Fast inward‐rectifying current accounts for anomalous rectification in olfactory cortex neurones.

Constanti, Andrew; Galvan, M.

doi:10.1113/jphysiol.1983.sp014526

Cited by 194 publications

(107 citation statements)

References 50 publications

(98 reference statements)

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“…The present results and those of and Constanti & Galvan (1983) suggest that time-dependent anomalous rectification produced by membrane hyperpolarization is due to activation of voltage-sensitive conductances separate from those activated during membrane depolarization. The hyperpolarization-activated conductance produces a region ofinward rectification in the steady-state current-voltage relationship.…”

Section: Block Of Ih By Impermeable Anion Substitutessupporting

confidence: 72%

“…Detailed information is not available on the ionic mechanism of the inward rectifier in hippocampal pyramidal neurones, but its Ba2+ resistance suggests similarity to the sensory neurone and cardiac conductances, although the Na+-K+ permeability ratio may be lower in hippocampal neurones . In olfactory cortex neurones the inward rectifier shows Ba2+ sensitivity and V-EK dependence, and thus resembles the muscle and marine egg conductances (Constanti & Galvan, 1983).…”

Section: Inward Rectifiers In Other Membranesmentioning

confidence: 83%

“…1978;Standen & Stanfield, 1978b) and Cs+ (Hagiwara et al 1976;Gay & Stanfield, 1977;Constanti & Galvan, 1983). The activation variable of this conductance shows V-EK dependence (Hagiwara et al 1976;Leech & Stanfield, 1981;Hestrin, 1981;Constanti & Galvan, 1983); that is it appears as if the conductance depends on the difference between the membrane and K+ equilibrium potentials, rather than on the membrane potential alone.…”

Section: Inward Rectifiers In Other Membranesmentioning

confidence: 97%

“…In all of these tissues the conductance is activated by hyperpolarization and is permeable to K+. The inward rectifier of marine eggs, muscle and olfactory cortex neurones is a relatively K+-specific conductance (Hagiwara & Takahashi, 1974;Standen & Stanfield, 1980;Constanti & Galvan, 1983) and is blocked by Ba2+ (Hagiwara et at. 1978;Standen & Stanfield, 1978b) and Cs+ (Hagiwara et al 1976;Gay & Stanfield, 1977;Constanti & Galvan, 1983).…”

Section: Inward Rectifiers In Other Membranesmentioning

confidence: 99%

“…The inward rectifier of marine eggs, muscle and olfactory cortex neurones is a relatively K+-specific conductance (Hagiwara & Takahashi, 1974;Standen & Stanfield, 1980;Constanti & Galvan, 1983) and is blocked by Ba2+ (Hagiwara et at. 1978;Standen & Stanfield, 1978b) and Cs+ (Hagiwara et al 1976;Gay & Stanfield, 1977;Constanti & Galvan, 1983). The activation variable of this conductance shows V-EK dependence (Hagiwara et al 1976;Leech & Stanfield, 1981;Hestrin, 1981;Constanti & Galvan, 1983); that is it appears as if the conductance depends on the difference between the membrane and K+ equilibrium potentials, rather than on the membrane potential alone.…”

Section: Inward Rectifiers In Other Membranesmentioning

confidence: 99%

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A voltage‐clamp analysis of inward (anomalous) rectification in mouse spinal sensory ganglion neurones.

Mayer

Westbrook

1983

The Journal of Physiology

426

320

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SUMMARY1. Mouse embryo dorsal root ganglion neurones were grown in tissue culture and voltage-clamped with two micro-electrodes. Hyperpolarizing voltage commands from holding potentials of -50 to -60 mV evoked slow inward current relaxations which were followed by inward tail currents on repolarization to the holding potential. These relaxations are due to the presence of a time-and voltage-dependent conductance provisionally termed Gh.2. Gh activates over the membrane potential range -60 to -120 mV. The presence of Gh causes time-dependent rectification in the current-voltage relationship measured between -60 and --120 mV. Gh does not inactivate within this range and thus generates a steady inward current at hyperpolarized membrane potentials.3. The current carried by Gh increases when the extracellular K+ concentration is raised, and is greatly reduced in Na+-free solutions. Current-voltage plots show considerably less inward rectification in Na+-free solution; conversely inward rectification is markedly enhanced when the extracellular K+ concentration is raised. The reversal potential of 'h is close to -30 mV in media of physiological composition.Tail-current measurement suggests that Ih is a mixed Na+-K+ current.4. Low concentrations ofCs+ reversibly block Ih and produce outward rectification in the steady-state current-voltage relationship recorded between membrane potentials of -60 and -120 mV. Cs+ also reversibly abolishes the sag and depolarizing overshoot that distort hyperpolarizing electrotonic potentials recorded in currentclamp experiments.5. Impermeant anion substitutes reversibly block Ih; this block is different from that produced by Cs+ or Na+-free solutions: Cs+ produces outward rectification in the steady-state current-voltage relationship recorded over the Ih activation range; in Na+-free solutions inward rectification, of reduced amplitude, can still be recorded since Ih is a mixed Na+-K+ current; in anion-substituted solutions the current-voltage relationship becomes approximately linear.6. It is concluded that in dorsal root ganglion neurones anomalous rectification is generated by the time-and voltage-dependent current Ih. The possible function of Ih in sensory neurones is discussed.

