Related Experiment Video
Updated: Jun 6, 2026
04:33
Primary Culture of Rat Adrenocortical Cells and Assays of Steroidogenic Functions
Published on: March 12, 2019
β-endorphin binding in cultured adrenal cortical cells
R A Gelfand1, A Bobrow, L Pham
1Department of Veteran Affairs Medical Center, Endocrinology and Research Services, Long Beach, CA.
Endocrine
|December 15, 2010
Summary
Bovine adrenal cells bind beta-endorphin via a naloxone-insensitive, non-opioid receptor. This receptor shares characteristics with those found in immune cells, suggesting a conserved signaling pathway.
Area of Science:
- Endocrinology
- Neuroscience
- Cell Biology
Background:
- Beta-endorphin is a polypeptide hormone with known roles in pain and stress.
- Adrenal cortical cells are key endocrine regulators.
- The existence of non-opioid receptors for beta-endorphin suggests diverse signaling mechanisms.
Purpose of the Study:
- To characterize the binding properties of beta-endorphin on cultured bovine adrenal cortical cells.
- To identify the molecular characteristics of the beta-endorphin receptor on these cells.
- To compare these binding characteristics with known non-opioid receptors.
Main Methods:
- Radioligand binding assays using [3H]-beta-endorphin.
- Competition binding studies with various peptides and fragments.
- Molecular cross-linking experiments to identify receptor subunits.
- Analysis of binding affinity (Kd) and receptor subunit molecular weights.
Main Results:
- Beta-endorphin binding is naloxone-insensitive, indicating a non-opioid mechanism.
- N-Acetyl-beta-endorphin is equipotent with beta-endorphin.
- Specific structural features of beta-endorphin influence binding affinity.
- Competition studies revealed a single affinity class with Kd = 33 nM.
- Cross-linking identified putative receptor subunits at 85, 64, 54, and 44 kD.
- Differential cross-linking suggests distinct subunit properties.
Conclusions:
- Bovine adrenal cortical cells possess a non-opioid receptor for beta-endorphin.
- The receptor structure involves multiple subunits with varying properties.
- These findings align with previously identified non-opioid beta-endorphin receptors in immune cells.
- Suggests a conserved non-opioid signaling pathway for beta-endorphin across different cell types.
Related Concept Videos
01:26Adrenergic 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...
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...
01:31Hormones of the Adrenal Glands
Adrenal hormones play a pivotal role in maintaining the body's electrolyte balance and orchestrating responses to stress, showcasing the intricate functions of the adrenal cortex and medulla.
The adrenal cortex, a powerhouse of hormone synthesis, generates over two dozen corticosteroid hormones. The zona glomerulosa produces mineralocorticoids, exemplified by aldosterone, influencing the electrolyte composition of body fluids. The synthesis of glucocorticoids such as cortisol and corticosterone...
The adrenal cortex, a powerhouse of hormone synthesis, generates over two dozen corticosteroid hormones. The zona glomerulosa produces mineralocorticoids, exemplified by aldosterone, influencing the electrolyte composition of body fluids. The synthesis of glucocorticoids such as cortisol and corticosterone...
01:19Cushing Syndrome II: Pathophysiology
Cortisol production is normally governed by the hypothalamic–pituitary–adrenal (HPA) axis, which maintains hormonal balance through tightly regulated feedback mechanisms. Disruption of this regulatory system is central to the development of Cushing syndrome, whether the excess cortisol originates from external medications or internal pathology. Persistent cortisol elevation alters metabolism, immune function, and endocrine signaling, producing the characteristic clinical features of the...
01:27Adrenergic 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...
α-Adrenoceptors
α-Adrenoceptors are classified into two main subtypes: α1 and α2. The α1 adrenoceptors, which are found on postsynaptic...
01:26Cushing Syndrome I: Introduction
Cushing syndrome refers to the collection of clinical manifestations that arise when tissues are exposed to excessive amounts of cortisol or cortisol-like medications over an extended period. Cortisol, a glucocorticoid produced by the adrenal cortex, regulates metabolism, immune responses, and the body’s adaptation to stress. When its concentration remains chronically elevated, these physiological pathways become dysregulated, resulting in the characteristic features of the syndrome.Exogenous...
01:09GPCRs Regulate Adenylyl Cylase Activity
Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
Two...