Mo1755 Recombinant Accessory Cholera Enterotoxin (ACE) of Vibrio Cholera Induces Diarrhea by Stimulation of a Chloride Channel and Inhibition of the Na+/ Glucose Co-Transporter SGLT1

2014 ◽  
Vol 146 (5) ◽  
pp. S-652
Author(s):  
Irshad A. Sheikh ◽  
Tanaya Chatterjee ◽  
Mikio Hayashi ◽  
Dhira Rani Saha ◽  
Pinak Chakrabarti ◽  
...  
2005 ◽  
Vol 1 ◽  
pp. 1744-8069-1-2 ◽  
Author(s):  
Shui-Wang Ying ◽  
Peter A Goldstein

Propofol is a widely used intravenous general anesthetic. Propofol-induced unconsciousness in humans is associated with inhibition of thalamic activity evoked by somatosensory stimuli. However, the cellular mechanisms underlying the effects of propofol in thalamic circuits are largely unknown. We investigated the influence of propofol on synaptic responsiveness of thalamocortical relay neurons in the ventrobasal complex (VB) to excitatory input in mouse brain slices, using both current- and voltage-clamp recording techniques. Excitatory responses including EPSP temporal summation and action potential firing were evoked in VB neurons by electrical stimulation of corticothalamic fibers or pharmacological activation of glutamate receptors. Propofol (0.6 – 3 μM) suppressed temporal summation and spike firing in a concentration-dependent manner. The thalamocortical suppression was accompanied by a marked decrease in both EPSP amplitude and input resistance, indicating that a shunting mechanism was involved. The propofol-mediated thalamocortical suppression could be blocked by a GABAA receptor antagonist or chloride channel blocker, suggesting that postsynaptic GABAA receptors in VB neurons were involved in the shunting inhibition. GABAA receptor-mediated inhibitory postsynaptic currents (IPSCs) were evoked in VB neurons by electrical stimulation of the reticular thalamic nucleus. Propofol markedly increased amplitude, decay time, and charge transfer of GABAA IPSCs. The results demonstrated that shunting inhibition of thalamic somatosensory relay neurons by propofol at clinically relevant concentrations is primarily mediated through the potentiation of the GABAA receptor chloride channel-mediated conductance, and such inhibition may contribute to the impaired thalamic responses to sensory stimuli seen during propofol-induced anesthesia.


2009 ◽  
Vol 136 (5) ◽  
pp. A-712
Author(s):  
Zhihong Lin ◽  
Olga Kovbasnjuk ◽  
Rakhilya Murtazina ◽  
Boyoung Cha ◽  
Nicholas C. Zachos ◽  
...  

1971 ◽  
Vol 50 (6) ◽  
pp. 1218-1230 ◽  
Author(s):  
Daniel V. Kimberg ◽  
Michael Field ◽  
Judith Johnson ◽  
Antonia Henderson ◽  
Elaine Gershon

1995 ◽  
Vol 19 (2) ◽  
pp. 65-72
Author(s):  
Nina I. Smirnova ◽  
Elena A. Zhuravlyova ◽  
Ludmila F. Livanova ◽  
Sophya V. Shopyreva

PLoS ONE ◽  
2015 ◽  
Vol 10 (11) ◽  
pp. e0141283 ◽  
Author(s):  
Tanaya Chatterjee ◽  
Irshad Ali Sheikh ◽  
Devlina Chakravarty ◽  
Pinak Chakrabarti ◽  
Paramita Sarkar ◽  
...  

2013 ◽  
Vol 465 (11) ◽  
pp. 1583-1597 ◽  
Author(s):  
Negah Rahmati ◽  
Karl Kunzelmann ◽  
Jie Xu ◽  
Sharon Barone ◽  
Lalida Sirianant ◽  
...  

1975 ◽  
Vol 62 (3) ◽  
pp. 696-703 ◽  
Author(s):  
Kanji Sato ◽  
Yukitaka Miyachi ◽  
Nakaaki Ohsawa ◽  
Kinori Kosaka

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