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H Kettenmann

Publications and source records attributed to H Kettenmann.

At least 73 records · Page 4Linked to original sources
PubMed1996

Neurotoxicity induced by interleukin-2: involvement of infiltrating immune cells.

Interleukin-2 (IL-2), a key regulator of immune functions, also has potent effects on neurons and glia. IL-2 modulates neural cell growth and survival and transmitter and hormone releases and is thought to mediate neuroimmune interactions. Investigating the neuroendocrine consequences of chronically elevated central nervous system (CNS) levels of IL-2, we recently observed marked neurotoxicity [Hanisch et al. (1994) Endocrinology 135:2465-2472]. In the present study, we characterize in detail the modifications in brain tissue architecture as they result in Sprague-Dawley rats from intracerebroventricular (i.c.v.) administration of low amounts of IL-2 (5 and 15 U/h, respectively, delivered by means of osmotic minipumps for up to 14 days). Histological inspection of the brains revealed massive cellular infiltrates in the ipsilateral hemisphere. The infiltrates were associated with pronounced angiogenesis and changes in the composition of the extracellular matrix. These anatomical changes apparently developed between day 7 and 14. They were specific for IL-2 and were not seen in animals treated, for example, with heat-inactivated IL-2 (controls). We further show that chronic central administration of IL-2 let to T and B lymphocyte invasion of the brain and an intracranial agglomeration of large numbers of MHC class II-positive cells. Immunocytochemistry revealed a widespread inundation of CNS tissue and a decoration of glial cells and neurons by endogenous antibodies. Tissue regions around the IL-2-induced infiltrates showed myelin destruction and neuronal cell loss. Chronically elevated CNS levels of IL-2 may, thus, not only interfere with neurotransmission and endocrine functions but also severely disturb tissue homeostasis. Therefore, the present findings could be relevant to brain injuries, CNS disorders, and clinical treatments associated with increased IL-2 levels or involving an immune component.

Animals↗
PubMed1996

Human central neurocytoma cells show neuronal physiological properties in vitro.

Central neurocytoma is a rare brain tumor composed of small round synaptophysin-positive cells, suggesting a neuronal origin of these tumor cells. Glial properties are inferred, however, from the observation that the tumor cells exhibit a strong morphological similarity to oligodendroglioma cells and show an astrocytic differentiation in vitro. To test for neuronal or glial physiological properties, we studied cultured neurocytoma cells derived from a surgical specimen from a 44-year-old man, employing the patch-clamp technique. Early primary cultures were composed of morphologically unique bi- or multipolar cells which were positive for synaptophysin and negative for the astrocyte marker glial fibrillary acidic protein. In the majority of these cells, whole-cell membrane current recordings revealed physiological properties of neurons, i.e., a high density of Na+ currents, the capacity to generate action potentials, and the expression of inotropic neurotransmitter receptors. Metabotropic neurotransmitter receptors could be demonstrated by Ca2+ imaging techniques. The remaining bi- or multipolar cells and almost all cells in later culture stages and in vitro passage lacked these neuronal properties and showed physiological features characteristic of glial cells. We conclude that the major population of neurocytoma cells shows physiological properties of neurons and that with time in culture this population is replaced by electrically passive cells.

Action Potentials↗
PubMed1996

Calcium signalling in glial cells.

Glial cells respond to a variety of external stimuli such as neurotransmitters, hormones or even mechanical stress by generating complex changes in the cytoplasmic Ca2+ concentration. This Ca2+ signal is controlled by an interplay of different mechanisms including plasmalemmal and intracellular Ca2+ channels, Ca2+ transporters and cytoplasmic Ca2+ buffers. In astrocytes, the Ca2+ signal can travel as waves within the syncytium spreading via gap junctions which might be regarded as a possible means for interglial communication. Ca2+ signalling is also an important medium for neurone-glia interaction: neuronal activity can trigger Ca2+ signals in glial cells and, in turn, there is evidence that glial Ca2+ signals can elicit responses in neurones. While glial cells are not equipped with the proper channels to generate action potentials, Ca2+ signalling could be the instrument by which these cells integrate and propagate signals in the CNS.

Animals↗
PubMed1996

Neuron-like physiological properties of cells from human oligodendroglial tumors.

