Increase of ryanodine receptors by dopamine D1 receptors is negatively regulated by γ-aminobutyric acid type B receptors in primary cultures of mouse cerebral cortical neurons

2012 ◽  
Vol 90 (8) ◽  
pp. 1626-1638 ◽  
Author(s):  
Kazuhiro Kurokawa ◽  
Koji Mizuno ◽  
Seitaro Ohkuma
Keyword(s):  
Cortical Neurons ◽  
Ryanodine Receptors ◽  
Primary Cultures ◽  
Aminobutyric Acid ◽  
D1 Receptors ◽  
Type B ◽  
Dopamine D1 Receptors ◽  
Acid Type ◽  
Cerebral Cortical Neurons

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

Neuroprotective effects of vitexin by inhibition of NMDA receptors in primary cultures of mouse cerebral cortical neurons

2013 ◽  
Vol 386 (1-2) ◽  
pp. 251-258 ◽  
Author(s):  
Le Yang ◽  
Zhi-ming Yang ◽  
Nan Zhang ◽  
Zhen Tian ◽  
Shui-bing Liu ◽  
...  
Keyword(s):  
Nmda Receptors ◽  
Cortical Neurons ◽  
Primary Cultures ◽  
Neuroprotective Effects ◽  
Cerebral Cortical Neurons

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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