...looking for mini pH sensor

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Hss's picture
...looking for mini pH sensor

We are looking for the best way to check the intracellular pH of cells. Do you know about some small pH sensors or some way to do this measurement?

Bluejay's picture
Traditionally, we've used

Traditionally, we've used fluorescent intracellular dyes such as 2′7′-bis(carboxyethyl)-5(6)-carboxyfluorescin  (BCECF) or SNARF to measure intracellular pH.  Try looking at Invitrogen's Molecular Probes handbook. for further details  A link is attached below.

Fraser Moss
Fraser Moss's picture
here's an example for

here's an example for you
Brain Research
Volume 1017, Issues 1-2, 13 August 2004, Pages 137-145

Intracellular pH and KATP channel activity in dorsal vagal neurons of juvenile rats in situ during metabolic disturbances

Tobias Raupach and Klaus Ballanyi

a II. Physiologisches Institut Universität Göttingen, Humboldtallee 23, D-37073, Göttingen, Germany
b Perinatal Research Centre, Department of Physiology, University of Alberta, 232 HMRC, Edmonton, Alberta, Canada T6G 2S2

Accepted 10 May 2004. 

Available online 20 June 2004.

Intracellular pH (pHi) is an important factor for understanding cellular processes associated with the response of central neurons to metabolic disturbances such as anoxia or ischemia. In the present study, pHi was fluorometrically measured in 2′7′-bis(carboxyethyl)-5(6)-carboxyfluorescin (BCECF)-filled, voltage-clamped dorsal vagal neurons (DVN) of brainstem slices from rats during metabolic disturbances activating ATP-sensitive K+ (KATP) channels. Chemical anoxia induced by cyanide, rotenone or p-trifluoromethoxy-phenylhydrazone (FCCP) decreased pHi by >0.4 pH units. Untreated neurons with normal pHi baseline (7.2) responded to glucose-free superfusate after a delay of 7–16 min with a progressive fall of pHi. In contrast, pHi increased by >0.2 pH units after 10 min in cells that had a mean pHi of 6.8 due to incomplete recovery from a CN–induced acid load prior to glucose depletion. Metabolic arrest, induced by cyanide in glucose-free solution after 30 min preincubation in glucose-free saline, caused a progressive glutamate-mediated inward current with no change of pHi. Upon metabolic arrest, depolarization-evoked pHi decreases (0.2 pH units) were abolished, whereas glucose-free superfusate slightly delayed their recovery without major effects on amplitude. The glucose-dependent pHi fall coincided with activation of the KATP channel-mediated outward current, while KATP currents due to anoxia or metabolic arrest could reach their maximum in the absence of a major pHi change. The results indicate that the anoxic pHi decrease is due to enhanced glycolysis and lactate formation with often no obvious effect on KATP channel activity. The origin of glucose-dependent acidosis and its relation to KATP channel activity remain to be determined.

Author Keywords: Aglycemia; BCECF; FCCP; Hypoxia; Intracellular pH; Ischemia