[5] Access resistance and space clamp problems associated with whole-cell patch clamping

Armstrong, Clay M.; Gilly, William F.

doi:10.1016/0076-6879(92)07007-b

Cited by 144 publications

(114 citation statements)

References 5 publications

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“…It is well established that the adequacy of space clamp diminishes as the dendritic trees of neurons increase Johnston and Brown, 1983). Series and access resistance errors also increase with larger currents (Armstrong and Gilly, 1992). Furthermore, the diff usion and time to equilibrium between pipette solutions and cellular contents that result in junction potentials may be delayed in larger cells (Neher, 1992).…”

Section: Possible Voltage-clamp Errors With Age In Culturementioning

confidence: 99%

Calcium Channel Density and Hippocampal Cell Death with Age in Long-Term Culture

et al. 1997

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The expression of voltage-gated calcium (Ca 2ϩ ) channel activity in brain cells is known to be important for several aspects of neuronal development. In addition, excessive Ca 2ϩ influx has been linked clearly to neurotoxicity both in vivo and in vitro; however, the temporal relationship between the development of Ca 2ϩ channel activity and neuronal survival is not understood. Over a period spanning 28 d in vitro, progressive increases in high voltage-activated whole-cell Ca 2ϩ current and L-type Ca 2ϩ channel activity were observed in cultured hippocampal neurons. On the basis of single-channel analyses, these increases seem to arise in part from a greater density of functionally available L-type Ca 2ϩ channels. An increase in mRNA for the ␣ 1 subunit of L-type Ca 2ϩ channels occurred over a similar time course, which suggests that a change in gene expression may underlie the increased channel density. Parallel studies showed that hippocampal neuronal survival over 28 d was inversely related to increasing Ca 2ϩ current density. Chronic treatment of hippocampal neurons with the L-type Ca 2ϩ channel antagonist nimodipine significantly enhanced survival. Together, these results suggest that age-dependent increases in the density of Ca 2ϩ channels might contribute significantly to declining viability of hippocampal neurons. The results also are analogous to patterns seen in neurons of aged animals and therefore raise the possibility that long-term primary neuronal culture could serve as a model for some aspects of aging changes in hippocampal Ca 2ϩ channel function.

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Section: Possible Voltage-clamp Errors With Age In Culturementioning

confidence: 99%

Calcium Channel Density and Hippocampal Cell Death with Age in Long-Term Culture

et al. 1997

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“…It is important in this comparison that the simulated spike had an amplitude and waveform identical to the control spike at the site of origin (soma). This is not possible to determine on the basis of electrical recording alone without an additional voltagemeasuring electrode in the soma, because series resistance compensation is never perfect (Armstrong and Gilly, 1992); however, a good match could be achieved by using optical measurement. The amplitude of the voltage-clamp command potential was adjusted until the optical signal from the soma in the TTX solution was very nearly identical to the control spike signal from the same area.…”

Section: Action Potential Initiation and Propagation In Secondary Denmentioning

confidence: 99%

Voltage Imaging from Dendrites of Mitral Cells: EPSP Attenuation and Spike Trigger Zones

Djurišić¹,

Antic²,

Chen³

et al. 2004

J. Neurosci.

118

130

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To obtain a more complete description of individual neurons, it is necessary to complement the electrical patch pipette measurements with technologies that permit a massive parallel recording from many sites on neuronal processes. This can be achieved by using voltage imaging with intracellular dyes. With this approach, we investigated the functional structure of a mitral cell, the principal output neuron in the rat olfactory bulb. The most significant finding concerns the characteristics of EPSPs at the synaptic sites and surprisingly small attenuation along the trunk of the primary dendrite. Also, the experiments were performed to determine the number, location, and stability of spike trigger zones, the excitability of terminal dendritic branches, and the pattern and nature of spike initiation and propagation in the primary and secondary dendrites. The results show that optical data can be used to deduce the amplitude and shape of the EPSPs evoked by olfactory nerve stimulation at the site of origin (glomerular tuft) and to determine its attenuation along the entire length of the primary dendrite. This attenuation corresponds to an unusually large mean apparent "length constant" of the primary dendrite. Furthermore, the images of spike trigger zones showed that an action potential can be initiated in three different compartments of the mitral cell: the soma-axon region, the primary dendrite trunk, and the terminal dendritic tuft, which appears to be fully excitable. Finally, secondary dendrites clearly support the active propagation of action potentials.

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“…Thus, the experimental approach could record ACh-induced current from multiple cells, which significantly enhanced the signal/ noise ratio. In the mean time, we were aware that the space-clamping problem existed for the cells that surround the recorded one, so that the I/V relation curves obtained might be distorted more or less (Armstrong et al, 1992;Lindau et al, 1988). To minimize such distortion, we used the thinnest and shortest vessel segments possible for whole-cell recording.…”

Section: Technical Issuesmentioning

confidence: 99%

ACh-induced depolarization in inner ear artery is generated by activation of a TRP-like non-selective cation conductance and inactivation of a potassium conductance

et al. 2008

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Adequate cochlear blood supply by the spiral modiolar artery (SMA) is critical for normal hearing. ACh may play a role in neuroregulation of the SMA but several key issues including its membrane action mechanisms remain poorly understood. Besides its well-known endothelium-dependent hyperpolarizing action, ACh can induce a depolarization in vascular cells. Using intracellular and whole-cell recording techniques on cells in guinea pig in vitro SMA, we studied the ionic mechanism underlying the ACh-depolarization and found that: 1) ACh induced a DAMP-sensitive depolarization when intermediate conductance K Ca channels were blocked by charybdotoxin or nitrendipine. The ACh-depolarization was associated with a decrease in input resistance (R input ) in high membrane potential (V m ) (~−40 mV) cells but with no change or an increase in R input in low V m (~−75 mV) cells. ACh-depolarization was attenuated by background membrane depolarization from ~−70 mV in the majority of cells; 2) ACh-induced inward current in smooth muscle cells embedded in a SMA segment often showed a U-shaped I/V curve, the reversal potential of its two arms being near E K and 0 mV respectively; 3) ACh-depolarization was reduced by low Na + , zero K + or 20 mM K + bath solutions; 4) ACh-depolarization was inhibited by La 3+ in all cells tested, by 4-AP and flufenamic acid in low V m cells, but was not sensitive to Cd 2+ , Ni 2+ , nifedipine, niflumic acid, DIDS, IAA94, linopirdine or amiloride. We conclude that ACh-induced vascular depolarization was generated mainly by activation of a TRP-like non-selective cation channel and by inactivation of an inward rectifier K + channel.

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[5] Access resistance and space clamp problems associated with whole-cell patch clamping

Cited by 144 publications

References 5 publications

Calcium Channel Density and Hippocampal Cell Death with Age in Long-Term Culture

Calcium Channel Density and Hippocampal Cell Death with Age in Long-Term Culture

Voltage Imaging from Dendrites of Mitral Cells: EPSP Attenuation and Spike Trigger Zones

ACh-induced depolarization in inner ear artery is generated by activation of a TRP-like non-selective cation conductance and inactivation of a potassium conductance

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