A versatile means of intracellular labeling: injection of biocytin and its detection with avidin conjugates

Horikawa, Kazuki; Armstrong, William E.

doi:10.1016/0165-0270(88)90114-8

Cited by 849 publications

(484 citation statements)

References 32 publications

Supporting

Mentioning

483

Contrasting

Order By: Relevance

“…Hampson et al, 1994), the coupling is termed dye coupling, and when non-fluorescent compounds are used, the coupling is termed tracer coupling. The most frequently used tracer compounds are biocytin (Horikawa and Armstrong, 1988) and Neurobiotin (Kita and Armstrong, 1991). They can be visualized by reacting with streptavidinbiotinylated-HRP (horseradish peroxidase) complex and diaminobenzidine (e.g.…”

Section: Evidence From Tracer Couplingmentioning

confidence: 99%

Electrical synapses between AII amacrine cells in the retina: Function and modulation

Hartveit

Veruki

2012

Brain Research

View full text Add to dashboard Cite

Adaptation enables the visual system to operate across a large range of background light intensities. There is evidence that one component of this adaptation is mediated by modulation of gap junctions functioning as electrical synapses, thereby tuning and functionally optimizing specific retinal microcircuits and pathways. The AII amacrine cell is an interneuron found in most mammalian retinas and plays a crucial role for processing visual signals in starlight, twilight and daylight. AII amacrine cells are connected to each other by gap junctions, potentially serving as a substrate for signal averaging and noise reduction, and there is evidence that the strength of electrical coupling is modulated by the level of background light. Whereas there is extensive knowledge concerning the retinal microcircuits that involve the AII amacrine cell, it is less clear which signaling pathways and intracellular transduction mechanisms are involved in modulating the junctional conductance between electrically coupled AII amacrine cells. Here we review the current state of knowledge, with a focus on recent evidence that suggests that the modulatory control involves activity-dependent changes in the phosphorylation of the gap junction channels between AII amacrine cells, potentially linked to their intracellular Ca 2+ dynamics.

show abstract

Section: Evidence From Tracer Couplingmentioning

confidence: 99%

Electrical synapses between AII amacrine cells in the retina: Function and modulation

Hartveit

Veruki

2012

Brain Research

View full text Add to dashboard Cite

show abstract

“…Sections were incubated in an avidin-biotin-peroxidase complex solution (ABC Elite kit, Vector Labs) and processed to reveal the intracellular peroxidase staining. 23 In addition, selected sections were counterstained with Thionin to verify the positions of the stimulating electrodes. Tissue shrinkage induced by fixation was estimated at ]15%.…”

Section: Histological Identification Of the Recorded Cells And Stimulmentioning

confidence: 99%

Inhibitory control of somatodendritic interactions underlying action potentials in neocortical pyramidal neurons in vivo: An intracellular and computational study

