Design of the EPC-9, a computer-controlled patch-clamp amplifier. 2. Software

Sigworth, Fred J.; Affolter, Hubert; Neher, Erwin

doi:10.1016/0165-0270(94)00129-5

Cited by 56 publications

(46 citation statements)

References 6 publications

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“…The input resistance of the examined neurons was determined by short, hyperpolarizing voltage steps from a 50 mV holding potential and was Ͼ1 G⍀ in most neurons with the recording solution (see above). The series resistance estimated by exponential fitting of the capacitance artifacts during brief hyperpolarizing voltage commands from 50 to 60 mV conformed well to the values obtained with the EPC9 capacitance cancellation paradigm (Sigworth et al, 1995). Series resistance compensation was used to improve the voltage-clamp control (60 -80%).…”

Section: Methodsmentioning

confidence: 99%

GSK-3β Inhibits Presynaptic Vesicle Exocytosis by Phosphorylating P/Q-Type Calcium Channel and Interrupting SNARE Complex Formation

Zhu

Liú²,

Hu³

et al. 2010

J. Neurosci.

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Glycogen synthase kinase-3 (GSK-3), a Ser/Thr protein kinase abundantly expressed in neurons, plays diverse functions in physiological and neurodegenerative conditions. Our recent study shows that upregulation of GSK-3 suppresses long-term potentiation and presynaptic release of glutamate; however, the underlying mechanism is elusive. Here, we show that activation of GSK-3␤ retards the synaptic vesicle exocytosis in response to membrane depolarization. Using calcium imaging, whole-cell patch-clamp, as well as specific Ca

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Section: Methodsmentioning

confidence: 99%

GSK-3β Inhibits Presynaptic Vesicle Exocytosis by Phosphorylating P/Q-Type Calcium Channel and Interrupting SNARE Complex Formation

Zhu

Liú²,

Hu³

et al. 2010

J. Neurosci.

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“…Current-clamp recordings were continued only if the initial uncompensated R s was Ͻ6 M⍀. With a residual uncompensated capacitance of ϳ2 pF in the EPC -9 fast currentclamp mode (F. Sigworth, personal communication;Sigworth et al, 1995), the time constant of the current-clamp recordings was estimated to be Ͻ12 sec.…”

Section: Methodsmentioning

confidence: 99%

Fine-Tuning an Auditory Synapse for Speed and Fidelity: Developmental Changes in Presynaptic Waveform, EPSC Kinetics, and Synaptic Plasticity

2000

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Fast, precise, and sustained synaptic transmission at high frequency is thought to be crucial for the task of sound localization in the auditory brainstem. However, recordings from the calyx of Held synapse have revealed severe frequency-dependent synaptic depression, which tends to degrade the exact timing of postsynaptic spikes. Here we investigate the functional changes occurring throughout the critical period of synapse refinement from immature calyx terminal [postnatal day 5 (P5)] to after the onset of hearing (P12-P14). Surprisingly, for recordings near physiological temperature (35°C), we find that P14 synapses are already able to follow extremely high input rates of up to 800 Hz. This ability stems in part from a remarkable shortening of presynaptic action potentials, which may lead to a lowering of release probability and decrease in synaptic delays during development. In addition, AMPA receptor-mediated EPSCs as well as quantal synaptic currents acquired progressively faster kinetics, although their mean amplitudes did not change significantly. NMDA receptor-mediated EPSCs, however, diminished with age, as indicated by a 50% reduction in mean amplitude and faster decay kinetics. Finally, the degree of synaptic depression was greatly attenuated with age, presumably because of a 2.5-fold or larger increase in the releasable pool of vesicles, which together with a decreasing release probability produces a fairly constant EPSC amplitude. This finely tuned orchestra of developmental changes thus simultaneously promotes speed while preventing premature vesicle pool depletion during prolonged bouts of firing. A few critical days in postnatal development can thus have a large impact on synaptic function.

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“…For measuring the capacitative current, hyperpolarizing square pulses (50 mV) were applied from a holding potential of −60 mV and data were sampled at 40 kHz. Most of the capacitance of the pipette-pipette holder assembly could be neutralized in the cell-attached configuration using the 'Cfast' capacitance neutralization network of the EPC_9 (Sigworth, Affolter & Neher, 1995). After establishing the whole-cell configuration the 'Cslow' capacitance neutralization network of the EPC_9 (Sigworth et al 1995) was used to determine cell membrane capacitance and access resistance.…”

Section: Electrophysiologymentioning

confidence: 99%

Low‐conductance intercellular coupling between mouse chromaffin cells in situ

Moser

1998

The Journal of Physiology

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Patch‐clamp experiments were used to compare membrane properties of mouse chromaffin cells in thin tissue slices and of isolated cells in primary culture. The mean membrane input resistance (Rin) and membrane capacitance were 3.1 ± 0.5 GΩ and 9.1 ± 0.5 pF in situ and 9.9 ± 1.8 GΩ and 8.2 ± 0.2 pF in isolated cells. Spike‐like currents were observed on top of the calcium currents during depolarizations in thirty out of forty‐nine cells in situ. They were not seen in isolated cells nor after addition of Cd2+ (100 μM) and TTX (10 μM) to the perfusate of the slices. The mean Rin of cells which displayed current spikes (2.3 ± 0.18 GΩ) was significantly smaller than that of cells lacking spikes (3.9 ± 0.25 GΩ). It is suggested that the current spikes represent intercellular currents which result from action potential firing in neighbouring cells during the depolarization of the patch‐clamped cell. Investigation of capacitative currents induced by square voltage pulses showed a slow component in twenty‐four out of twenty‐seven cells in situ. It is concluded that a large fraction of mouse chromaffin cells in situ are electrically coupled. From the slow capacitative currents and the amplitude of the intercellular current spikes a junctional conductance between chromaffin cells of below 1 nS was deduced. This junctional conductance appears to be too low to support spreading of electrical activity in cases where a single cell is stimulated by an action potential. However, the junctional conductance could allow longer depolarizations of one cell or simultaneous firing of several cells to trigger electrical activity in neighbouring cells.

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Design of the EPC-9, a computer-controlled patch-clamp amplifier. 2. Software

Cited by 56 publications

References 6 publications

GSK-3β Inhibits Presynaptic Vesicle Exocytosis by Phosphorylating P/Q-Type Calcium Channel and Interrupting SNARE Complex Formation

GSK-3β Inhibits Presynaptic Vesicle Exocytosis by Phosphorylating P/Q-Type Calcium Channel and Interrupting SNARE Complex Formation

Fine-Tuning an Auditory Synapse for Speed and Fidelity: Developmental Changes in Presynaptic Waveform, EPSC Kinetics, and Synaptic Plasticity

Low‐conductance intercellular coupling between mouse chromaffin cells in situ

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