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Section: Block Of Ih By Impermeable Anion Substitutessupporting

confidence: 72%

Section: Inward Rectifiers In Other Membranesmentioning

confidence: 83%

Section: Inward Rectifiers In Other Membranesmentioning

confidence: 97%

Section: Inward Rectifiers In Other Membranesmentioning

confidence: 99%

Section: Inward Rectifiers In Other Membranesmentioning

confidence: 99%

See 3 more Smart Citations

A voltage‐clamp analysis of inward (anomalous) rectification in mouse spinal sensory ganglion neurones.

Mayer

Westbrook

1983

The Journal of Physiology

426

320

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In vitro electrophysiology of rat subicular bursting neurons

1997

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Intracellular recordings were used to study the electrophysiological properties of rat subicular neurons in a brain slice preparation in vitro. Cells were classified as bursting neurons (n = 102) based on the firing pattern induced by depolarizing current pulses. The bursting response recorded at resting membrane potential (−66.1 ± 6.2 mV, mean ± SD n = 94) was made up of a cluster of fast action potentials riding on a slow depolarization and was followed by an afterhyperpolarization. Tonic firing occurred at a membrane potential of approximately −55 mV. A burst also occurred upon termination of a hyperpolarizing current pulse. Tetrodotoxin (TTX, 1 μM) blocked the burst and decreased or abolished the underlying slow depolarization. These effects were not induced by the concomitant application of the Ca2+ channel blockers Co2+ (2 mM) and Cd2+ (1 mM). Subicular bursting neurons displayed voltage‐ and time‐dependent inward rectifications of the membrane during depolarizing and hyperpolarizing current pulses. The inward rectification in the depolarizing direction was abolished by TTX, while that in the hyperpolarizing direction was blocked by extracellular Cs+ (3 mM), but not modified by Ba2+ (0.5–1 mM), TTX, or Co2+ and Cd2+. Tetraethylammonium (10 mM)‐sensitive, outward rectification became apparent in the presence of TTX. These results suggest that neurons in the rat subiculum can display voltage‐dependent bursts of action potentials as well as membrane rectification in the depolarizing and hyperpolarizing directions. These results also indicate that activation of a voltage‐gated Na+ conductance may be instrumental in the initiation of bursting activity. Hippocampus 7:48–57, 1997. © 1997 Wiley‐Liss, Inc.

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Cellular and subcellular localization of Kir2.1 subunits in neurons and glia in piriform cortex with implications for K⁺ spatial buffering

Howe

Feig

Osting

et al. 2007

J of Comparative Neurology

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Potassium channels of the Kir2 family are widely expressed in neurons and glia, where they form strong inwardly rectifying channels. Existing functional hypotheses for these channels in neurons are based on the weak outward conductance, whereas the leading hypothesis for glia, that they promote potassium spatial buffering, is based on inward conductance. Although the spatial buffering hypothesis has been confirmed for Müller glia in retina, many aspects of Kir2 channels that will be required for understanding their functional roles in neurons and other forms of glia have received little or no study. Particularly striking is the paucity of data regarding their cellular and subcellular localization. We address this gap for Kir2.1-containing channels by using light and electron microscopic immunocytochemistry. The analysis was of piriform cortex, a highly epileptogenic area of cerebral cortex, where pyramidal cells have K(+)-selective strong inward rectification like that observed in Müller cells, where Kir2.1 is the dominant Kir2 subunit. Pyramidal cells in adult piriform cortex also lack I(h), the mixed Na(+)-K(+) current that mediates a slower form of strong inward rectification in large pyramidal cells in neocortex and hippocampus. The experiments demonstrated surface expression of Kir2.1-containing channels in astrocytes and in multiple populations of pyramidal and nonpyramidal cells. Findings for astrocytes were not consistent with predictions for K(+) spatial buffering over substantial distance. However, findings for pyramidal cells suggest that they could be a conduit for spatially buffering K(+) when it is highly elevated during seizure.

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Fast inward‐rectifying current accounts for anomalous rectification in olfactory cortex neurones.

Cited by 194 publications

References 50 publications

A voltage‐clamp analysis of inward (anomalous) rectification in mouse spinal sensory ganglion neurones.

A voltage‐clamp analysis of inward (anomalous) rectification in mouse spinal sensory ganglion neurones.

In vitro electrophysiology of rat subicular bursting neurons

Cellular and subcellular localization of Kir2.1 subunits in neurons and glia in piriform cortex with implications for K⁺ spatial buffering

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Fast inward‐rectifying current accounts for anomalous rectification in olfactory cortex neurones.

Cited by 194 publications

References 50 publications

A voltage‐clamp analysis of inward (anomalous) rectification in mouse spinal sensory ganglion neurones.

A voltage‐clamp analysis of inward (anomalous) rectification in mouse spinal sensory ganglion neurones.

In vitro electrophysiology of rat subicular bursting neurons

Cellular and subcellular localization of Kir2.1 subunits in neurons and glia in piriform cortex with implications for K+ spatial buffering

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Product

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Cellular and subcellular localization of Kir2.1 subunits in neurons and glia in piriform cortex with implications for K⁺ spatial buffering