Membrane properties of identified embryonic nerve and glial cells of the leech central nervous system

Schirrmacher, K.; Deitmer, Joachim W.

doi:10.1007/bf00614507

Cited by 6 publications

(1 citation statement)

References 33 publications

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“…It was surprising that 50 mM KC1 did not cause a detectable calcium influx in these neurons even though the physiological recordings proved that this concentration does depolarize them, since elevated KC1 causes sustained rises in [Ca2+], in a variety of other neurons (Lipscombe et al, 1988;Collins et al, 1991;Rehder and Kater, 1992). Adult AP cells in culture have significant inward calcium currents at the membrane potentials reported here (-20 to 0 mV; Stewart et al, 1989), and embryonic Retzius cells in situ do have a voltage-dependent calcium current at comparable ages (Schirrmacher and Deitmer, 1989). A possible explanation is that these embryonic AP cells may have a rapidly desensitizing voltage-dependent calcium conductance that ends too quickly to be seen with our methods, the temporal resolution of this calcium imaging system being limited to detecting changes in ratios on the order of seconds instead of milliseconds.…”

Section: Discussionmentioning

confidence: 58%

Calcium wave fronts that cross gap junctions may signal neuronal death during development

et al. 1994

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Embryonic anterior pagoda (AP) neurons in the leech interact with their segmental homologs in adjacent ganglia through transient axons that overlap during a critical period of development and then retract. However, when an AP neuron is ablated mechanically or by irradiation during this period, an adjacent homolog responds by reinitiating growth of its overlapped axon and thereby taking over vacated territory (Gao and Macagno, 1987b; Gao, 1989). The death of an AP cell is therefore communicated to its homolog, but the mechanism underlying this signaling is presently unknown. Since it was recently found that AP homologs are electrically and dye coupled through their transient axons (Wolszon et al., 1994), we investigated the possibility that gap junctions may mediate the cell death signal that could occur between developing neurons. Among several candidate intercellular signals, we began by studying calcium dynamics in embryonic AP cells, in situ, since calcium is known to cross gap junctions and is implicated in cell death in many systems. We found that elements that usually increase [Ca2+]i in adult neurons, such as releasable internal stores or voltage-dependent calcium channels, were not present at the critical period. Instead, mechanisms that reduce free calcium, such as buffering and pumping, were the most robust. When a large, focal calcium rise was produced in an AP axon by making a lesion with a UV microbeam (leading to eventual death of these neurons), calcium did not rise quickly throughout the cell, but rather moved in a slow (0.05-0.25 micron/sec) wave front away from the lesion site, into other processes of the damaged cell. Furthermore, when a calcium wave front reached the growth cone of a transient axon, it crossed at the gap junctions into the coupled axon of the neighboring AP neuron, but went no further. Since it is known that an AP responds to a neighbor's death by reinitiating growth only in that axon that contacts the dying cell (Gao and Macagno, 1987b; Gao, 1989), these observations are consistent with calcium playing a role in the signaling of cell death to homologs that are coupled to a dying cell.

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Section: Discussionmentioning

confidence: 58%

Calcium wave fronts that cross gap junctions may signal neuronal death during development

et al. 1994

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Developmental changes of potassium currents of embryonic leech ganglion cells in primary culture

Meis

Deitmer

1997

J. Neurosci. Res.

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The expression of calcium-activated potassium currents (IK(Ca)), delayed outward rectifier potassium currents (IK(slow)), and transient outward currents (IA) was studied during the development of the nervous system of the leech using the whole-cell patch-clamp recording technique. Dissociated cells were isolated from leech embryos between stage E7 and E16 and maintained in primary culture. K+ currents were recorded at E7, when only few anterior ganglia had formed beneath the primordial mouth. IK(slow) was present in all cells tested, while IK(Ca) was expressed in only 67% of the cells studied. Even as early as E7, different types of IK(Ca) have been found. Neither frequency of occurrence nor the charge density of IK(Ca) showed significant changes between E7 and E16. The density of IK(slow), however, increased by a factor of two between E7 and E8, which resulted in a significant increase in the total K+ current of these cells. This rise in potassium outward current developed in parallel with the appearance of Na+ and Ca2+ inward currents (Schirrmacher and Deitmer: J Exp Biol 155:435-453, 1991) during early development, shaping the electrical excitability in embryonic leech neurones. I(A) could be separated by its voltage-dependence and pharmacological properties. The current was detected at stage E9, when all 32 ganglia are formed in the embryo. The frequency of occurrence of I(A) increased from 16% at E9 to 70% at E15. The channel density, steady state inactivation, and kinetics showed no significant changes during development.

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Single K + Channels in Embryonic Leech Ganglion Cells

Frey

Schlue

1996

Journal of Membrane Biology

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We investigated the properties of single K+ channels in the soma membrane of embryonic leech ganglion cells using the patch-clamp technique. We compared these K+ channels with the K+ channels found previously in Retzius neurons of the adult leech. In ganglion cells of 9- to 15-day-old embryos we characterized eight different types of K+ channels with mean conductances of 21, 55, 84, 111, 122, 132, 149 and 223 pS. The 55 pS and 84 pS channels showed flickering and were active for less than 2 min after excising the patch. The 111 pS channel was an outward rectifier, and the open state probability (po) decreased in the inside-out configuration when the Ca2+ concentration was raised from pCa 7 to pCa 3. The 122 pS channel also showed outward rectification. This type of channel was activated after changing from the cell-attached to the inside-out configuration and it did not inactivate during more than 30 min. The po was Ca2+- and voltage-insensitive. One hundred micron glibenclamide reversibly reduced po. The 132 pS channel was an outward rectifier and was Ca2+-insensitive. The 149 pS channel inactivated in the inside-out configuration. The 149- and the 223 pS channel showed inward rectification. The 111 pS channel had similar properties to the Ca2+-dependent K+ channel and the 122 pS channel resembled the ATP-inhibited K+ channel found previously in Retzius neurons of the adult leech.

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Membrane properties of identified embryonic nerve and glial cells of the leech central nervous system

Cited by 6 publications

References 33 publications

Calcium wave fronts that cross gap junctions may signal neuronal death during development

Calcium wave fronts that cross gap junctions may signal neuronal death during development

Developmental changes of potassium currents of embryonic leech ganglion cells in primary culture

Single K + Channels in Embryonic Leech Ganglion Cells

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