Glial Cells

Orkand, Richard K.

doi:10.1002/cphy.cp010123

Cited by 35 publications

(25 citation statements)

References 127 publications

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“…In this respect, the report that TTX can be toxic to astrocytes in culture (Sontheimer et al, 1994) may be relevant. Because astrocytes are needed to maintain appropriate ionic conditions at the Nodes of Ranvier (Orkand, 1977;Newman, 1993), a possible TTX-mediated astrocytic toxicity in vivo could contribute to the long conduction block we observed. Current electron microscopic studies in our laboratory may shed light on this possibility.…”

Section: Discussionmentioning

confidence: 93%

Local Blockade of Sodium Channels by Tetrodotoxin Ameliorates Tissue Loss and Long-Term Functional Deficits Resulting from Experimental Spinal Cord Injury

1997

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Although relatively little is known of the mechanisms involved in secondary axonal loss after spinal cord injury (SCI), recent data from in vitro models of white matter (WM) injury have implicated abnormal sodium influx as a key event. We hypothesized that blockade of sodium channels after SCI would reduce WM loss and long-term functional deficits. To test this hypothesis, a sufficient and safe dose (0.15 nmol) of the potent Na ϩ channel blocker tetrodotoxin (TTX) was determined through a doseresponse study. We microinjected TTX or vehicle (VEH) into the injury site at 15 min after a standardized contusive SCI in the rat. Behavioral tests were performed 1 d after injury and weekly thereafter. Quantitative histopathology at 8 weeks postinjury showed that TTX treatment significantly reduced tissue loss at the injury site, with greater effect on sparing of WM than gray matter. TTX did not change the pattern of chronic histopathology typical of this SCI model, but restricted its extent, tripled the area of residual WM at the epicenter, and reduced the average length of the lesions. Serotonin immunoreactivity caudal to the epicenter, a marker for descending motor control axons, was nearly threefold that of VEH controls. The increase in WM at the epicenter was significantly correlated with the decrease in functional deficits. The TTX group exhibited a significantly enhanced recovery of coordinated hindlimb functions, more normal hindlimb reflexes, and earlier establishment of a reflex bladder. The results demonstrate that Na ϩ channels play a critical role in WM loss in vivo after SCI.

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Section: Discussionmentioning

confidence: 93%

Local Blockade of Sodium Channels by Tetrodotoxin Ameliorates Tissue Loss and Long-Term Functional Deficits Resulting from Experimental Spinal Cord Injury

1997

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“…70) (Rall, 1977) and they are much smaller in glia (Orkand, 1977) and so are too fast to affect the time course of the K+ signal). Our experience during recording suggested that we were only a few micrometers from the cell membrane, not the 15 ,um necessitated by the calculation.…”

Section: Extraneuronal K+mentioning

confidence: 99%

“…From Williams, Grossman & Edmunds (1980), the cell surface to cell volume ratio (fi) of a glial cell is probably in the range 5000 cm-" to 50000 cm-'. If Rm = 400 Q1 cm2 (Orkand, 1977) and Ri = 100Q cm (Rall, 1977) and X = ,(1-cx) then 300 ,m > A > 90,um.…”

Section: Di8persal Of K+ In a Glial 8yncytiummentioning

confidence: 99%

Potassium accumulation around individual purkinje cells in cerebellar slices from the guinea‐pig.

Hounsgaard¹,

Nicholson²

1983

The Journal of Physiology

111

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6. The diffusion characteristics of the slices were determined by an ionophoretic method using tetramethylammonium and ion-selective micropipettes. The extracellular volume fraction of the slice averaged 028 while the tortuosity averaged 1-84.These values were close to those found previously in the intact rat cerebellum:. These data were used to make quantitative estimates of the expected [K+]o accumulation in the vicinity of a single cell (see Appendix). Such estimates showed reasonable agreement with the measured values.

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“…Communication between these different types of cells is indirectly mediated via the extracellular space. One of the best, and most extensively described examples of neurone-glia interaction is the regulation of extracellular K+ by the glial syncytium thereby influencing neuronal excitability (Orkand, 1977;Coles & Tsacopoulos, 1981). But K+ is not the only ion in the extracellular space which undergoes changes during neuronal activity.…”

Section: Introductionmentioning

confidence: 99%

Intracellular pH regulation in cultured mouse oligodendrocytes.

Kettenmann

Schlue

1988

The Journal of Physiology

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SUMMARY1. Intracellular pH (pHi) and the mechanism of pHi regulation have been investigated in cultured oligodendrocytes from mouse spinal cord using doublebarrelled neutral-carrier H+-selective microelectrodes. The distribution of H+ was not in electrochemical equilibrium. The pHi was more alkaline than the pH of the bathing medium (pHO), namely 7-5 at pHo 7-2 and 7-6 at pHo 7-4. 2. Removal of HCO3-from the bathing medium reduced the steady-state pHi by 0 4 units. An increase in extracellular K+ caused, with a delay, an increase in pHi. A decrease in pHO to 6-2 caused an acidification of pHi by 0 5 units.3. The pHi regulation was studied by applying and subsequently removing NH4, which resulted in an acidification of the cell. The subsequent recovery of pHi could then be analysed. The recovery from an acidification by 1 pH unit lasted 3-10 min.In HCO3--free solution pHi recovery was slowed. 4. In HCO3--free solution pHi recovery was completely blocked when either Na+ was removed or when amiloride was applied indicating an exclusive activation of the Na+-H+ exchanger.5. In the presence of HCO3 , removal of Na+ also completely blocked pH1 recovery. When Na+ was readded, pHi recovered. In HCO3--containing solution amiloride slightly slowed, but did not block pHi recovery.6. Removal of Cl-or application of SITS, DIDS or furosemide, blockers of Cl--coupled transport mechanisms, did not affect the pHi recovery in the presence of HCO3-.7. In conclusion, oligodendrocytes possess two mechanisms regulating pHi, a Na+-H+ exchanger and a Na+-HCO3-co-transporter while the latter is clearly more potent. It follows that pHi regulation of oligodendrocytes is dependent on the transmembrane Na+ gradient and is strictly separated from regulation of internal Cl.

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Glial Cells

Cited by 35 publications

References 127 publications

Local Blockade of Sodium Channels by Tetrodotoxin Ameliorates Tissue Loss and Long-Term Functional Deficits Resulting from Experimental Spinal Cord Injury

Local Blockade of Sodium Channels by Tetrodotoxin Ameliorates Tissue Loss and Long-Term Functional Deficits Resulting from Experimental Spinal Cord Injury

Potassium accumulation around individual purkinje cells in cerebellar slices from the guinea‐pig.

Intracellular pH regulation in cultured mouse oligodendrocytes.

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