Measurement of passive membrane parameters with whole-cell recording from neurons in the intact amphibian retina

Coleman, Paul A.; Miller, Robert F.

doi:10.1152/jn.1989.61.1.218

Cited by 111 publications

(68 citation statements)

References 15 publications

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“…A previous compartmental model of an alpha cell (22) based on a low specific membrane resistance (2500 fl.cm2) suggested that nonlinear subunits correspond to discrete regions of the alpha dendritic tree. This scheme is unlikely, however, since the subunits coalesce into a single large subunit as the specific membrane resistance approaches currently published values (>8000 fQcm2) (19,20,22). A more plausible model is a rectifying amacrine cell interposed between the bipolar cell and the ganglion cell.…”

Section: Discussionmentioning

confidence: 90%

“…However, when the b1 surround is represented as an exponential (instead of a Gaussian), then the form of the alpha surround was indeed altered (Fig. 5D, heavy (13)(14)(15)(16)(17)(18)(19)(20) are opened by single quanta of transmitter at other central nervous system synapses (36,37). About 450 b, synapses contact the alpha cell (12).…”

Section: Discussionmentioning

confidence: 99%

“…This article must therefore be hereby marked (20). This may be due to a difference of species and/or temperature (21).…”

mentioning

confidence: 99%

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Computational model of the on-alpha ganglion cell receptive field based on bipolar cell circuitry.

Freed

Smith

Sterling

1992

Proc. Natl. Acad. Sci. U.S.A.

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The on-alpha ganglion cell in the area cen- its receptive field has a center and surround (13).Here we combine the general structure of the analytical models with detailed anatomical data to compute the contribution of the b, array to the on-alpha receptive field. The computation assumes, like the analytical models, that the on-alpha cell sums its inputs linearly. Although there are temporal nonlinearities within the on-alpha receptive field, given moderate stimulus contrast, these nonlinearities apparently sum in a spatially linear fashion (9, 11). The computation also assumes that every b, synapse evokes the same conductance increase in the on-alpha cell (for a given depolarization of the bipolar cell) and that this conductance increase depolarizes the on-alpha cell. These assumptions simplify the computation of the on-alpha receptive field to a weighted summation of bipolar receptive fields. A bipolar cell's weight depends on the number of synapses it contributes to the on-alpha dendrites and the electrotonic effects of these synapses at the soma.The receptive fields of both on and off types of alpha (Y) ganglion cells are tuned to low spatial frequencies (cutoff frequency, 2 c/degree in area centralis) (1). The Y cell contributes the major retinal input to area 18, which may explain the low-frequency tuning of this area (2, 3). The alpha cell's contribution to the visual system depends critically on the structure of its receptive field. There are two overlapping regions: a relatively broad center and a still broader antagonistic surround, each with a roughly Gaussian distribution of sensitivity (4-7).The question we address here is how does the alpha (Y) receptive field structure arise from retinal circuitry? Analytical models of the alpha receptive field give some important clues (8-11). Such models, as schematized in Fig. 1, hypothesize the receptive field to arise from a pooling of linear subunits. Each linear subunit has a center and surround with Gaussian distributions of sensitivity. These linear subunits are weighted individually and summed in a linear fashion. If appropriate distributions of sensitivity for the subunits are chosen, as well as the correct weightings, then the summed subunit centers duplicate the alpha center and the summed subunit surrounds duplicate the alpha surround (8). Although correspondence has not been established between linear subunits and any particular elements of retinal circuitry, they closely resemble, by their individual properties and their array, the bipolar cells that contact the on-alpha cell. We had previously described this source ofinput by reconstructing an on-alpha cell from serial, electron microscopic sections.Most bipolar synapses (82-89%) derive from a single bipolar METHODS An on-alpha ganglion cell from the area centralis had been filled with horseradish peroxidase, blackened with diaminobenzidine, and drawn with a camera lucida (12). Almost half of the dendritic arbor, spanning the full-field diameter, had been reconstructed by electron microsco...

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Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

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Computational model of the on-alpha ganglion cell receptive field based on bipolar cell circuitry.

Freed

Smith

Sterling

1992

Proc. Natl. Acad. Sci. U.S.A.