One of the most common symptoms of patients with oligodendrogliomas is the high frequency of epileptic seizures. We thus studied the physiological properties of cells in six human oligodendrogliomas and two oligoastrocytomas obtained from surgical material. The majority of tumor cells in living brain slices can generate action potentials as recorded with the patch-clamp technique indicating that this tissue is dominated by electrically excitable cells. In cultures from the same material, the action potential generating cells prevail within the first days and are subsequently replaced by electrically inexcitable cells. From histopathological and immunohistochemical data, the histogenesis of human oligodendroglial tumor is still uncertain. Our physiological study has not settled the debate on the origin of these tumors but revealed important findings with regard to this question. Since action potential generating glial cells have not been described in situ so far their occurrence in oligodendroglial tumors implies that oligodendroglial tumor cells may belong to the neuronal cell lineage.

Adult↗
PubMed1996

Complement 5a controls motility of murine microglial cells in vitro via activation of an inhibitory G-protein and the rearrangement of the actin cytoskeleton.

Microglial cells respond to most pathological events by rapid transformation from a quiescent to an activated phenotype characterized by increased cytotoxicity and motile activity. To investigate the regulation of microglial motility by different inflammatory mediators, we studied cultured murine microglia by time-lapse video microscopy and a computer-based motility assay. Microglial cells exhibited a high resting motility. The acute application of complement 5a (C5a) immediately induced intense ruffling of microglial membranes followed by lamellipodia extension within few seconds, while formyl-Met-Leu-Phe-OH, bacterial endotoxin (lipopolysaccharide) or inflammatory cytokines did not increase motility. This process was accompanied by a rapid rearrangement of the actin cytoskeleton as demonstrated by labelling with fluorescein isothiocyanate-phalloidin and could be inhibited by cytochalasin B. A GTP-binding protein was involved in the signal cascade, since pertussis toxin inhibited motility and actin assembly in response to C5a. Chemotactic migration in a gradient of C5a was also completely blocked by pertussis toxin and cytochalasin B. The C5a-induced motility reaction was accompanied by an increase in intracellular calcium ([Ca2+]i) as measured by a Fluo-3 based imaging system. Ca2+ transients were, however, not a prerequisite for triggering the increase in motility; motility could be repeatedly evoked by C5a in nominally Ca(2+)-free solution, while Ca2+ signals occurred only upon the first stimulation. Moreover, conditions mimicking intracellular Ca2+ transients, like incubation with thapsigargin or Ca2+ ionophore A23187, were not able to induce any motility reaction, suggesting that Ca2+ transients are not necessary for, but are associated with, microglial motility. Motile activity was shown to be restricted to a defined concentration range of [Ca2+]i as revealed by lowering [Ca2+]i with BAPTA-AM or increasing [Ca2+]i with A23187. Since complement factors are released at pathological sites, this signal cascade could serve to increase motility and to direct microglial cells to the lesioned or damaged area by means of a G-protein-dependent pathway and via the rearrangement of the actin cytoskeleton.

Actins↗
PubMed1996

Complement factor C5a and epidermal growth factor trigger the activation of outward potassium currents in cultured murine microglia.

Microglia, the resident macrophages of the brain, are transformed from a quiescent into an activated phenotype in a number of pathological conditions. The signalling mechanisms which control such transformations are not yet understood. In the present study, we have characterized fast electrophysiological responses in cultured microglia, induced by two putative signalling substances, complement 5a (C5a), a chemotactic agent for macrophages and microglia, and epidermal growth factor, the receptor of which is up-regulated during pathological conditions in the brain. Both factors transiently activate an outwardly rectifying K+ conductance, while the membrane of the unstimulated microglial cell is dominated by an inwardly rectifying K+ conductance. The C5a-stimulated current developed within about 20s and decayed within a slightly slower time course. It was activated by depolarlizing voltage steps positive to the resting membrane potential of about -70 mV, and neither inactivated nor showed a delayed activation following voltage steps. The epidermal growth factor-stimulated current showed similar characteristics. When G-proteins were specifically blocked, the K+ conductance could no longer be activated by C5a or epidermal growth factor, suggesting that for both agonists an inhibitory G-protein is involved in the intracellular signalling cascade. We tested if the induction of the K+ conductance is causally linked to other C5a-induced cellular responses, like transient cytosolic Ca2+ elevation and mobility. The K+ conductance was not activated when a Ca2+ transient was induced by thapsigargin, nor did a blockade of the C5a-induced K+ conductance by K+ channel blockers affect the motility response. This implies that after activation of the C5a receptor and the G-protein, the K+ conductance activation, the Ca2+ mobilization and the motility response are governed by independent intracellular pathways, and that the K+ conductance increase must serve other functions than the control of motility.

