scholarly journals Molecular Mechanism of Secreted Amyloid-β Precursor Protein in Binding and Modulating GABABR1a

2021 ◽  
Author(s):  
Mei Feng ◽  
Yi Song ◽  
Serena H. Chen ◽  
Yuanzhao Zhang ◽  
Ruhong Zhou
Keyword(s):  
Molecular Mechanism ◽  
Amyloid Β ◽  
Precursor Protein ◽  
Aminobutyric Acid ◽  
Type B ◽  
Intrinsically Disordered ◽  
Acid Type ◽  
Extension Domain

A recent phenomenal study discovered that the extension domain of secreted amyloid-β precursor protein (sAPP) can bind to the intrinsically disordered sushi 1 domain of the γ-aminobutyric acid type B...

Synthesis and Pharmacological Evaluation of Novel γ-Aminobutyric Acid Type B (GABAB) Receptor Agonists as Gastroesophageal Reflux Inhibitors

2008 ◽  
Vol 51 (14) ◽  
pp. 4315-4320 ◽  
Author(s):  
Christer Alstermark ◽  
Kosrat Amin ◽  
Sean R. Dinn ◽  
Thomas Elebring ◽  
Ola Fjellström ◽  
...  
Keyword(s):  
Gastroesophageal Reflux ◽  
Gabab Receptor ◽  
Aminobutyric Acid ◽  
Type B ◽  
Receptor Agonists ◽  
Pharmacological Evaluation ◽  
Acid Type

Evaluation of Difluoromethyl Ketones as Agonists of the γ-Aminobutyric Acid Type B (GABAB) Receptor

2013 ◽  
Vol 56 (6) ◽  
pp. 2456-2465 ◽  
Author(s):  
Changho Han ◽  
Amy E. Salyer ◽  
Eun Hoo Kim ◽  
Xinyi Jiang ◽  
Rachel E. Jarrard ◽  
...  
Keyword(s):  
Gabab Receptor ◽  
Aminobutyric Acid ◽  
Type B ◽  
Acid Type

Effects of baclofen on the Hering-Breuer inspiratory-inhibitory and deflation reflexes in rats

1998 ◽  
Vol 274 (2) ◽  
pp. R462-R469 ◽  
Author(s):  
Erin Seifert ◽  
Teresa Trippenbach
Keyword(s):  
Aminobutyric Acid ◽  
Type B ◽  
Rapid Adaptation ◽  
Inspiratory Time ◽  
Airway Occlusion ◽  
Acid Type ◽  
Tracheal Pressure ◽  
The Difference ◽  
Respiratory Phases ◽  
Stimulation Of

The objective of this study was to evaluate effects of baclofen, a γ-aminobutyric acid type B (GABAB) receptor agonist, injected into the nucleus of the solitary tract, on the Hering-Breuer inspiratory-inhibitory (Ti-inhibitory) and deflation reflexes in urethan-anesthetized adult Wistar rats ( n = 7). The Ti-inhibitory reflex was estimated from changes in peak amplitude of the integrated diaphragmatic electromyogram and inspiratory time (Ti) provoked by airway occlusion at end expiration. The deflation reflex was evaluated from changes in Ti and expiration (Te) of the first two breaths (Ti-1, Te-1 and Ti-2, Te-2) immediately after a decrease in tracheal pressure (Ptr). Under control conditions, airway occlusion at end-Te prolonged Ti (66 ± 5%; mean ± SE) and the following Te (54 ± 11%). Decreases in Ptr, from −2 to −5 cmH2O, evoked an increase in Ti and shortening of Te of both breaths. Both effects were Ptr dependent, and Ti-1 and Te-1 differed from Ti-2 and Te-2, suggesting a rapid adaptation to the stimulus. At Ptr of −5 cmH2O, Ti-1 and Ti-2 increased by 30 ± 2 and 43 ± 6%, respectively, and Te-1 and Te-2 decreased by 53 ± 4 and 33 ± 7%, respectively. During unloaded breathing, 60 pmol baclofen prolonged Ti by 120 ± 11% and left Te unaffected. Baclofen abolished vagally mediated changes in Te. On the other hand, the Ti increases caused by either airway occlusion (24 ± 8%) or Ptr of −5 cmH2O (Ti-1; 16 ± 5%) were still significant, but Ti-1 and Ti-2 were not different. A GABAB receptor antagonist, CGP-35348 (2.8 nmol), reversed these effects of baclofen. These results imply that stimulation of GABAB receptors attenuates but does abolish vagally mediated control of Ti. The difference in effects of baclofen on the central and vagal control of Ti and Te suggests different distribution of GABAB receptors in neuronal networks controlling each of these respiratory phases.

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