scholarly journals The vasodepressor mechanism of action of 2-(l-octynyl)-adenosine, a novel adenosine A2 receptor agonist, does not involve inhibitory G protein in rats

1992 ◽  
Vol 58 ◽  
pp. 398
Author(s):  
So Furukawa ◽  
Keisuke Satoh ◽  
Norio Taira
Keyword(s):  
G Protein ◽  
Mechanism Of Action ◽  
Receptor Agonist ◽  
Adenosine A2 Receptor ◽  
Inhibitory G Protein

Opioid modulation of calcium current in cultured sensory neurons: μ-modulation of baroreceptor input

1999 ◽  
Vol 277 (2) ◽  
pp. H705-H713 ◽  
Author(s):  
Mary Hamra ◽  
Robert S. McNeil ◽  
Martin Runciman ◽  
Diana L. Kunze
Keyword(s):  
G Protein ◽  
Sensory Neurons ◽  
Mechanism Of Action ◽  
Pertussis Toxin ◽  
Calcium Current ◽  
Receptor Agonist ◽  
Age Groups ◽  
Opiate Receptor ◽  
Μ Opiate Receptor ◽  
Patch Technique

We used the whole cell open-patch or perforated-patch technique to characterize μ-opioid modulation of Ca2+ current ( I Ca) in nodose sensory neurons and in a specific subpopulation of nodose cells, aortic baroreceptor neurons. The μ-opiate receptor agonist Tyr-d-Ala-Gly-MePhe-Gly-ol enkephalin (DAGO) inhibited I Ca in 95% of neonatal [postnatal day (P)1–P3] nodose neurons. To the contrary, only 64% of juvenile cells (P20–P35) and 61% of adult cells (P60–P110) responded to DAGO. DAGO-mediated inhibition of I Ca was naloxone sensitive, irreversible in the presence of guanosine 5′- O-(3-thiotriphosphate), absent with guanosine 5′- O-(2-thiodiphosphate), and eliminated with pertussis toxin; DAGO’s inhibition of I Ca was G protein mediated. Incubation of neurons with ω-conotoxin GVIA eliminated the effect of DAGO in neonatal but not in juvenile cells. In the latter, DAGO reduced 37% of the current remaining in the presence of ω-conotoxin. In the subset of nodose neurons, aortic baroafferents, the effect of DAGO was concentration dependent, with an IC50 of 1.82 × 10−8 M. DAGO slowed activation of I Ca, but activation curves constructed from tail currents were the same with and without DAGO (100 nM). In summary, μ-opiate modulation of I Ca in nodose neurons was demonstrated in three age groups, including specifically labeled baroafferents. The demonstration of a mechanism of action of μ-opioids on baroreceptor afferents provides a basis for the attenuation of the baroreflex that occurs at the level of the nucleus tractus solitarii.

Reciprocal inhibition of voltage-gated potassium currents (IK(V)) by activation of cannabinoid CB1and dopamine D1receptors in ON bipolar cells of goldfish retina

2005 ◽  
Vol 22 (1) ◽  
pp. 55-63 ◽  
Author(s):  
SHIH-FANG FAN ◽  
STEPHEN YAZULLA
Keyword(s):  
G Protein ◽  
Receptor Agonist ◽  
Lucifer Yellow ◽  
Reciprocal Inhibition ◽  
Receptor Activation ◽  
Light Signal ◽  
Bipolar Cells ◽  
Protein G ◽  
Calcium Dependent ◽  
Voltage Dependent

Cannabinoid CB1receptor (viaGs) and dopamine D2receptor (viaGi/o) antagonistically modulate goldfish cone membrane currents. As ON bipolar cells have CB1and D1receptors, but not D2receptors, we focused on whether CB1receptor agonist and dopamine interact to modulate voltage-dependent outward membrane K+currentsIK(V)of the ON mixed rod/cone (Mb) bipolar cells. Whole-cell currents were recorded from Mb bipolar cells in goldfish retinal slices. Mb bipolar cells were identified by intracellular filling with Lucifer yellow. The bath solution was calcium-free and contained 1 mM cobalt to block indirect calcium-dependent effects. Dopamine (10 μM) consistently increasedIK(V)by a factor of 1.57 ± 0.12 (S.E.M.,n= 15). A CB receptor agonist, WIN 55212-2 (0.25–1 μM), had no effect, but 4 μM WIN 55212-2 suppressedIK(V)by 60%. IfIK(V)was first increased by 10 μM dopamine, application of WIN 55212-2 (0.25–1 μM) reversibly blocked the effect of dopamine even though these concentrations of WIN 55212-2 had no effect of their own. If WIN 55212-2 was applied first and dopamine (10 μM) was added to the WIN-containing solution, 0.1 μM WIN 55212-2 blocked the effect of dopamine. All effects of WIN 55212-2 were blocked by coapplication of SR 141716A (CB1antagonist) and pretreatment with pertussis toxin (blocker of Gi/o) indicating actionviaCB1receptor activation of G protein Gi/o. Coactivation of CB1and D1receptors on Mb bipolar cells produces reciprocal effects onIK(V). The CB1-evoked suppression ofIK(V)is mediated by G protein Gi/o, whereas the D1-evoked enhancement is mediated by G protein Gs. As dopamine is a retinal “light” signal, these data support our notion that endocannabinoids function as a “dark” signal, interacting with dopamine to set retinal sensitivity.

Receptors for bitter, sweet and umami taste couple to inhibitory G protein signaling pathways

2004 ◽  
Vol 489 (3) ◽  
pp. 139-149 ◽  
Author(s):  
Mark Ozeck ◽  
Paul Brust ◽  
Hong Xu ◽  
Guy Servant
Keyword(s):  
Signaling Pathways ◽  
G Protein ◽  
G Protein Signaling ◽  
Protein Signaling ◽  
Umami Taste ◽  
Inhibitory G Protein

scholarly journals 199 Takotsubo syndrome associated mir-16 and mir-26a reduce contractility of cardiomyocytes in vitro by an inhibitory g-?protein dependent mechanism

Heart ◽  
2017 ◽  
Vol 103 (Suppl 5) ◽  
pp. A135.1-A135
Author(s):  
Liam Couch ◽  
Anselm A Derda ◽  
Thomas Thum ◽  
Cesare Terracciano ◽  
Sian Harding
Keyword(s):  
G Protein ◽  
Takotsubo Syndrome ◽  
Inhibitory G Protein ◽  
Dependent Mechanism
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