Perforated Patch Recording

Korn, Stephen J.; Marty, Alain; Connor, John A.; Horn, Richard

doi:10.1016/b978-0-12-185257-3.50027-6

Cited by 98 publications

(76 citation statements)

References 13 publications

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“…Our results demonstrate that ET_1 has no significant effects on basal, unstimulated ICa,L in guinea-pig ventricular myocytes, a finding which is in contrast with recent studies reporting a decrease in basal ICa,L in guinea-pig atrial (Ono et al 1994) and ventricular (Xie et al 1996) as well as human atrial and ventricular myocytes (Cheng et al 1995). One plausible explanation for these differences reflects the fact that we utilized the perforated patch configuration to record ICa,L which avoids the disruption of normal intracellular Ca¥ buffering mechanisms (Korn et al 1991). ICa,L recorded using perforated patch configuration in these experiments was maintained nearly constant for up to 60 min, with negligible rundown compared with the significant rundown usually observed in conventional whole cell recordings.…”

Section: Discussion Et_1 and Basal Ical Activitycontrasting

confidence: 54%

“…Macroscopic ICa,L was studied by using the nystatin-perforated patch configuration (Korn et al 1991) at room temperature. All recordings were made using an Axopatch 1D amplifier (Axon Instruments).…”

Section: Perforated Patch Recordingmentioning

confidence: 99%

“…perforated patch configuration, thus creating a physiological intracellular milieu where ICa,L and responses to neurotransmitters are maintained for considerably longer periods of time (Kurachi, Asano, Takikawa & Sigimoto, 1989;Korn, Marty, Connor & Horn, 1991). ET_1 has been demonstrated to decrease isoprenaline-enhanced ICa,L under some conditions (Ono et al 1994;Cheng et al 1995;Xie et al 1996).…”

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confidence: 99%

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Differential Effects of Endothelin‐1 on Basal and Isoprenaline‐Enhanced Ca²⁺ Current in Guinea‐Pig Ventricular Myocytes

Thomas

Sims

Karmazyn

1997

The Journal of Physiology

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We examined the effect of endothelin‐1 (ET‐1) on basal and isoprenaline‐enhanced L‐type Ca2+ current (ICa,L) in guinea‐Pig ventricular myocytes under nystatin‐perforated patch configuration. ET‐1 at concentrations of 1, 5 and 10 nM had little effect on basal ICa,L. However, ICa,L enhanced by isoprenaline (500 nM) was significantly attenuated by 5 nM ET‐1 by more than 50%. This effect was reversed upon washout. ICa,L enhanced by forskolin was also decreased by ET‐1. The inhibitory effect of ET‐1 against isoprenaline was completely blocked by the ETA receptor antagonist BQ‐123 (1 μm). In myocytes incubated with pertussis toxin (PTX, 2 μg ml−1) for 5 h, ET‐1 did not inhibit isoprenaline‐enhanced ICa,L. Although ET‐1 has been shown to activate specific protein kinase C (PKC) isoforms, a significant inhibitory effect of ET‐1 was maintained in the presence of the PKC inhibitor bisindolylmaleimide (20 nm). The nitric oxide (NO) donor SIN‐1 (10 μm) attenuated but failed to prevent the ET‐1 effect. In summary, our results demonstrate that ET‐1 is devoid of any significant effects on basal ICa,L. However, it exerts a potent inhibitory effect against isoprenaline‐enhanced ICa,L. This effect is mediated through ETA receptors coupled to PTX‐sensitive G‐proteins and occurs in the presence of PKC inhibition and NO generation.

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Section: Discussion Et_1 and Basal Ical Activitycontrasting

confidence: 54%

Section: Perforated Patch Recordingmentioning

confidence: 99%

mentioning

confidence: 99%

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Differential Effects of Endothelin‐1 on Basal and Isoprenaline‐Enhanced Ca²⁺ Current in Guinea‐Pig Ventricular Myocytes

Thomas

Sims

Karmazyn

1997

The Journal of Physiology

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“…Bicuculline methobromide (1 M) was routinely added to the extracellular medium to reduce inhibition. Recordings from single cells were performed using either perforated-patch (Korn et al, 1991) or whole-cell (Hamill et al, 1981;Edwards et al, 1989) recording configurations with an Axopatch 1-D amplifier (Axon Instruments) in current-clamp mode. Tight-seal (Ͼ 1 G⍀), whole-cell recordings were performed under visual control using a 40ϫ Hoffman, waterimmersion, objective (Zeiss).…”