Animals↗
PubMed1996

ATP-induced membrane currents in ameboid microglia acutely isolated from mouse brain slices.

Microglial cells were harvested from the surface of corpus callosum slices acutely isolated from the brain of neonatal (five- to seven-day-old) mice. Transmembrane ionic currents were measured employing a standard whole-cell voltage-clamp technique. The extracellular application of 1 mM ATP triggered the generation of a complex membrane current comprising three components: (i) an initial fast inward current which had a reversal potential at about -20 to -15 mV; (ii) this initial component was followed by a steady-state inward current with reversal potential about -50 to -40 mV; and (iii) a delayed inward current with a reversal potential close to 0 mV. The first two components (fast and steady-state) had an activation threshold at 10 microM ATP, and 100 microM ATP evoked an almost maximal response. In contrast, the third component of ATP-induced inward membrane current could be observed only while 1 mM ATP was applied. The increase in concentration of tetra-anionic form of ATP (ATP4-) by removal of divalent cations from the bath solution substantially lowered the activation threshold for the delayed component of ATP-induced membrane current; conversely, lowering the ATP4- concentration (by replacing Ca2+ with Mg2+) resulted in its disappearance. These results suggest that ATP4- acts as a true agonist for the activation of the delayed ATP-induced membrane current. We conclude that microglial cells express several purinoreceptor subtypes. The activation of these receptors might play a role in intracellular signal transduction in brain microglia.

Adenosine Triphosphate↗
PubMed1996

Expression of glycine receptor subunits in glial cells of the rat spinal cord.

We previously demonstrated that the inhibitory neurotransmitter glycine induced membrane currents in glial cells from rat spinal cord. In this present study, the patch-clamp technique was combined with the reverse transcription-mediated PCR to analyze the glycine receptor-subunit expression in individual glial cells of rats age 3-18 days. Using the patch-clamp technique in the whole-cell configuration, glial cells were identified by their membrane current pattern and tested for responsiveness to glycine. Subsequently, the cytoplasm was harvested followed by reverse transcription of total cytoplasmic RNA. Subunit-specific cDNA fragments were amplified and analyzed by agarose gel electrophoresis, Southern blotting, and sequencing. In all cell types investigated, transcripts of the alpha1 subunit, but not of alpha 2 or alpha 3 subunits, were detected. In addition, about one-half the glial cells analyzed contained beta-subunit mRNA. These results illustrate that glial cells of rat spinal cord express functional glycine receptors in contrast to cultured glial cells. Glial cells are in intimate contact with synaptic regions making it likely that these nonneuronal receptors may be activated during glycinergic transmission and may trigger yet unknown responses in the glial cells.

Age Factors↗
PubMed1996

Calcium signalling in mouse Bergmann glial cells mediated by alpha1-adrenoreceptors and H1 histamine receptors.

The presence of adrenergic and histaminergic receptors in Bergmann glial cells from cerebellar slices from mice aged 20-25 days was determined using fura-2 Ca2+ microfluorimetry. To measure the cytoplasmic concentration of Ca2+ ([Ca2+]i), either individual cells were loaded with the Ca2+-sensitive probe fura-2 using the whole-cell patch-clamp technique or slices were incubated with a membrane permeable form of the dye (fura-2/AM) and the microfluorimetric system was focused on individual cells. The monoamines adrenalin and noradrenalin (0.1-10 microM) and histamine (10-100 microM) triggered a transient increase in [Ca2+]i. The involvement of the alpha1-adrenoreceptor was inferred from the observations that monoamine-triggered [Ca2+]i responses were locked by the selective alpha1-adreno-antagonist prazosin and were mimicked by the alpha1-adreno-agonist phenylephrine. The monoamine-induced [Ca2+]i signals were not affected by beta- and alpha2-adrenoreceptor antagonists (propranolol and yohimbine), and were not mimicked by beta- and alpha2-adrenoreceptor agonists (isoproterenol and clonidine). Histamine-induced [Ca2+]i responses demonstrated specific sensitivity to only H1 histamine receptor modulators. [Ca2+]i responses to monoamines and histamine did not require the presence of extracellular Ca2+ and they were blocked by preincubation of slices with thapsigargin (500 nM), indicating that the [Ca2+]i responses were recorded after application of aspartate, bradykinin, dopamine, GABA, glycine, oxytocin, serotonin, somatostatin, substance P, taurine or vasopressin. We conclude that cerebellar Bergmann glial cells are endowed with alpha1-adrenoreceptors and H1 histamine receptors which induce the generation of intracellular [Ca2+]i signals via activation of Ca2+ release from inositol-1,4,5-trisphosphate-sensitive intracellular stores.

