Intracellular marking with Lucifer Yellow CH and horseradish peroxidase of cells electrophysiologically characterized as glia in the cerebral cortex of the cat

Takato, Michiaki; Goldring, Sidney

doi:10.1002/cne.901860205

Cited by 57 publications

(17 citation statements)

References 25 publications

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“…These cells (n = 3) (Fig. 6, upper left) had the features of protoplasmic astro cytes as noted in previous studies (Takato and Goldring, 1979;Chesler and Kraig, 1987). Second, HRP was similarly injected (n = 14) into living as trocytes, but animals were then killed by cardiac arrest, and perfusion-fixation was delayed for 20-40 min to allow ischemic-morphologic changes to occur.…”

Section: Horseradish Peroxidase Stainingmentioning

confidence: 66%

Astrocytic Acidosis in Hyperglycemic and Complete Ischemia

Kraig

Chesler

1990

J Cereb Blood Flow Metab

161

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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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Section: Horseradish Peroxidase Stainingmentioning

confidence: 66%

Astrocytic Acidosis in Hyperglycemic and Complete Ischemia

Kraig

Chesler

1990

J Cereb Blood Flow Metab

161

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“…However, the morphologies of neurons and glia have been extensively described (Fairen et al, 1977;Jones, 1975;Lund, 1973;Lund and Boothe, 1975;Peters and Jones, 1984a;Peters and Jones, 1984b;Takato and Goldring, 1979). These studies have established criteria that allow for discrimination between several cell types, based on their unique morphologies (e.g.…”

Section: Species Differences In the Distribution Of Dj-1 Protein In Hmentioning

confidence: 99%

Selective enrichment of DJ‐1 protein in primate striatal neuronal processes: Implications for Parkinson's disease

Olzmann

Bordelon

Muly

et al. 2006

J of Comparative Neurology

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Mutations in DJ-1 cause autosomal recessive, early-onset Parkinson's disease (PD). The precise function and distribution of DJ-1 in the central nervous system remain unclear. In this study, we performed a comprehensive analysis of DJ-1 expression in human, monkey, and rat brains using antibodies that recognize distinct, evolutionarily conserved epitopes of DJ-1. We found that DJ-1 displays region-specific neuronal and glial labeling in human and non-human primate brain, sharply contrasting the primarily neuronal expression pattern observed throughout rat brain. Further immunohistochemical analysis of DJ-1 expression in human and non-human primate brains showed that DJ-1 protein is expressed in neurons within the substantia nigra pars compacta and striatum, two regions critically involved in PD pathogenesis. Moreover, immunoelectron microscopic analysis revealed a selective enrichment of DJ-1 within primate striatal axons, presynaptic terminals, and dendritic spines with respect to the DJ-1 expression in prefrontal cortex. Together, these findings indicate neuronal and synaptic expression of DJ-1 in primate subcortical brain regions and suggest a physiological role for DJ-1 in the survival and/or function of nigral-striatal neurons. KeywordsPARK7; substantia nigra; striatum; electron microscopy; primate brain; distribution Parkinson's disease (PD) is a debilitating neurodegenerative movement disorder characterized by the relatively selective degeneration of nigral dopaminergic neurons (Lang and Lozano, 1998a;Lang and Lozano, 1998b). Recently, mutations in the gene encoding DJ-1 have been identified as the genetic defect responsible for the PARK7-associated autosomal recessive, early-onset form of familial PD (Abou-Sleiman et al., 2004;Bonifati et al., 2003). Accumulating evidence suggests that loss of DJ-1 function results in neurodegeneration, but the exact role of DJ-1 in the pathogenesis of PD is unknown (Cookson, 2005;Moore et al., 2005). Using X-ray crystallography, we and others have shown that DJ-1 is a 189 amino acid protein that adopts a helix-strand-helix dimeric structure with homology to the bacterial NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript protease PH1704 and Escherichia coli chaperone protein Hsp31 (Huai et al., 2003;Lee et al., 2003;Tao and Tong, 2003). Although the precise physiological function of DJ-1 remains unclear, DJ-1 has been implicated in several cellular processes including regulation of transcription, protein quality control, and oxidative stress response (Bonifati et al., 2004;Cookson, 2005;Moore et al., 2005). In addition, targeted disruption of DJ-1 gene expression in mice leads to altered dopamine D2 receptor signaling (Chen et al., 2005;Goldberg et al., 2005) and increased susceptibility to MPTP (1-methyl 4-phenyl 1,2,3,6-tetrahydropyridine)-induced neurodegeneration (Kim et al., 2005).The distribution of DJ-1 protein is controversial and remains poorly characterized. We previously showed that DJ-1 is mainly neuronal in cortical and subcor...

