Inactivation characteristics of a sustained, Ca(2+)‐independent K+ current of rat hippocampal neurones in vitro.

Nistri, Andrea; Cherubini, Enrico

doi:10.1113/jphysiol.1992.sp019395

Cited by 11 publications

(6 citation statements)

References 32 publications

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“…In keeping with previous studies (Sim and Cherubini, 1990;Neuman et al, 1991;Nistri and Cherubini, 1992), CA3 neurons fromjuvenile and adult rats had a resting membrane potential more negative than -55 mV, spike overshoots of 10-15 mV and a resting input resistance of 54 + 14 MQ (ranging from 28 to 83 MQ, n = 42). This value was significantly different (P < 0.05) from that found at PO-P6.…”

Section: P7-p31supporting

confidence: 88%

Developmental Changes in Spontaneous GABA_A‐mediated Synaptic Events in Rat Hippocampal CA3 Neurons

Hosokawa

Sciancalepore

Stratta

et al. 1994

Eur J of Neuroscience

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Ongoing spontaneous postsynaptic potentials (SPSPs) were intracellularly recorded at 34-36 degrees C from hippocampal CA3 neurons in slices obtained from postnatal days (P) 0-6 and 7-31. SPSPs occurred randomly, and their frequency distribution was fitted by a single exponential function. They were little affected by kynurenic acid, but were reversibly blocked by bicuculline, implying that they were mediated by GABAA receptors. The mean amplitude was 4.53 +/- 0.89 mV in control conditions and 4.07 +/- 0.79 mV in kynurenic acid. In kynurenic acid (with CsCl-filled microelectrodes), SPSPs reversed polarity at 2.4 +/- 2 mV. When tetrodotoxin (1 microM) was added to kynurenic acid solution, GABAA-mediated miniature postsynaptic potentials (MPSPs) were recorded. Under these conditions large events disappeared. The mean amplitude of MPSPs was 2.51 +/- 0.43 mV. The mean frequency decreased from 2.96 +/- 1.04 Hz in kynurenic acid to 0.4 +/- 0.15 Hz in kynurenic acid plus tetrodotoxin. In contrast with P0-P6, at P7-P31 SPSPs were significantly affected by kynurenic acid. The mean amplitude of SPSPs shifted from 4.71 +/- 0.82 mV in control conditions to 3.79 +/- 0.76 mV in kynurenic acid. At this developmental stage, the reversal potential of GABAA-mediated SPSPs shifted towards more negative values (-23.7 +/- 1.3 mV). Addition of tetrodotoxin to kynurenic acid solution abolished larger events and revealed GABAergic MPSPs. The mean amplitude of MPSPs was 2.72 +/- 0.5 mV, a value very close to that observed at P0-P6. Synaptic currents were recorded at 22-24 degrees C from voltage-clamped CA3 pyramidal neurons (at P6) using the tight-seal whole-cell recording technique.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: P7-p31supporting

confidence: 88%

Developmental Changes in Spontaneous GABA_A‐mediated Synaptic Events in Rat Hippocampal CA3 Neurons

Hosokawa

Sciancalepore

Stratta

et al. 1994

Eur J of Neuroscience

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“…In immature CAI pyramidal cells a fast inactivating component is dominant (Spigelman et al 1992). It has previously been shown that the slowly inactivating component can become activated either very slowly, reaching peak amplitude within several hundred milliseconds (Segal & Barker 1984, Numann et al 1987Nistri & Cherubini, 1992), or with a fast time course of a few milliseconds (Halliwell et al 1986;Sah, Gibb & Gage, 1988;Ficker & Heinemann, 1992). Under our experimental conditions, the a 1-5 6 1 -0 1 40 mV ensemble current reached its peak value with a time constant close to 2 ms, and a slowly activating component was never observed.…”

Section: Discussionmentioning

confidence: 45%

Somatic voltage‐gated potassium currents of rat hippocampal pyramidal cells in organotypic slice cultures.

Bossu¹,

Capogna²,

Debanne³

et al. 1996

The Journal of Physiology

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1. The dominant voltage-gated K+ currents in the somatic membrane of CA3 pyramidal cells from hippocampal slice cultures were characterized using the cell-attached configuration of the patch-clamp recording method. The kinetics, the voltage dependence of activation and inactivation, and the pharmacological properties of the current were determined from ensemble averages of large numbers of episodes from multichannel patches. 2. Steady-state analysis revealed that this current was half-inactivated at the resting membrane potential (Vr), and fully inactivated when patches were held 40 mV positive to Vr.Inactivation was removed when patches were hyperpolarized by 50 mV from Vr. Inactivation was well described by the Boltzmann equation with a slope factor of 12-6 mV. Removal of inactivation of the peak outward current could be described by a time-dependent monoexponential function with a time constant of the order of 100 ms. In contrast, the time course of inactivation was very slow: a +40 mV depolarization relative to Vr of several seconds was required for complete inactivation of the total outward current. 3. When steady-state inactivation was removed by hyperpolarization, the outward current activated with a threshold 10 mV positive to Vr and was half-activated at a potential 57 mV positive to Vr. The conductance can be described in terms of a single Boltzmann equation with a slope factor of 13-5 mV. Activation and inactivation properties of the somatic conductance produce a small window current between +10 and +20 mV relative to Vr.4. The outward current activated in a voltage-dependent manner in less than 10 ms with 500 ms depolarizing steps. A kinetic analysis of its decay revealed at least three components, with the following time constants: a fast (17 ms), a slowly (-150 ms), and a very slowly inactivating component (in the range of seconds). 5. External application of 4-aminopyridine (4-AP) induced a dose-dependent block of the peak outward current with an IC50 of 28 #UM. The inhibitory effect of 4-AP saturated at a concentration of 200 /LM which blocked 80% of the total current. The slowly and very slowly inactivating components of the current were not observed with 20 mM tetraethylammonium (TEA) in the pipette solution. A fast transient ensemble current (mean decay time constant, 24 ms) persisted in the presence of extracellular TEA in 29 % of the patches. 6. In summary, at least two distinct voltage-gated K+ currents were present at the somatic level of hippocampal pyramidal cells. The dominant one, which we named IK(AT), is sensitive to micromolar concentrations of 4-AP and millimolar concentrations of TEA, and contributes three kinetic components to the total outward current. The second is TEA insensitive, and contributes only a fast transient component of outward current probably corresponding to the classic A-type K+ current. Intracellular recordings in CA3 pyramidal cells showed that IK(AT) plays an important role in regulating the duration of the action potential.

