Related Experiment Video
Updated: Aug 8, 2026
06:40
Impact of Intracardiac Neurons on Cardiac Electrophysiology and Arrhythmogenesis in an Ex Vivo Langendorff System
Published on: May 22, 2018
Relation between catecholamine-induced cyclic AMP changes and hyperpolarization in isolated rat sympathetic ganglia
The Journal of Physiology
|May 1, 1979
Summary
Catecholamines stimulate cyclic adenosine monophosphate (cAMP) production via beta-receptors in rat ganglia, but do not mediate hyperpolarization. Exogenous cAMP hyperpolarizes ganglia, suggesting an action on adenosine receptors, not intracellular signaling pathways.
Area of Science:
- Neuroscience
- Pharmacology
- Cellular Signaling
Background:
- Catecholamines modulate neuronal function through various signaling pathways.
- Cyclic adenosine monophosphate (cAMP) is a key intracellular second messenger.
- Ganglion hyperpolarization affects neuronal excitability.
Purpose of the Study:
- To investigate the role of cyclic adenosine monophosphate (cAMP) in catecholamine-induced hyperpolarization of isolated rat superior cervical ganglia.
- To determine the receptor subtypes involved in catecholamine effects on cAMP production and ganglion hyperpolarization.
Main Methods:
- Measurement of cAMP levels in isolated rat superior cervical ganglia after incubation with various catecholamines and receptor antagonists.
- Assessment of ganglion hyperpolarization induced by catecholamines and exogenous cAMP.
- Use of specific agonists and antagonists for alpha- and beta-adrenergic receptors.
- Inhibition of phosphodiesterase activity.
Main Results:
- Isoprenaline (a beta-agonist) significantly increased cAMP levels, mediated via beta-receptors.
- Alpha-agonists (phenylephrine, dopamine, clonidine) did not increase ganglionic cAMP levels.
- Exogenous cAMP induced ganglion hyperpolarization, an effect mimicked by adenosine and adenosine monophosphate.
- Neither theophylline nor a phosphodiesterase inhibitor enhanced catecholamine-induced hyperpolarization.
Conclusions:
- Cyclic AMP production is primarily mediated by beta-receptors, while catecholamine-induced hyperpolarization involves alpha-receptors.
- Cyclic AMP is unlikely to be the mediator of catecholamine-induced hyperpolarization in rat superior cervical ganglia.
- The hyperpolarizing effect of exogenous cAMP may involve interactions with external adenosine receptors.
Related Concept Videos
01:21G-Protein Gated Ion Channels
GPCRs are primarily responsible for our sense of smell, taste, and vision. The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory organs,...
Sensory organs,...
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...
01:25cAMP-dependent Protein Kinase Pathways
Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
01:23Drugs Acting on Autonomic Ganglia: Stimulants
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 sympathetic or...
01:27Adrenergic 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...
Synthesis: Catecholamine synthesis requires tyrosine, which is taken...
01:30Parasympathetic Signaling
Parasympathetic signaling plays a crucial role in regulating various physiological processes. It involves the release of acetylcholine (ACh) by parasympathetic neurons, which can have localized and short-lived effects. The majority of ACh released is rapidly inactivated at the synapse by the enzyme acetylcholinesterase (AChE), which hydrolyzes Ach into choline and acetate. Additionally, the tissue cholinesterase deactivates any ACh diffusing into the surrounding tissues.
The effects of...
The effects of...