Electrophysiological Properties of Astrocytes

Ransom, Bruce R.; Carlini, Walter G.

doi:10.1016/b978-0-12-250452-5.50005-x

Cited by 38 publications

(33 citation statements)

References 210 publications

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“…Connors et al (1984) have reported that dye coupling in astrocytes in in vitro neocortical slices is very sensitive to C02 acidification of the bathing medium. Similar results were reported for the electrically and dye coupled ependymal cells in the turtle cortex (Ransom and Carlini, 1986). Therefore, dye coupling, presumably via gap junctions, can be abolished by decreasing pHi.…”

Section: Discussionsupporting

confidence: 87%

Lactic acid inhibition of gap junctional intercellular communication in in vitro astrocytes as measured by fluorescence recovery after laser photobleaching

Anders

1988

Glia

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Lactic acid can permeate plasma membranes, causing intracellular acidosis. Gap junctions are sensitive to pHi and can be reversibly uncoupled by weak acids. In this study, dye coupling between in vitro astrocytes, presumably mediated by gap junctions, was measured in the absence and presence of lactic acid. Fluorescence recovery after laser photobleaching (gap-FRAP analysis) was used to measure dye coupling. Astrocytes bathed in Eagle's minimum essential medium (EMEM) with lactic acid, pHo 5.5-6, showed no difference in their dye coupling (mean recovery of fluorescence 30%) when compared to control astrocytes (mean recovery of fluorescence 26%). However, 24 mM lactic acid in EMEM, pHo 4.5, decreased dye coupling (mean recovery of fluorescence 2.0%). This effect occurred within 5 min of treatment. When lactic acid-EMEM, pH 4.5, was removed from astrocytes after 30 min and the cells were incubated in EMEM for 24 hr, decreased coupling was not reversed (mean recovery 4.0%). When lactic acid-treated astrocytes were incubated in EMEM for 48 hr, the mean recovery of fluorescence increased to 15% (i.e., 42% of the recovery seen in controls). These observations suggest that brief exposure to high concentrations of lactic acid can have immediate and long-lasting effects on glial gap junctional communication. Under pathological circumstances, such a sequence could be initiated, and this might impair astrocytic control of the central nervous system microenvironment mediated by spatial buffering.

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Section: Discussionsupporting

confidence: 87%

Lactic acid inhibition of gap junctional intercellular communication in in vitro astrocytes as measured by fluorescence recovery after laser photobleaching

Anders

1988

Glia

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“…The widespread occurrence of a gap junction protein, in this case connexin43, that is involved in the formation of gap junctions between astrocytes is consistent with the general belief that astrocytic gap junctions are ubiquitous in CNS (Bennett and Goodenough, 1978;Dudek et al, 1983;Massa and Mugnaini, 1982;Mugnaini, 1986;Ransom and Carlini, 1986;Waxman and Black, 1984). However, based on previous anatomical studies of such junctions and on considerations of their equally ubiquitous role in forming astrocytic syncytial networks that contribute to the important process of potassium spatial buffering (Galambos, 1989;Orkand, 1977;Walz, 1989;Walz and Hertz, 1983), the degree of connexin43 heterogeneity observed in brain was entirely unexpected.…”

Section: Introductionsupporting

confidence: 73%

Quantitative immunohistochemical and biochemical correlates of connexin43 localization in rat brain

Nagy

Yamamoto

Sawchuk

et al. 1992

Glia

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We have shown by immunohistochemical methods that the gap junction protein connexin43 is heterogeneously distributed in rat brain (Yamamoto et al: J Comp Neurol 302:853, 1990). Here we have compared quantitatively the relative amount of connexin43 detected on Western blots of seven central nervous system (CNS) regions with the density of connexin43-immunoperoxidase reactivity in these regions. As has been observed on Western blots of several cell types, homogenates of these CNS regions contained two forms of connexin43, its dephospho form with an apparent mobility of approximately 41 kDa and its approximately 43 kDa phosphorylated form. While the relative quantities of connexin43 varied considerably among the brain regions, the ratio of the 43/41 kDa forms, 0.71, was relatively uniform (correlation coefficient, r = 0.92). Sections of brain processed for connexin43-immunolocalization by the peroxidase-antiperoxidase (PAP) method showed that chromogen deposition was linear with incubation time in reaction medium. Optical density of tissue connexin43-immunoreactivity in each of the seven areas plotted against the density of connexin43 bands on Western blots gave a correlation coefficient of r = 0.90. Connexin43-immunoreactivity had a similar appearance in sections processed by PAP or immunofluorescence procedures and consisted of isolated or aggregates of puncta.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Resistance increased by approximately an order of magnitude during hyperglycemic and com plete ischemia. Normally, astrocytes also have a membrane time constant of less than 1 ms (Tracht enberg and Pollen, 1970;Ransom and Carlini, 1986). In experiments reported here the astrocytic membrane time constant was increased by approx imately 1 order of magnitude, suggesting an in crease in specific membrane resistance.…”