Section: Methodsmentioning

confidence: 99%

Long-Term Potentiation in Distinct Subtypes of Hippocampal Nonpyramidal Neurons

1996

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We have investigated NMDA receptor-dependent long-term potentiation (LTP) in distinct subtypes of nonpyramidal neurons of the CA1 hippocampus using induction protocols that permitted the differentiation between a direct form of LTP and plasticity resulting simply from the "passive propagation" of LTP occurring on CA1 pyramidal neurons. Two types of stratum (st.) oriens/ alveus interneurons received passive propagation of synaptic potentiation via the recurrent collaterals of CA1 pyramidal cells, but neither subtype possessed direct plasticity. In st. radiatum, two distinct classes of cells were observed: st. radiatum interneurons that showed neither direct nor propagated forms of synaptic plasticity, and "giant cells" for which EPSPs were robustly potentiated after a pairing protocol. This potentiation is similar to the LTP described in pyramidal cells, and its induction requires NMDA receptor activation. Thus, a large heterogeneity of synaptic plasticity exists in morphologically distinct neurons and suggests that complex changes in the CA1 network properties will occur after the induction of LTP.Key words: hippocampus; interneurons; LTP; plasticity; GABAergic; CA1 Synaptic plasticity of the CA1 subfield of the rat hippocampus has been extensively studied and characterized in pyramidal cells (Bliss and Collingridge, 1993;Malenka and Nicoll, 1993;Lisman, 1994). Although many issues still are under debate (Kullmann and Siegelbaum, 1995), the mechanisms involved in the induction of long-term potentiation (LTP) and long-term depression (LTD) have been elucidated (Bliss and Collingridge, 1993;Malenka, 1994). Both forms of plasticity require the activation of postsynaptic NMDA receptors (NMDARs) and an elevation of intracellular calcium levels (Collingridge et al., 1983; Malenka et al., 1988, Dudek andBear, 1992;Mulkey and Malenka, 1992), which lead to phosphorylation or dephosphorylation processes (Malinow et al., 1988;Malenka et al., 1989;Mulkey at al, 1993;Lisman, 1994).At the level of the hippocampal network, the net flow of information in the CA1 region is strongly modulated by the action of the nonpyramidal neurons, the cell bodies of which are distributed throughout all layers of the hippocampus (Lacaille et al., 1987(Lacaille et al., , 1989 Lacaille and Schwartzkroin, 1988a,b;Buhl et al., 1994;Sik et al., 1994Sik et al., , 1995Cobb et al., 1995;Maccaferri and McBain, 1995) (for review, see Freund and Buzsaki, 1996). The vast majority (ϳ90%) of these cells have been shown to be glutamate decarboxylase (GAD)-positive inhibitory interneurons (Woodson et al., 1989), the axons of which target different domains of the pyramidal cell dendritic tree (Gulyás et al., 1993;Buhl et al., 1994;Sik et al., 1995). Therefore, the possibility of additional synaptic plasticity occurring in nonpyramidal cells would greatly increase both the power and the level of complexity of signal processing in the CA1 subfield. Indeed, several reports have shown that after tetanic stimulation, changes occur in (1) evoked nonpyramidal cell f...

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“…lA,B). This washout effect was apparently attributable to intracellular dialysis (Korn et al, 1991) One cell (open circles) was tested with 17P-estradiol (100 nM). The application of 17P-estradiol (solid circles) significantly retarded the decline in the amplitude of kainatc-induced currents.…”

Section: Kainate-induced Currentsmentioning

confidence: 99%

17β-Estradiol Potentiates Kainate-Induced Currents via Activation of the cAMP Cascade

1996

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Evidence for nongenomic actions of steroids is now coming from a variety of fields of steroid research. Mechanisms of steroid action are being studied with regard to the membrane receptors and the activation of second messengers. The present study investigated the mechanism for the rapid effect of estrogen on acutely dissociated hippocampal CA1 neurons by using the whole-cell, voltage-clamp recording. Under the perforated patch configuration, 17P-estradiol potentiated kainateinduced currents in 38% of tested neurons. The potentiation was stereospecific, rapid in onset, and reversible after the removal of the steroid. Dose-response curves show that the potentiation by l-/P-estradiol was evident at a concentration as low as 10 nM and saturated at IO PM. 17/3-Estradiol did not affect the kinetics (i.e., affinity and cooperativity) and reversal potential of kainate-induced currents. This suggests that the potentiation did not result from direct interaction with kainate receptors nor the activation of ion channels other than kainate receptor-channels.The potentiation by 17/3-estradiol was similar to the enhancement of kainate-induced currents evoked by 8-bromo-CAMP, and was modulated by an inhibitor of phosphodiesterase (IBMX). The estrogen potentiation was blocked by a specific blocker of PKA (&I-CAMPS). Under standard recording configuration, the effect was significantly affected by intracellular perfusing with GDP-p-S or GTP-y-S. The data suggest that the potentiation of kainate-induced currents by 17P-estradiol was likely a G-protein(s) coupled, CAMPdependent phosphorylation event. By involvement of this nongenomic mechanism, estrogen may play a role in the modulation of excitatory synaptic transmission in the hippocampus.

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Perforated Patch Recording

Cited by 98 publications

References 13 publications

Differential Effects of Endothelin‐1 on Basal and Isoprenaline‐Enhanced Ca²⁺ Current in Guinea‐Pig Ventricular Myocytes

Differential Effects of Endothelin‐1 on Basal and Isoprenaline‐Enhanced Ca²⁺ Current in Guinea‐Pig Ventricular Myocytes

Long-Term Potentiation in Distinct Subtypes of Hippocampal Nonpyramidal Neurons

17β-Estradiol Potentiates Kainate-Induced Currents via Activation of the cAMP Cascade

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Perforated Patch Recording

Cited by 98 publications

References 13 publications

Differential Effects of Endothelin‐1 on Basal and Isoprenaline‐Enhanced Ca2+ Current in Guinea‐Pig Ventricular Myocytes

Differential Effects of Endothelin‐1 on Basal and Isoprenaline‐Enhanced Ca2+ Current in Guinea‐Pig Ventricular Myocytes

Long-Term Potentiation in Distinct Subtypes of Hippocampal Nonpyramidal Neurons

17β-Estradiol Potentiates Kainate-Induced Currents via Activation of the cAMP Cascade

Contact Info

Product

Resources

About

Differential Effects of Endothelin‐1 on Basal and Isoprenaline‐Enhanced Ca²⁺ Current in Guinea‐Pig Ventricular Myocytes

Differential Effects of Endothelin‐1 on Basal and Isoprenaline‐Enhanced Ca²⁺ Current in Guinea‐Pig Ventricular Myocytes