The G-protein activates a downstream signalling cascade that causes increased level of cyclic-AMP ( cAMP ), which trigger neurotransmitter release.

When glucose level is low, glucagon is released into the bloodstream, triggering a cAMP signal cascade.

cAMP is known as a second messenger.

cAMP ( cyclic adenosine monophosphate ) is an important molecule in eukaryotic signal transduction, a so-called second messenger.

This is a useful technique for researchers in neuroscience because it allows them to quickly increase the intracellular cAMP levels in particular neurons, and to study the effect of that increase in neural activity on the behavior of the organism.

The cAMP Dependent Pathway is used as a signal transduction pathway for many hormones including:

** Cyclic nucleotide-gated channels: This family of channels is characterized by activation due to the binding of intracellular cAMP or cGMP, with specificity varying by member.

Dopamine is a neurotransmitter that acts on D1 type ( D1 and D5 ) Gs coupled receptors, which increase cAMP and PKA, and D2 type ( D2, D3, and D4 ) receptors, which activate Gi-coupled receptors that decrease cAMP and PKA.

A phosphodiesterase inhibitor is a drug that blocks one or more of the five subtypes of the enzyme phosphodiesterase ( PDE ), therefore preventing the inactivation of the intracellular second messengers cyclic adenosine monophosphate ( cAMP ) and cyclic guanosine monophosphate ( cGMP ) by the respective PDE subtype ( s ).

PDE10A is almost exclusively expressed in the striatum and subsequent increase in cAMP and cGMP after PDE10A inhibition ( e. g. by papaverine ) is " a novel therapeutic avenue in the discovery of antipsychotics ".

This is mediated via the A1 receptor, inhibiting adenylyl cyclase, reducing cAMP and so causing cell hyperpolarization by increasing outward K + flux.

Glucagon is the specific antidote for beta-blocker poisoning, because it increases intracellular cAMP and cardiac contractility.

The Na < sup >+</ sup >/ K < sup >+</ sup >- ATPase is upregulated by cAMP.

* Direct sympathetic innervation of the salivary glands takes place via preganglionic nerves in the thoracic segments T1-T3 which synapse in the superior cervical ganglion with postganglionic neurons that release norepinephrine, which is then received by β-adrenergic receptors on the acinar and ductal cells of the salivary glands, leading to an increase in cyclic adenosine monophosphate ( cAMP ) levels and the corresponding increase of saliva secretion.

In decidual cells and in lymphocytes the distal promoter and thus prolactin expression is stimulated by cAMP.

Responsivness to cAMP is mediated by an imperfect cAMP – responsive element and two CAAT / enhancer binding proteins ( C / EBP ).

One explanation is most basically due to an increased amount of cyclic AMP ( cAMP ) in the ventricular cardiac myocytes leading to increased flow of calcium ions into the cell.

In Dictyostelium, aggregation is signalled by cAMP, but others use different chemicals.

The effect of this is to relay the signal throughout the nearby population of amoebae and cause inward movement to the area of highest cAMP concentration.

One important note is the differential effects of increased cAMP in smooth muscle compared to cardiac muscle.

* cAMP receptor protein ( also known as catabolite gene activator protein ) is a regulatory protein in bacteria

In cell biology, Protein kinase A ( PKA ) refers to a family of enzymes whose activity is dependent on cellular levels of cyclic AMP ( cAMP ).

Under low levels of cAMP, the holoenzyme remains intact and is catalytically inactive.

The α subunit is thought to be the effector region responsible for stimulation of adenylate cyclase ( involved the generation of cAMP ).

CREB is closely related in structure and function to CREM ( cAMP response element modulator ) and ATF-1 ( activating transcription factor-1 ) proteins.

An increase in cAMP results in an increase in the active form of PKA, which is directly related with an inhibition in platelet aggregation.

# competitive nonselective phosphodiesterase inhibitors which raise intracellular cAMP, activate PKA, inhibit TNF-alpha and leukotriene synthesis, and reduce inflammation and innate immunity and

Upon ligand binding, the receptor undergoes conformation changes that stimulate the enzyme adenylyl cyclase, which leads to an increase in intracellular cAMP and subsequent activation of protein kinase A.

The rise in cAMP then triggers the insertion of aquaporin-2 water channels by exocytosis of intracellular vesicles, recycling endosomes.

Agonist binding thus causes a rise in the intracellular concentration of the second messenger cAMP.

Downstream effectors of cAMP include cAMP-dependent protein kinase ( PKA ), which mediates some of the intracellular events following hormone binding.

β receptors couple to Gs alpha subunit | G < sub > s </ sub >, and increases intracellular cyclic amp | cAMP activity, resulting in e. g. heart muscle contraction, smooth muscle relaxation and glycogenolysis.

These receptors generally function via intracellular second messengers, including cyclic AMP ( cAMP ), inositol 1, 4, 5-trisphosphate ( IP3 ) and the calcium ( Ca < sup > 2 +</ sup >)- calmodulin system.

229: 119-127 PMID 11133158 </ Ref > The activated OR in turn activates the intracellular G-protein, GOLF ( GNAL ), adenylate cyclase and production of cyclic AMP ( cAMP ) opens ion channels in the cell membrane, resulting in an influx of sodium and calcium ions into the cell, and an efflux of chloride ions.

The histamine receptors act by increasing intracellular cAMP, whereas the muscarinic and gastrin receptors increase intracellular Ca < sup > 2 +</ sup > levels.

Activation of D < sub > 1 </ sub >- like family receptors is coupled to the G protein G < sub > αs </ sub >, which subsequently activates adenylate cyclase, increasing the intracellular concentration of the second messenger cyclic adenosine monophosphate ( cAMP ).

An influx of Ca < sup > 2 +</ sup > produces increased intracellular cAMP levels and thus, an increase in motility.

Epinephrine activates adenylate cyclase through a seven transmembrane receptor coupled to G < sub > s </ sub > which, in turn, activates adenylate cyclase to increase intracellular concentrations of cAMP.

In the lung, cAMP causes a decrease in the intracellular calcium concentration and, via activation of protein kinase A, both inactivates myosin light chain kinase and activates myosin light chain phosphorylase.

Like other methylated xanthine derivatives, pentoxifylline is a competitive nonselective phosphodiesterase inhibitor which raises intracellular cAMP, activates PKA, inhibits TNF and leukotriene synthesis, and reduces inflammation and innate immunity.

This pathway increases the intracellular levels of 12-HPETE ( 12-Hydroperoxy-5, 8, 10, 14-Eicosatetraenoic Acid ), which induces cGMP signaling and subsequently causes a decrease in the cAMP / cGMP ratio.

# competitive nonselective phosphodiesterase inhibitor which raises intracellular cAMP, activates PKA, inhibits TNF-alpha and leukotriene synthesis, and reduces inflammation and innate immunity and