Immunocytochemical localization of the mammalian voltage-dependent sodium channel using polyclonal antibodies against the purified protein

Haimovich, Beatrice; Bonilla, Edmundo; Casadei, Jan; Barchi, Robert L.

doi:10.1523/jneurosci.04-09-02259.1984

Cited by 49 publications

(27 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The specific loss of the peripheral large gap junctions in the disks of hibernating myocardium is potentially critical. Recent findings suggest that tetrodotoxin-insensitive voltagedependent sodium channels, essential for the rapid early upstroke of the cardiac action potential, 37 have been localized to the lateral sarcolemma 38 and may be preferentially concentrated around the intercalated disks. 39 The peripheral intercalated disk conductance, determined by these large junctional plaques, may be of particular importance because of this spatial relationship.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of Immunodetectable Connexin43 and Decreased Gap Junction Size in the Pathogenesis of Chronic Hibernation in the Human Left Ventricle

et al. 1998

View full text Add to dashboard Cite

Background-The regional wall motion impairment and predisposition to arrhythmias in human ventricular hibernation may plausibly result from abnormal intercellular propagation of the depolarizing wave front. This study investigated the hypothesis that altered patterns of expression of connexin43, the principal gap junctional protein responsible for passive conduction of the cardiac action potential, contribute to the pathogenesis of hibernation. Methods and Results-Patients with poor ventricular function and severe coronary artery disease underwent thallium scanning and MRI to predict regions of normally perfused, reversibly ischemic, or hibernating myocardium. Twenty-one patients went on to coronary artery bypass graft surgery, during which biopsies representative of each of the above classes were taken. Hibernation was confirmed by improvement in segmental wall motion at reassessment 6 months after surgery.

show abstract

Section: Discussionmentioning

confidence: 99%

Downregulation of Immunodetectable Connexin43 and Decreased Gap Junction Size in the Pathogenesis of Chronic Hibernation in the Human Left Ventricle

et al. 1998

View full text Add to dashboard Cite

show abstract

“…Both electrophysiological measurements and measurements of numbers of saxitoxin binding sites indicate a high density of Na+ channels in nodes of Ranvier (reviewed in Waxman and Ritchie, 1985;Black et al, 1990). Immunocytochemical experiments with Na+ channel-specific antibodies confirm the high density of Na+ channels at nodes (Ellisman and Levinson, 1982;Haimovich et al, 1984). In contrast, there are few if any Na+ channels under the myelin because internodal regions of acutely demyelinated axons are not immunocytochemically stained with polyclonal antibodies against Na+ channels (Ellisman and Levinson, 1982;Black et al, 1990) and only small Na+ currents are recorded from acutely demyelinated internodal regions (Chiu and Ritchie, 1982;Shrager, 1987;reviewed in Black et al, 1990).…”

Section: Cellular Location Of Increased Na+ Channel Densitymentioning

confidence: 95%

Elevated expression of type II Na+ channels in hypomyelinated axons of shiverer mouse brain

1992

View full text Add to dashboard Cite

Type I and type III Na+ channels are localized mainly in neuronal cell bodies in mouse brain. Type II channels are preferentially localized in unmyelinated fiber tracts but are not detectable in normally myelinated fibers. In shiverer mice, which lack compact myelin due to a defect in the myelin basic protein gene, elevated expression of type II Na+ channels was observed in the hypomyelinated axons of large-caliber fiber tracts such as the corpus callosum, internal capsule, fimbria, fornix, corpus medullare of the cerebellum, and nigrostriatal pathway by immunocytochemical analysis with subtype-specific antibodies. No difference was observed in the localization of type I and type III Na+ channels between wild-type and shiverer mice. These findings support the hypothesis that type II Na+ channels are preferentially localized in axons of brain neurons and suggest that their density and localization are regulated by myelination. The selective increase in the number of type II channels in hypomyelinated fiber tracts may contribute to the hyperexcitable phenotype of the shiverer mouse.

show abstract

“…Since TTX-resistant channels are undetectable in innervated adult muscle (Caldwell and Milton, 1988), they can be ruled out. Other muscle Na+ channel subtypes (Haimovich et al, 1984(Haimovich et al, , 1987 have been observed, and the possibility that one or several of these subtypes is not bound by otScTx cannot be excluded. However, no subtype difference between the synaptic-perisynaptic zone and the rest of the surface has been reported.…”

Section: Na+ Channel Distribution On Presynaptic Structuresmentioning

confidence: 99%

Autoradiographic localization of voltage-dependent sodium channels on the mouse neuromuscular junction using 125I-alpha scorpion toxin. II. Sodium distribution on postsynaptic membranes

1992

View full text Add to dashboard Cite

A radioiodinated alpha-scorpion toxin (toxin II from Androctonus australis Hector) (alpha ScTx) was used as a probe for EM autoradiography to study the distribution of voltage-dependent sodium channels (Na+ channel) on the postsynaptic side of the mouse neuromuscular junction. Silver grain distribution was analyzed by the cross-fire method to assess the relative Na+ channel density in each membrane domain measured by stereology. This analysis showed that the maximum Na+ channel density was located on the edge of the synaptic gutter, where it reached about twice the mean density in the postsynaptic fold membrane. Na+ channel densities have been calculated using ACh receptor (AChR) density in fold crests as reference. Sodium channel density on the edge of the synaptic gutter was estimated at about 5000/microns 2. Sodium channel distribution in the postsynaptic folds was compared to AChR distribution using density distribution analysis (Fertuck and Salpeter, 1976). The results confirmed that, as already observed by immunogold labeling (Flucher and Daniels, 1989), there are no Na+ channels on fold crests. Na+ channels are located in the rest of the fold membrane (bottom) and may be distributed according to two possible models. In the first, density would be uniformly high, although lower than on the gutter edge. In the second, density would decrease from the crest border, where the value was that of the gutter edge, to the fold end, where the value would be 50% lower. Based on the latter model, which was the “best-fit model,” we propose that the postsynaptic membrane includes two domains. The first is the fold crest, which contains almost exclusively AChRs. This domain is devoted to reception-transduction of the chemical signal. The second includes both the fold bottom membrane and the perisynaptic membrane. Sodium channel density is highest along the crest border and decreases moving away. Its functions are the integration of postsynaptic potentials and generation-conduction of the muscle action potential.

show abstract

Immunocytochemical localization of the mammalian voltage-dependent sodium channel using polyclonal antibodies against the purified protein

Cited by 49 publications

References 15 publications

Downregulation of Immunodetectable Connexin43 and Decreased Gap Junction Size in the Pathogenesis of Chronic Hibernation in the Human Left Ventricle

Downregulation of Immunodetectable Connexin43 and Decreased Gap Junction Size in the Pathogenesis of Chronic Hibernation in the Human Left Ventricle

Elevated expression of type II Na+ channels in hypomyelinated axons of shiverer mouse brain

Autoradiographic localization of voltage-dependent sodium channels on the mouse neuromuscular junction using 125I-alpha scorpion toxin. II. Sodium distribution on postsynaptic membranes

Contact Info

Product

Resources

About