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“…Initially, there is a large outward current component that inactivates in ϳ100 ms to a sustained plateau; these two components are due, respectively, to activation of I K(Ca) and activation of I K(V) . I K(Ca) are activated by the [Ca 2ϩ ] c transient generated by the prepulse and inactivate upon clearance of such transient to give rise to the sustained plateau, that is due to voltage-dependent K ϩ channels, which remain open for the entire 400-ms depolarizing pulse (52). Figure 2E shows that the I K(Ca) and I K(V) components of I K were present in mSOD1 cells; they, however, were substantially lower than those recorded in the WT cell.…”

Section: Resultsmentioning

confidence: 99%

Depressed excitability and ion currents linked to slow exocytotic fusion pore in chromaffin cells of the SOD1^G93A mouse model of amyotrophic lateral sclerosis

Calvo-Gallardo

Pascual

Fernández-Morales

et al. 2015

American Journal of Physiology-Cell Physiology

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Altered synaptic transmission with excess glutamate release has been implicated in the loss of motoneurons occurring in amyotrophic lateral sclerosis (ALS). Hyperexcitability or hypoexcitability of motoneurons from mice carrying the ALS mutation SOD1(G93A) (mSOD1) has also been reported. Here we have investigated the excitability, the ion currents, and the kinetics of the exocytotic fusion pore in chromaffin cells from postnatal day 90 to postnatal day 130 mSOD1 mice, when motor deficits are already established. With respect to wild-type (WT), mSOD1 chromaffin cells had a decrease in the following parameters: 95% in spontaneous action potentials, 70% in nicotinic current for acetylcholine (ACh), 35% in Na(+) current, 40% in Ca(2+)-dependent K(+) current, and 53% in voltage-dependent K(+) current. Ca(2+) current was increased by 37%, but the ACh-evoked elevation of cytosolic Ca(2+) was unchanged. Single exocytotic spike events triggered by ACh had the following differences (mSOD1 vs. WT): 36% lower rise rate, 60% higher decay time, 51% higher half-width, 13% lower amplitude, and 61% higher quantal size. The expression of the α3-subtype of nicotinic receptors and proteins of the exocytotic machinery was unchanged in the brain and adrenal medulla of mSOD1, with respect to WT mice. A slower fusion pore opening, expansion, and closure are likely linked to the pronounced reduction in cell excitability and in the ion currents driving action potentials in mSOD1, compared with WT chromaffin cells.

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Inactivation characteristics of a sustained, Ca(2+)‐independent K+ current of rat hippocampal neurones in vitro.

Cited by 11 publications

References 32 publications

Developmental Changes in Spontaneous GABA_A‐mediated Synaptic Events in Rat Hippocampal CA3 Neurons

Developmental Changes in Spontaneous GABA_A‐mediated Synaptic Events in Rat Hippocampal CA3 Neurons

Somatic voltage‐gated potassium currents of rat hippocampal pyramidal cells in organotypic slice cultures.

Depressed excitability and ion currents linked to slow exocytotic fusion pore in chromaffin cells of the SOD1^G93A mouse model of amyotrophic lateral sclerosis

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Inactivation characteristics of a sustained, Ca(2+)‐independent K+ current of rat hippocampal neurones in vitro.

Cited by 11 publications

References 32 publications

Developmental Changes in Spontaneous GABAA‐mediated Synaptic Events in Rat Hippocampal CA3 Neurons

Developmental Changes in Spontaneous GABAA‐mediated Synaptic Events in Rat Hippocampal CA3 Neurons

Somatic voltage‐gated potassium currents of rat hippocampal pyramidal cells in organotypic slice cultures.

Depressed excitability and ion currents linked to slow exocytotic fusion pore in chromaffin cells of the SOD1G93A mouse model of amyotrophic lateral sclerosis

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Developmental Changes in Spontaneous GABA_A‐mediated Synaptic Events in Rat Hippocampal CA3 Neurons

Developmental Changes in Spontaneous GABA_A‐mediated Synaptic Events in Rat Hippocampal CA3 Neurons

Depressed excitability and ion currents linked to slow exocytotic fusion pore in chromaffin cells of the SOD1^G93A mouse model of amyotrophic lateral sclerosis