" as they contain a catechol moiety and an amine side chain. The five stages of neurotransmitter release involve their synthesis, storage, release, reuptake and metabolism.
Synthesis: Catecholamine synthesis requires tyrosine, which is taken...

You might also read

Related Articles

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

Sort by
Same author

Corrigendum to "Revisiting subcallosal cingulate deep brain stimulation for depression: Long-term safety and effectiveness outcomes from a pooled analysis of 172 implanted patients" [Brain Stimul 18 (2025) 1632-1640].

Brain stimulation·2026
Same author

Exercise evokes retained motor performance without neuroprotection in a mouse model of Parkinson's disease.

Frontiers in physiology·2026
Same author

Microglial sTREM2 limits dyskinesia and acts on TrkB to support circuit plasticity.

bioRxiv : the preprint server for biology·2026
Same author

Magnetic resonance-guided focused ultrasound for the management of tremor: update on the position statement of the American Society for Stereotactic and Functional Neurosurgery.

Journal of neurosurgery·2026
Same author

Neuropsychological outcomes comparing traditional surgical approaches and laser interstitial therapy for refractory mesial temporal lobe epilepsy: A systematic review and meta-analysis.

Epilepsia·2026
Same author

A wireless, 60-channel, AI-enabled neurostimulation platform.

Brain stimulation·2025

Related Experiment Video

Updated: Jun 22, 2026

Two-photon Imaging of Microglial Processes' Attraction Toward ATP or Serotonin in Acute Brain Slices
07:27

Two-photon Imaging of Microglial Processes' Attraction Toward ATP or Serotonin in Acute Brain Slices

Published on: January 31, 2019

Adenosine A(2A) receptor mediates microglial process retraction.

Anna G Orr1, Adam L Orr, Xiao-Jiang Li

  • 1Department of Pharmacology, Emory University School of Medicine, Atlanta, Georgia, USA. anna.orr@gladstone.ucsf.edu

Nature Neuroscience
|June 16, 2009
PubMed
Summary
This summary is machine-generated.

Microglia cell processes normally extend but retract during brain inflammation due to a newly identified molecular pathway. This switch, involving A(2A) adenosine receptor upregulation, explains the characteristic amoeboid shape of activated microglia in CNS inflammation.

More Related Videos

Targeted Knockdown of Genes in the Choroid Plexus
04:43

Targeted Knockdown of Genes in the Choroid Plexus

Published on: June 16, 2023

Related Experiment Videos

Last Updated: Jun 22, 2026

Two-photon Imaging of Microglial Processes' Attraction Toward ATP or Serotonin in Acute Brain Slices
07:27

Two-photon Imaging of Microglial Processes' Attraction Toward ATP or Serotonin in Acute Brain Slices

Published on: January 31, 2019

Targeted Knockdown of Genes in the Choroid Plexus
04:43

Targeted Knockdown of Genes in the Choroid Plexus

Published on: June 16, 2023

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Microglia are brain immune cells with motile processes crucial for surveying and scavenging.
  • Microglial process retraction during prolonged brain injury or disease is a common but unexplained feature of neuroinflammation.

Purpose of the Study:

  • To identify the molecular mechanism responsible for microglial process retraction during brain inflammation.
  • To elucidate the signaling pathway that causes a switch from process extension to retraction in microglia.

Main Methods:

  • Investigated molecular pathways in mouse and human microglia.
  • Analyzed changes in receptor expression (A(2A) adenosine receptor and P2Y(12)) and their role in microglial morphology.
  • Studied the effects of purine nucleotides and their breakdown products on microglial cell behavior.

Main Results:

  • Identified a pathway where inflammation upregulates the A(2A) adenosine receptor while downregulating the P2Y(12) receptor in microglia.
  • Demonstrated that adenosine, a breakdown product of extracellular ATP, stimulates the A(2A) receptor, causing activated microglia to retract their processes and adopt an amoeboid morphology.
  • Revealed a chemotactic switch driven by purine nucleotide signaling.

Conclusions:

  • The study uncovers a novel molecular mechanism explaining microglial process retraction and amoeboid morphology during CNS inflammation.
  • This purinergic signaling switch, mediated by A(2A) adenosine receptor activation, is a key driver of a hallmark feature of brain inflammation.
  • Findings offer insights into context-dependent receptor signaling and potential therapeutic targets in neuroinflammatory diseases.