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“…The average long and short diameters of the soma were 5.9 and 3 9 ,tm, respectively (twenty-four cells), although these values were possibly over-estimated owing to the fluorescent halo. These structural features of the inexcitable cell generally conform to those of astrocytes (Dennis & Gerschenfeld, 1969;Kelly & van Essen, 1974;Takato & Goldring, 1979;Gutnick, Connors & Ransom, 1981 Dennis & Gerschenfeld, 1969), in vivo (38 mV, Ransom & Goldring, 1973a) and in culture (52 mV, Kettenmann, Sonnhof & Schachner, 1983;51 mV, Walz, Wuttke & Hertz, 1984). [K+o (mM) The input conductance of inexcitable cells during the slow potential was measured by passing hyperpolarizing current pulses of constant intensity (Fig.…”

Section: Morphology Of Inexcitable Cellsmentioning

confidence: 99%

“…They have demonstrated that the glial cell membrane behaves like T. TAKAHASHI AND H. TSURUHARA a K+ electrode and that a transient extracellular K+ accumulation caused by a nerve impulse produces a slow depolarizing potential in glial cells. Slow depolarizing potentials have also been observed in mammalian glia in vivo after tetanic nerve stimulation (Karahashi & Goldring, 1966;Somjen, 1970;Ransom & Goldring, 1973b;Lothman & Somjen, 1975;Takato & Goldring, 1979) or during drug-induced seizures (Sugaya, Goldring & O'Leary, 1964;Futamachi & Pedley, 1976). However, in the mammalian central nervous system in vivo, detailed studies of glial cells have been limited by the difficulties in attaining stable intracellular recordings and in controlling the extracellular ionic environment.…”

Section: Introductionmentioning

confidence: 99%

Slow depolarizing potentials recorded from glial cells in the rat superficial dorsal horn.

Takahashi

Tsuruhara

1987

The Journal of Physiology

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SUMMARY1. Intracellular potentials were recorded from inexcitable cells in the superficial dorsal horn of the rat lumbar spinal cord in vitro.2. These cells had a large resting membrane potential (up to -90 mV) but when depolarized were unable to produce action potentials. The resting potential was highly dependent upon extracellular K+ concentrations ([K+]0), with a slope of about 45 mV for a 10-fold change in [K+].3. Electrical stimulation of dorsal roots evoked a slow depolarizing potential lasting for many seconds in the inexcitable cells. The slow potentials were not accompanied by any appreciable change in input conductance, nor were their amplitudes dependent upon the membrane potential.4. The morphology of the inexcitable cells marked by intracellular injection of a fluorescent dye, Lucifer Yellow, was consistent with their being glial cells.5. [K+]. values were measured by K+-sensitive electrodes simultaneously with intracellular glial potentials. Changes in the K+-electrode potential occurred in parallel with slow depolarizing potentials following stimulation of dorsal roots. When the stimulus intensity was altered, changes in the magnitude of the K+-electrode response were correlated with those of the slow potentials.6. Replacement of extracellular Ca2+ by Mg2+ abolished both the slow potentials and K+-electrode responses evoked by afferent stimulation, suggesting that impulses in primary afferent fibres do not directly contribute to the glial slow potentials.7. It is concluded that the slow potentials in glial cells result from a transient increase in [K+]. at the superficial dorsal horn, which is induced by activation of neighbouring internuncial neurones.

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Intracellular marking with Lucifer Yellow CH and horseradish peroxidase of cells electrophysiologically characterized as glia in the cerebral cortex of the cat

Cited by 57 publications

References 25 publications

Astrocytic Acidosis in Hyperglycemic and Complete Ischemia

Astrocytic Acidosis in Hyperglycemic and Complete Ischemia

Selective enrichment of DJ‐1 protein in primate striatal neuronal processes: Implications for Parkinson's disease

Slow depolarizing potentials recorded from glial cells in the rat superficial dorsal horn.

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