Adrenergic Agonists↗
PubMed1995

Blockade of K+ channels induced by AMPA/kainate receptor activation in mouse oligodendrocyte precursor cells is mediated by Na+ entry.

AMPA/kainate receptor activation in cultured oligodendrocyte precursor cells from embryonic mouse cortex leads to a blockade of delayed rectifying K+ currents. In the present study, we provide evidence using the patch-clamp technique in the whole-cell configuration that the mechanism linking kainate receptor activation and K+ conductance blockade is due to the receptor-mediated Na+ entry: 1) The blockade was not observed in Na(+)-free bathing solution nor when intracellular [Na+] was elevated by dialzying the cell with a pipette solution containing high [Na+]. 2) Elevation of intracellular [Na+] alone led to a blockade of outward currents in contrast to cells dialyzed by sucrose. High [Li+]i also reduced the outward currents, and in Li(+)-containing bathing solution the kainate-induced blockade of K+ channels was more pronounced. Probably, Li+ accumulates intracellularly after permeation through the receptor pore due to slower extrusion mechanisms. Experiments with GTP gamma S or GDP beta S and pertussis toxin indicated that GTP-binding protein-mediated mechanisms were not of importance for the kainate-induced K+ conductance blockade. Our data suggest that in glial precursor cells AMPA/kainate receptor activation leads to an intracellular [Na+] increase which blocks delayed rectifying K+ channels.

Animals↗
PubMed1995

Glycine- and GABA-activated currents in identified glial cells of the developing rat spinal cord slice.

In the neonatal rat spinal cord, four types of glial cells, namely astrocytes, oligodendrocytes and two types of precursor cells, can be distinguished based on their membrane current patterns and distinct morphological features. In the present study, we demonstrate that these cells respond to the inhibitory neurotransmitters glycine and GABA, as revealed with the whole-cell recording configuration of the patch-clamp technique. All astrocytes and glial precursor cells and a subpopulation of oligodendrocytes responded to glycine. The involvement of glycine receptors was inferred from the observation that the response was blocked by strychnine and that the induced current reversed close to the Cl- equilibrium potential. GABA induced large membrane currents in astrocytes and precursor cells while oligodendrocytes showed only small responses. The GABA-activated current was due to the activation of GABAA receptors since muscimol mimicked and bicuculline blocked the response; moreover, the reversal potential was close to the Cl- equilibrium potential. Besides the increase in a Cl- conductance, GABAA receptor activation also induced a block of the resting K+ conductance, as observed previously in Bergmann glial cells. Our experiments show that while glial GABAA receptors are found in many brain regions and the spinal cord, glial glycine receptors have so far been detected only in the spinal cord. The restricted coexpression of glial and neuronal glycine receptors in a defined central nervous system grey matter area implies that such glial receptors may be involved in synaptic transmission.

Aging↗
PubMed1995

Lines of murine oligodendroglial precursor cells immortalized by an activated neu tyrosine kinase show distinct degrees of interaction with axons in vitro and in vivo.

Replication-defective retroviruses expressing the t-neu oncogene, or a hybrid protein with the neu tyrosine kinase linked to the external region of the human epidermal growth factor receptor (egfr-neu), were used to establish lines of murine oligodendroglial precursor cells. Differentiation of the t-neu lines into myelin-associated glycoprotein (MAG)-positive oligodendrocytes was induced by dibutyryl cAMP, and the egfr-neu line showed limited differentiation in vitro upon withdrawal of epidermal growth factor. Cerebellar granule cell neurons expressed mitogens for the cell lines. Upon transplantation into demyelinated lesions, t-neu line cells engaged with the demyelinated axons whereas the egfr-neu line cells differentiated further and ensheathed the axons. These cell lines thus interact with neurons in vitro and in vivo and can be used as tools to define the molecules involved in different stages of neuron-glia interaction.