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Section: Methodsmentioning

confidence: 99%

“…In the majority of experiments examining iontophoretic responses, tetrodotoxin (0.5-1 1uM) was included to block sodium-dependent action potentials. Currents were recorded with an Axopatch 1B amplifier from neurons in the CA1 and CA3 pyramidal cell layers and granule cell layer of the dentate gyrus using the "blind" whole-cell recording technique (15,16 To measure glutamate desensitization, currents were recorded from outside-out patches pulled from the somata of pyramidal and granule neurons. Patches were maneuvered within the slice chamber to an apparatus constructed for the rapid application of agonists (6,8,17 solution containing kainate or glutamate to one containing the agonist but with a 10-fold lower concentration of NaCl (18).…”

Section: Methodsmentioning

confidence: 99%

Aniracetam reduces glutamate receptor desensitization and slows the decay of fast excitatory synaptic currents in the hippocampus.

Isaacson

Nicoll²

1991

Proc. Natl. Acad. Sci. U.S.A.

184

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Aniracetam is a nootropic drug that has been shown to selectively enhance quisqualate receptor-mediated responses in Xenopus oocytes injected with brain mRNA and in hippocampal pyramidal cells [Ito, I., Tanabe, S., Kohda, A. & Sugiyama, H. (1990) J. Physiol. (London) 424, 533-544]. We have used patch clamp recording techniques in hippocampal slices to elucidate the mechanism for this selective action. We find that aniracetam enhances glutamate-evoked currents in whole-cell recordings and, in outside-out patches, strongly reduces glutamate receptor desensitization. In addition, aniracetam selectively prolongs the time course and increases the peak amplitude of fast synaptic currents. A general property of neurotransmitter receptor channels is that in the cQntinuous presence of agonist the response rapidly diminishes. Although this desensitization, which results from a conformational change in the receptors, is readily demonstrated for a number of neurotransmitters, including acetylcholine (1, 2), y-aminobutyric acid (3), glycine (4), serotonin (5), and glutamate (6-12), a physiological role for desensitization in synaptic transmission has not been established. Rapid perfusion experiments with the non-N-methyl-D-aspartate (NMDA) type of glutamate receptor indicate that this receptor desensitizes extremely quickly in the presence of glutamate (6,7,(10)(11)(12) with a time course similar to that of glutamate-mediated synaptic responses. We have investigated whether desensitization could contribute to the decay of excitatory postsynaptic currents (EPSCs) (6, 7). We find that aniracetam, a drug reported to enhance glutamate responses (13), strongly reduces glutamate receptor desensitization. In addition, this drug prolongs the time course and increases the peak amplitude of synaptic currents. These findings suggest that receptor desensitization governs the strength of excitatory synaptic transmission in the brain. MATERIALS AND METHODSExperiments were performed on guinea pig hippocampal slices (500 jmm) prepared by standard methods (14). After a 1-hr recovery period, slices were placed in a laminar flow recording chamber and superfused with amedium containing (in mM) 125 NaCl, 5 KCI, 4 MgCl2, 4 CaCl2, 26 NaHCO3, 1 NaH2PO4, and 10 glucose and equilibrated with 95% 02/5% CO2. For all experiments examining synaptic currents or iontophoretic responses in slices, picrotoxin (50-100 lOM) and DL-2-amino-5-phosphonovaleric acid (50 ,uM) were added to the medium to block y-aminobutyric acid type A (GABAA) receptors and NMDA receptors, respectively. In the majority of experiments examining iontophoretic responses, tetrodotoxin (0.5-1 1uM) was included to block sodium-dependent action potentials. Currents were recorded with an Axopatch 1B amplifier from neurons in the CA1 and CA3 pyramidal cell layers and granule cell layer of the dentate gyrus using the "blind" whole-cell recording technique (15,16 NaCI, pH 8). All experiments were performed at room temperature at a holding potential of -80 mV, unless otherwise state...

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Automatic characterization and classification of ganglion cells from the salamander retina

Costa

Velte

1999

J. Comp. Neurol.

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Measurement of passive membrane parameters with whole-cell recording from neurons in the intact amphibian retina

Cited by 111 publications

References 15 publications

Computational model of the on-alpha ganglion cell receptive field based on bipolar cell circuitry.

Computational model of the on-alpha ganglion cell receptive field based on bipolar cell circuitry.

Aniracetam reduces glutamate receptor desensitization and slows the decay of fast excitatory synaptic currents in the hippocampus.

Automatic characterization and classification of ganglion cells from the salamander retina

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