Paré¹,

Lang²,

Destexhe³

1998

Neuroscience

View full text Add to dashboard Cite

Abstract--The effect of synaptic inputs on somatodendritic interactions during action potentials was investigated, in the cat, using in vivo intracellular recording and computational models of neocortical pyramidal cells. An array of 10 microelectrodes, each ending at a different cortical depth, was used to preferentially evoke synaptic inputs to different somatodendritic regions. Relative to action potentials evoked by current injection, spikes elicited by cortical microstimuli were reduced in amplitude and duration, with stimuli delivered at proximal (somatic) and distal (dendritic) levels evoking the largest and smallest decrements, respectively. When the inhibitory postsynaptic potential reversal was shifted to around 50 mV by recording with KCl pipettes, synaptically-evoked spikes were significantly less reduced than with potassium acetate or cesium acetate pipettes, suggesting that spike decrements are not only due to a shunt, but also to voltage-dependent effects. Computational models of neocortical pyramidal cells were built based on available data on the distribution of active currents and synaptic inputs in the soma and dendrites. The distribution of synapses activated by extracellular stimulation was estimated by matching the model to experimental recordings of postsynaptic potentials evoked at different depths. The model successfully reproduced the progressive spike amplitude reduction as a function of stimulation depth, as well as the effects of chloride and cesium. The model revealed that somatic spikes contain an important contribution from proximal dendritic sodium currents up to ]100 µm and ]300 µm from the soma under control and cesium conditions, respectively. Proximal inhibitory postsynaptic potentials can prevent this dendritic participation thus reducing the spike amplitude at the soma. The model suggests that the somatic spike amplitude and shape can be used as a ''window'' to infer the electrical participation of proximal dendrites.Thus, our results suggest that inhibitory postsynaptic potentials can control the participation of proximal dendrites in somatic sodium spikes.1998 IBRO. Published by Elsevier Science Ltd.Key words: multicompartment models, intrinsic electrophysiological properties, in vivo intracellular recordings, action potentials, dendritic integration.By comparing the shape of antidromic, orthodromic and current-evoked action potentials (APs) in motoneurons, Coombs et al. 7 provided compelling evidence for the idea that APs are initiated at the initial segment (IS) and then invade the somatodendritic compartment. However, the applicability of this model to other cell types was questioned when the first intradendritic recordings revealed that dendrites can sustain active electrogenesis. 33,34,63 In neocortical and hippocampal pyramidal neurons for instance, intracellular recordings revealed that dendritic spikes can be elicited by synaptic inputs 5,9,30,52 and that they can amplify synaptic inputs electrotonically distant from the soma to initiate APs. 5 Moreover, the prox...

show abstract

“…Horikawa and Armstrong 1988) was injected intracellularly by passing negative current (0.2 to 0.4 nA) through the recording electrode for at least 5 min. Usually only 1 or 2 cells were labeled per slice.…”

Section: Histologymentioning

confidence: 99%

Contribution of NMDA receptors to postsynaptic potentials and paired-pulse facilitation in identified neurons of the rat nucleus accumbens in vitro

et al. 1991

View full text Add to dashboard Cite

Summary. The principal aim of this study was to characterize the transmitter mechanisms mediating fast postsynaptic potentials in identified neurons of the rat nucleus accumbens. Using the biocytin-avidin labeling technique, impaled neurons were identified as medium spiny neurons. The basic membrane characteristics of these neurons were determined. Local electrical stimulation or stimulation of the corpus callosum elicited a depolarizing postsynaptic potential consisting of an EPSP often followed by an IPSP. The quisqualate/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (4 gM) abolished most of the depolarizing postsynaptic potential. The N-methyl-D-aspartate receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid depressed a small part of the decay phase of the depolarizing postsynaptic potential. Paired-pulse facilitation of postsynaptic potentials was found using interstimulus-intervals between 10 and 150 ms. N-methyl-D-aspartate receptors were found to contribute only slightly to the facilitation of the decay phase of the depolarizing postsynaptic potential, but not to its rising phase. This contribution was particularly clear under conditions of reduced GABAA receptor mediated inhibition. The present study indicates that postsynaptic responses of medium spiny neurons in the nucleus accumbens to local stimulation or stimulation of neocortical afferents are primarily mediated by quisqualate/kainate receptors. The contribution of NMDA receptors is normally limited to a portion of the decay phase of these responses, but is enlarged in the absence of GABAergic inhibition and following paired-pulse stimulation.

show abstract

A versatile means of intracellular labeling: injection of biocytin and its detection with avidin conjugates

Cited by 849 publications

References 32 publications

Electrical synapses between AII amacrine cells in the retina: Function and modulation

Electrical synapses between AII amacrine cells in the retina: Function and modulation

Inhibitory control of somatodendritic interactions underlying action potentials in neocortical pyramidal neurons in vivo: An intracellular and computational study

Contribution of NMDA receptors to postsynaptic potentials and paired-pulse facilitation in identified neurons of the rat nucleus accumbens in vitro

Contact Info

Product

Resources

About