Animals↗
PubMed1995

Adult rat optic nerve oligodendrocyte progenitor cells express a distinct repertoire of voltage- and ligand-gated ion channels.

Cultured oligodendrocyte progenitor cells derived from the developing central nervous system (CNS) express a pattern of ion channels that is distinct from mature oligodendrocytes and other cell types of the CNS. In the present study, we used the whole-cell patch-clamp technique and the fura-2-based Ca++ imaging system to study the ion channel expression of oligodendrocyte progenitor cells derived from the optic nerves of adult rats. We found that the adult oligodendrocyte progenitor cell membrane is dominated by K+ currents, both delayed outward and inward rectifying. The inwardly rectifying K+ currents were often as large as the outward delayed rectifying K+ currents. The delayed rectifying outward currents were partially blocked by 50 mM tetraethylammonium or 1 mM 4-aminopyridine, but not by 2 or 5 mM BaCl2. This suggests that the delayed rectifier channels expressed by adult progenitor cells are different from those expressed by perinatal cells. Most adult oligodendrocyte progenitor cells showed no or only small A-type K+ currents. Both Ca++ and Na+ channels were also detected in these cells. Furthermore, adult progenitor cells responded to the neurotransmitters GABA and kainate and the pharmacology of these responses indicated that these cells express GABAA receptors and kainate receptors that are Ca(++)-permeable. Our study suggests that adult oligodendrocyte progenitor cells are electrophysiologically distinct and that these cells share electrophysiological characteristics with both perinatal progenitor cells and immature oligodendrocytes.

Animals↗
PubMed1995

Preferential localization of active mitochondria in process tips of immature retinal oligodendrocytes.

Active mitochondria were visualized with a laser scanning confocal microscope using the dye rhodamine 123, which is accumulated in mitochondria with a high respiratory activity. In glial precursor cells cultured from rabbit retina the fluorescence signal of active mitochondria was confined to the tips of processes, while in oligodendrocytes an even distribution was found. The developmental stage of cultured oligodendrocytes was determined by staining with O4 and O10 antibodies after the end of microfluorometric measurements. In glial precursor cells, the mitochondrial uncoupler CCCP generated an increase in the cytoplasmic calcium concentration ([Ca2+]i) in regions corresponding to those revealed by rhodamine 123 staining. In mature oligodendrocytes CCCP evoked [Ca2+]i elevation without significant spatial heterogeneity. However, electron microscopy did not reveal an uneven distribution of mitochondria in either immature or mature oligodendrocytes. We conclude that in the precursor cells, active mitochondria are confined to process tips and serve as a Ca2+ pool, while in oligodendrocytes such a spatial heterogeneity cannot be detected. This preferential localization of active mitochondria may play a role in the neurone-glia interaction during the formation of the contact between the myelinating glial process and the axonal membrane.

Aniline Compounds↗
PubMed1995

Activation of P2-purinoreceptors triggered Ca2+ release from InsP3-sensitive internal stores in mammalian oligodendrocytes.

1. The subcellular characteristics of an ATP-induced elevation of the cytoplasmic free calcium concentration ([Ca2+]i) were studied in cultured cells of the oligodendrocyte lineage obtained from mouse cortex and rabbit retina, as well as in oligodendrocytes from mouse corpus callosum slices, using laser scanning confocal microfluorometry. 2. With the stage- and lineage-specific antibodies O4 and O10, three developmental stages within the oligodendrocyte lineage were distinguished prior to Ca2+ recording. 3. Bath application of 1-100 microM ATP induced a transient increase of [Ca2+]i in late precursors and oligodendrocytes but not in early glial precursor cells from retinal and cortical cultures and from corpus callosum slices. This effect of ATP was observed in Ca(2+)-free extracellular solution, suggesting that the ATP-mediated elevation of [Ca2+]i is due to a Ca2+ liberation from intracellular stores. 4. In both late precursors and oligodendrocytes from retina, the amplitude of ATP-induced [Ca2+]i transients was significantly higher in processes as compared with the soma; in cortical cultures such an uneven response was only observed in oligodendrocytes, while in immature cells responses in soma and processes were of similar amplitude. 5. The rank order of potency for the purine and pyrimidine nucleotides was UTP > or = ATP > ADP >> AMP = adenosine = Me-ATP for retinal oligodendrocytes, and ADP > or = ATP >> UTP = AMP = adenosine = Me-ATP for cortical oligodendrocytes. The response to ATP and related nucleotides was blocked by suramin, indicating the involvement of a P2-purinoreceptor in the ATP-mediated [Ca2+]i response. 6. ATP-induced elevation of the cytosolic Ca2+ concentration was inhibited by incubating cells with thapsigargin (10 microM) and by intracellular administration of heparin (1 microM). These findings indicate that ATP triggers a release of Ca2+ ions from InsP3-sensitive internal stores. 7. The ATP receptors may play a role in neuron-glial signal transfer; ATP is released as neurotransmitter, but also under pathological conditions from damaged cells.

