Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Adrenergic Antagonists: Pharmacological Actions of ɑ-Receptor Blockers

Adrenergic Antagonists: Pharmacological Actions of ɑ-Receptor Blockers

α-Adrenergic antagonists, known as α-blockers, exert their effects by inhibiting α-adrenoceptors, leading to specific physiological actions. α1-blockers and α2-blockers have distinct pharmacological actions and therapeutic applications.
α1-blockers: These drugs inhibit α1-adrenoceptors on smooth muscle cells, resulting in vasodilation. This vasodilation lowers blood pressure, making α1-blockers valuable in treating hypertension. Additionally, α1-blockers effectively address urinary obstruction...

Adrenergic Receptors: β Subtype

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...

Adrenergic Antagonists: Chemistry and Classification of ɑ-Receptor Blockers

Adrenergic Antagonists: Chemistry and Classification of ɑ-Receptor Blockers

Adrenergic antagonists, or sympatholytics, inhibit adrenoceptor activation driven by catecholamines or agonists. Based on their adrenoceptor specificity, adrenergic blockers can be categorized into two primary groups: α-adrenergic blockers (α-blockers) and β-adrenergic blockers (β-blockers). α-blockers interact with α1 and α2 subtypes of α-adrenoceptors.
Nonselective α-blockers: Nonselective α-blockers contain haloalkylamine or imidazoline moieties. Phenoxybenzamine, with a haloalkylamine...

Drugs Affecting Neurotransmitter Release or Uptake

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...

Adrenergic Receptors: ɑ Subtype

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 (Adrenoceptors): Classification

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...

You might also read

Related Articles

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

Sort by

Same author

Impact of local and systemic antimicrobials on leukocyte- and platelet rich fibrin: an in vitro study.

Scientific reports·2022

Same author

Prospective international validation of the predisposition, infection, response and organ dysfunction (PIRO) clinical staging system among intensive care and general ward patients.

Annals of intensive care·2021

Same author

The effect of agricultural intensification and water-locking on the world's largest coastal lagoonal system.

The Science of the total environment·2021

Same author

Impact of g force and timing on the characteristics of platelet-rich fibrin matrices.

Scientific reports·2021

Same author

Background levels of trace elements in brown and red seaweeds from Trindade, a remote island in South Atlantic Ocean.

Marine pollution bulletin·2018

Same author

Diazoxide enhances excitotoxicity-induced neurogenesis and attenuates neurodegeneration in the rat non-neurogenic hippocampus.

Neuroscience·2016

Search research articles

Related Experiment Video

Updated: May 31, 2026

Disrupting Reconsolidation of Fear Memory in Humans by a Noradrenergic β-Blocker

Disrupting Reconsolidation of Fear Memory in Humans by a Noradrenergic β-Blocker

Published on: December 18, 2014

Br-16a does not interfere with alpha - 2 noradrenergic and dopamine postsynaptic receptor functioning.

C Andrade¹, J George, T Joseph

¹Chiitaranjan Andrade, MD, Associate Professor, Department of Psychopharmacology, NIMHANS, Bangalore - 560 029.

Indian Journal of Psychiatry

|July 12, 2011

Summary

This study investigated the effects of the herbal preparation BR-16A on neurotransmitter systems. Results indicate BR-16A does not interfere with alpha-2 noradrenergic or dopamine receptor function in rats.

More Related Videos

Methods for the Discovery of Novel Compounds Modulating a Gamma-Aminobutyric Acid Receptor Type A Neurotransmission

Methods for the Discovery of Novel Compounds Modulating a Gamma-Aminobutyric Acid Receptor Type A Neurotransmission

Published on: August 16, 2018

Optimized Automated Analysis of Live Neuronal Mitochondria Homeostasis Modulation by Isoform-Specific Retinoic Acid Receptors

Optimized Automated Analysis of Live Neuronal Mitochondria Homeostasis Modulation by Isoform-Specific Retinoic Acid Receptors

Published on: July 28, 2023

Related Experiment Videos

Last Updated: May 31, 2026

Disrupting Reconsolidation of Fear Memory in Humans by a Noradrenergic β-Blocker

Disrupting Reconsolidation of Fear Memory in Humans by a Noradrenergic β-Blocker

Published on: December 18, 2014

Methods for the Discovery of Novel Compounds Modulating a Gamma-Aminobutyric Acid Receptor Type A Neurotransmission

Methods for the Discovery of Novel Compounds Modulating a Gamma-Aminobutyric Acid Receptor Type A Neurotransmission

Published on: August 16, 2018

Optimized Automated Analysis of Live Neuronal Mitochondria Homeostasis Modulation by Isoform-Specific Retinoic Acid Receptors

Optimized Automated Analysis of Live Neuronal Mitochondria Homeostasis Modulation by Isoform-Specific Retinoic Acid Receptors

Published on: July 28, 2023

Area of Science:

Neuroscience
Pharmacology
Herbal Medicine Research

Background:

BR-16A is a herbal preparation with proposed psychotropic effects.
Previous research suggests BR-16A may enhance cognition and mitigate amnesia in animal models.
The central nervous system's noradrenergic and dopaminergic pathways are crucial for cognitive functions.

Purpose of the Study:

To determine if BR-16A influences central noradrenergic and dopaminergic functioning.
To assess the impact of BR-16A on neurotransmitter receptor activity in vivo.

Main Methods:

Adult male Sprague-Dawley rats were administered BR-16A (200mg/kg) or vehicle for one month.
Animals were challenged with clonidine (alpha-2 noradrenergic agonist) or apomorphine (dopamine agonist).
Locomotor activity was measured in an open field to assess receptor-mediated responses.

Main Results:

BR-16A did not alter clonidine-induced hypomotility, indicating no interference with alpha-2 noradrenergic receptor function.
BR-16A did not affect apomorphine-induced hypermotility, suggesting no impact on dopamine postsynaptic receptor function.
The herbal preparation showed no significant effect on the tested neurotransmitter pathways.

Conclusions:

BR-16A does not appear to modulate alpha-2 noradrenergic or dopamine postsynaptic receptor activity.
These findings suggest BR-16A's psychotropic effects, if any, may operate through different neurobiological mechanisms.
Further research is needed to elucidate the precise mechanisms underlying BR-16A's purported cognitive and amnesia-ameliorating properties.