Section: Astrocytic Mtmbrane Characteristics During Ischemiamentioning

confidence: 53%

“…The input resistance of normal cortical astrocytes is typically less than 10 MD (Trachtenberg and Pol len, 1970; also for review, see Ransom and Carlini, 1986). Resistance increased by approximately an order of magnitude during hyperglycemic and com plete ischemia.…”

Section: Astrocytic Mtmbrane Characteristics During Ischemiamentioning

confidence: 99%

Astrocytic Acidosis in Hyperglycemic and Complete Ischemia

Kraig

Chesler

1990

J Cereb Blood Flow Metab

160

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Summary: Nearly complete brain ischemia under normo glycemic conditions results in death of only selectively vulnerable neurons. With prior elevation of brain glucose, such injury is enhanced to include pancel1ular necrosis (i.e., infarction), perhaps because an associated, severe lactic acidosis preferentially injures astrocytes. However, no direct physiologic measurements exist to support this hypothesis. Therefore, we used microelectrodes to mea sure intracellular pH and passive electrical properties of cortical astrocytes as a first approach to characterizing the physiologic behavior of these cel1s during hypergly cemic and complete ischemia, conditions that produce infarction in reperfused brain. Anesthesized rats (n = 26) were made extremely hyperglycemic (blood glucose, 51.4 ± 2.8 mM) so as to create potentially the most extreme acidic conditions possible; then ischemia was induced by cardiac arrest. Two loci more acidic than the interstitial space (6.17-6.20 pH) were found. The more acidic locus [4.30 ± 0.19 (n = 5); range: 3.82-4.89] was occasional1y seen at the onset of anoxic depolarization, 3-7 min after Excessive brain acidosis is thought to be required for infarction from nearly complete ischemia under hyperglycemic conditions (Myers and Yamaguchi, 1fJ77; Ginsberg et aI., 1980; Welsh et aI., 1980; Ka limo et aI., 1981; Rehncrona et aI., 1981; Pulsinelli et aI., 1982). However, the cellular and physiological bases for such injury remain incompletely defined. Abbreviations used: HA, neutral lactic acid; HRP, horseradish peroxidase; NMR, nuclear magnetic resonance; pHj, intracellu lar pH; pHo' interstitial pH. 104cardiac arrest. The less acidic locus [5.30 ± 0.07 (n = 53); range 4.46-5.93)] was seen 5-46 min after cardiac arrest. A smal1 negative change in DC potential [8 ± 1 m V (n = 5); range -3 to -12 mV and 7 ± 2 mV (n = 53); range + 3 to -31 m V , respectively] was always seen upon im palement of acidic loci, suggesting cellular penetration. In a separate group of five animals, electrical characteristics of these cells were specifically measured (n = 17): mem brane potential was -12 ± 0.2 m V (range -3 to -24 mY), input resistance was 114 ± 16 Mil (range 25-250 Mil), and time constant was 4.4 ± 0.4 ms (range 3.0-7.9 ms). Injection of horseradish peroxidase into cells from either animal group uniformly stained degenerating astro cytes. These findings establish previously unrecognized properties of ischemic astrocytes that may be prerequi sites for infarction from nearly complete ischemia: the capacity to develop profound cellular acidosis and a con comitant reduction in cel1 membrane ion permeability.

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Electrophysiological Properties of Astrocytes

Cited by 38 publications

References 210 publications

Lactic acid inhibition of gap junctional intercellular communication in in vitro astrocytes as measured by fluorescence recovery after laser photobleaching

Lactic acid inhibition of gap junctional intercellular communication in in vitro astrocytes as measured by fluorescence recovery after laser photobleaching

Quantitative immunohistochemical and biochemical correlates of connexin43 localization in rat brain

Astrocytic Acidosis in Hyperglycemic and Complete Ischemia

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