Adenosine Triphosphate↗
PubMed1995

Distinct populations of identified glial cells in the developing rat spinal cord slice: ion channel properties and cell morphology.

Four types of glial cells could be distinguished in the grey matter of rat spinal cord slices at postnatal days 1-19 (P1-P19), based on their pattern of membrane currents as revealed by the whole cell patch clamp technique, and by their morphological and immunocytochemical features. The recorded cells were labelled with Lucifer Yellow, which allowed the subsequent identification of cells using cell-type-specific markers. Astrocytes were identified by positive staining for glial fibrillary acidic protein (GFAP). These were morphologically characterized by multiple, very fine and short processes and electrophysiologically by symmetrical, non-decaying K+ selective currents. Oligodendrocytes were identified by a typical oligodendrocyte-like morphology, lack of GFAP staining and positive labelling with a combination of O1 and O4 antibodies (markers of the oligodendrocyte lineage), and their membrane was dominated by symmetrical, passive, decaying K+ currents. The third population of glial cells was also characterized by positive staining for O1/O4 or only for O4 antigens, lack of GFAP staining and, in some cells, oligodendrocyte-like morphology. However, these cells could be distinguished by the presence of inwardly rectifying (KIR), delayed outwardly rectifying (KDR) and A-type K+ currents (KA), representing the most likely glial precursor cells of the oligodendrocyte lineage. The fourth population of glial cells had small somata and a widespread network of long processes with no apparent orientation preference. In one case, processes were positively labelled with GFAP, while 30% were characterized by faint, diffuse staining. These cells expressed a complex pattern of voltage-gated channels, namely Na+, KDR, KA and KIR channels. In contrast to neurons, the amplitude of Na+ currents was at least one order of magnitude smaller than the K+ currents, and none of these cells showed the ability to generate action potentials in the current clamp mode. Since none of these cells could be labelled by oligodendrocyte markers we assume that they were either astrocytes or glial precursor cells of the astrocyte lineage. The four cell types were found in all regions of the grey matter. When randomly accessing the glial cells, the probability of recording from the oligodendrocyte precursor cells and the glial cells with Na+ currents decreased during development. At P1-P3, 50% of the cells revealed the Na+ current, while at P13-P15 only 18% did. Concomitantly, the number of glial cells with astrocyte- and oligodendrocyte-like membrane currents increased from 19 and 12% to 41 and 35.5% respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1995

Subcellular heterogeneity of voltage-gated Ca2+ channels in cells of the oligodendrocyte lineage.

We studied the distribution of voltage-gated Ca2+ channels in cells of the oligodendrocyte lineage from retinal and cortical cultures. Influx of Ca2+ via voltage-gated channels was activated by membrane depolarization with elevated extracellular K+ concentration ([K+]e) and local, subcellular increases in cytosolic free Ca2+ concentration ([Ca2+]in) could be monitored with a fluometric system connected to a laser scanning confocal microscope. In glial precursor cells from both retina and cortex, small depolarizations (with 10 or 20 mM K+) activated Ca2+ transients in processes indicating the presence of low-voltage-activated Ca2+ channels. Larger depolarizations (with 50 mM K+) additionally activated high-voltage-activated Ca2+ channels in the soma. An uneven distribution of Ca2+ channels was also observed in the mature oligodendrocytes; Ca2+ transients in processes were considerably larger. Recovery of Ca2+ levels after the voltage-induced influx was achieved by the activity of the plasmalemmal Ca2+ pump, while mitochondria played a minor role to restore Ca2+ levels after an influx through voltage-operated channels. During the development of white matter tracts, cells of the oligodendrocyte lineage contact axons to form myelin. Neuronal activity is accompanied by increases in [K+]e; this may lead to Ca2+ changes in the processes and the Ca2+ increases might be a signal for the glial precursor cell to start myelin formation.

Animals↗