pH transients due to monosynaptic activation of GABAA receptors in rat hippocampal slices

Kaila, Kai; Paalasmaa, Pekka; Taira, Tomi; Voipio, Juha

doi:10.1097/00001756-199201000-00028

Cited by 94 publications

(60 citation statements)

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“…Neuronal activity causes rapid alkalosis by a tenth of a pH unit, which is followed by longer lasting acidosis by about two-tenths of a pH unit [for example in the cerebellum (477), in the cortex (942), in the hippocampus (431) or in the spinal cord (423)]. In the optic nerve, a white matter tract, the onset of neuronal activity only triggers an acid shift (191).…”

Section: E Proton Channelsmentioning

confidence: 99%

Physiology of Microglia

Kettenmann

Hanisch

Нода

et al. 2011

Physiological Reviews

3,144

2,981

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Microglial cells are the resident macrophages in the central nervous system. These cells of mesodermal/mesenchymal origin migrate into all regions of the central nervous system, disseminate through the brain parenchyma, and acquire a specific ramified morphological phenotype termed “resting microglia.” Recent studies indicate that even in the normal brain, microglia have highly motile processes by which they scan their territorial domains. By a large number of signaling pathways they can communicate with macroglial cells and neurons and with cells of the immune system. Likewise, microglial cells express receptors classically described for brain-specific communication such as neurotransmitter receptors and those first discovered as immune cell-specific such as for cytokines. Microglial cells are considered the most susceptible sensors of brain pathology. Upon any detection of signs for brain lesions or nervous system dysfunction, microglial cells undergo a complex, multistage activation process that converts them into the “activated microglial cell.” This cell form has the capacity to release a large number of substances that can act detrimental or beneficial for the surrounding cells. Activated microglial cells can migrate to the site of injury, proliferate, and phagocytose cells and cellular compartments.

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Section: E Proton Channelsmentioning

confidence: 99%

Physiology of Microglia

Kettenmann

Hanisch

Нода

et al. 2011

Physiological Reviews

3,144

2,981

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“…This was necessary because of the extremely brief (20-ms) orthodromic stimulus train used to elicit rapid alkaline transients (see following text and DISCUSSION). Picrotoxin (100 M) was included to prevent the generation of extracellular alkaline transients arising from HCO 3 Ϫ efflux across GABA A anion channels (Chen and Chesler 1992b;Kaila et al 1992). Exogenous CA, added to the saline in some experiments, consisted of purified bovine type II isoform.…”

Section: Preparation and Solutionsmentioning

confidence: 99%

“…In hippocampus, two kinds of alkaline transients occur with stimulation of the Schaffer collaterals. One form arises from the efflux of HCO 3 Ϫ across ␥-aminobutyric acid type A (GABA A ) anion channels and is blocked by inhibitors of extracellular carbonic anhydrase (ECA) (Chen and Chesler 1992b;Kaila et al 1992). A second form of alkaline shift, addressed in this study, is independent of HCO 3 Ϫ (Chesler and Chan 1988; and is amplified by ECA blockers such as benzolamide (Chen and Chesler 1992b,c).…”

Section: Introductionmentioning

confidence: 99%

Kinetics of Activity-Evoked pH Transients and Extracellular pH Buffering in Rat Hippocampal Slices

Tong¹,

Chen²,

Chesler³

2006

Journal of Neurophysiology

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Tong, Chi-Kun, Kevin Chen, and Mitchell Chesler. Kinetics of activity-evoked pH transients and extracellular pH buffering in rat hippocampal slice. J Neurophysiol 95: 3686 -3697, 2006. First published April 12, 2006 doi:10.1152/jn.01312.2005. The kinetics of activity-dependent, extracellular alkaline transients, and the buffering of extracellular pH (pH e ), were studied in rat hippocampal slices using a fluorescein-dextran probe. Orthodromic stimuli generated alkaline transients Յ0.05 pH units that peaked in 273 Ϯ 26 ms and decayed with a half-time of 508 Ϯ 43 ms. Inhibition of extracellular carbonic anhydrase (ECA) with benzolamide increased the rate of rise by 25%, doubled peak amplitude, and prolonged the decay three-to fourfold. The slow decay in benzolamide allowed marked temporal summation, resulting in a severalfold increase in amplitude during long stimulus trains. Addition of exogenous carbonic anhydrase reduced the rate of rise, halved the peak amplitude, but had no effect on the normalized decay. A simulation of extracellular buffering kinetics generated recoveries from a base load consistent with the observed decay of the alkaline transient in the presence of benzolamide. Under control conditions, the model approximated the observed decays with an acceleration of the CO 2 hydration-dehydration reactions by a factor of 2.5. These data suggest low endogenous ECA activity, insufficient to maintain equilibrium during the alkaline transients. Disequilibrium implies a time-dependent buffering capacity, with a CO 2 /HCO 3 Ϫ contribution that is small shortly after a base load. It is suggested that within 100 ms, extracellular buffering capacity is about 1% of the value at equilibrium and is provided mainly by phosphate. Accordingly, in the time frame of synaptic transmission, small base loads would generate relatively large changes in interstitial pH.

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“…A number of experiments have revealed the presence of carbonic anhydrase (CA) activity in the extracellular space of the brain, using inhibitors of the enzyme that do not readily cross cell membranes (Chen and Chesler, 1992a, b;Kaila et al, 1992;Huang et al, 1995). The cellular localization of extracellular CA and the particular isoforms responsible for this activity remain unclear.…”

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confidence: 99%

Surface carbonic anhydrase activity on astrocytes and neurons facilitates lactate transport

Svichar

Chesler

2003

Glia

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A number of studies have provided physiological evidence for extracellular carbonic anhydrase (CA) in brain. Association of extracellular CA with glia has been limited to functional studies of gliotic slices and retinal Muller cells. While astrocytes contain intracellular CA, there has been no direct evidence for surface CA on these cells. In fact, some morphological studies suggest that the extracellular CA in brain parenchyma resides on neurons, not glia. There has been no functional demonstration of extracellular CA activity on CNS neurons, however. Here we capitalized on the H ϩ dependence of inward lactate transport to reveal functional extracellular CA activity on cultured astrocytes and acutely isolated hippocampal pyramidal neurons. Exposure to 20 mM L-lactate produced a rapid acidification of astrocytes that was reversibly blocked by 10 M benzolamide. The lactate-induced acidification (LIA) was also blocked by a dextran-conjugated CA inhibitor. In CO 2 /HCO 3 Ϫ -free, HEPES-buffered media, the LIA was largely unaffected. Acutely dissociated hippocampal pyramidal neurons underwent a similar LIA that was reversibly blocked by benzolamide. Surface CA is likely to facilitate lactate transport by enabling rapid replenishment (i.e., buffering) of surface H ϩ required for inward lactate-H ϩ cotransport. These results demonstrate functional surface CA for the first time on individual mammalian astrocytes and neurons and suggest that this enzyme may play a role in the utilization of monocarboxylate substrates such as lactate and pyruvate by the brain. GLIA 41:415-419, 2003.

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pH transients due to monosynaptic activation of GABAA receptors in rat hippocampal slices

Cited by 94 publications

References 0 publications

Physiology of Microglia

Physiology of Microglia

Kinetics of Activity-Evoked pH Transients and Extracellular pH Buffering in Rat Hippocampal Slices

Surface carbonic anhydrase activity on astrocytes and neurons facilitates lactate transport

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