Metabolic Coupling, Ionic Coupling and Cell Contacts

Gilula, Norton B.; Reeves, O. R.; Steinbach, Alan

doi:10.1038/235262a0

Cited by 639 publications

(220 citation statements)

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“…For example, diffusion of apoptotic vesicles from tk + cells to tk − cells 7 and an increased immune response 8,9 have been considered. Transfer of toxic phosphorylated nucleotides between tumor cells through gap junctions was shown long ago 10 and has been proposed as the basis for a new form of cancer therapy. 11,12 In our laboratory, we have demonstrated the transfer of toxic agents from one cell to another via gap junctional intercellular communication (GJIC), leading to the selective killing of tumorigenic cells…”

Section: Introductionmentioning

confidence: 99%

Long-term connexin-mediated bystander effect in highly tumorigenic human cells in vivo in herpes simplex virus thymidine kinase/ganciclovir gene therapy

et al. 1998

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Section: Introductionmentioning

confidence: 99%

Long-term connexin-mediated bystander effect in highly tumorigenic human cells in vivo in herpes simplex virus thymidine kinase/ganciclovir gene therapy

et al. 1998

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“…Gap junctions were identified based on established criteria (Goodenough and Revel, 1970;Gilula et al, 1972;Rash et al, 1997Rash et al, ,1998, including: a) uniform 8−9 nm diameter IMPs in their P-faces and uniform 8−9 nm diameter pits in their E-faces, both having 10-nm centerto-center spacing; b) close packing of IMPs/pits, often in regular hexagonal array; c) maintained alignment of the rows of P-face IMPs and E-face pits where the fracture plane steps from Pface to E-face within the gap junction; and d) narrowing of the extracellular space to 2−3 nm within the border of those few gap junctions in which both P-and E-faces are exposed. This report uses the internationally-recognized terminology for describing membrane faces in freeze-fracture replicas (Branton et al, 1975), wherein replicated "protoplasmic" fracture faces are designated by the mnemonic "P-face" and the complementary "extraplasmic" leaflets (extracellular, extranuclear, extramitochondrial) are designated "E-faces".…”

Section: Criteria For Identifying Gap Junctions In Freeze-fracture Rementioning

confidence: 99%

Identification of connexin36 in gap junctions between neurons in rodent locus coeruleus

et al. 2007

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Locus coeruleus neurons are strongly coupled during early postnatal development, and it has been proposed that these neurons are linked by extraordinarily abundant gap junctions consisting of connexin32 and connexin26, and that those same connexins abundantly link neurons to astrocytes. Based on the controversial nature of those claims, immunofluorescence imaging and freeze-fracture replica immunogold labeling were used to re-investigate the abundance and connexin composition of neuronal and glial gap junctions in developing and adult rat and mouse locus coeruleus. In early postnatal development, connexin36 and Cx43 immunofluorescent puncta were densely distributed in the locus coeruleus, whereas connexin32 and connexin26 were not detected. By freeze-fracture replica immunogold labeling, connexin36 was found in ultrastructurally-defined neuronal gap junctions, whereas connexin32 and connexin26 were not detected in neurons and only rarely detected in glia. In 28-day postnatal (adult) rat locus coeruleus, immunofluorescence labeling for connexin26 was always co-localized with the glial gap junction marker connexin43; connexin32 was associated with the oligodendrocyte marker CNPase; and connexin36 was never co-localized with connexin26, Cx32 or connexin43. Ultrastructurally, connexin36 was localized to gap junctions between neurons, whereas connexin32 was detected only in oligodendrocyte gap junctions; and Cx26 was found only rarely in astrocyte junctions but abundantly in pia mater. Thus, in developing and adult locus coeruleus, neuronal gap junctions contain connexin36 but do not contain detectable connexin32 or connexin26, suggesting that the locus coeruleus has the same cell-type specificity of connexin expression as observed ultrastructurally in other regions of the central nervous system. Moreover, in both developing and adult locus coeruleus, no evidence was found for gap junctions or connexins linking neurons with astrocytes or oligodendrocytes, indicating that neurons in this nucleus are not linked to the pan-glial syncytium by connexin32-or connexin26-containing gap junctions or by abundant free connexons composed of those connexins. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2008 July 29. Published in final edited form as:Neuroscience. In the developing mammalian central nervous system (CNS), electrical coupling between neurons is well documented by electrophysiological and dye-coupling approaches (Peinado et al., 1993;Fulton, 1995;Montoro and Yuste, 2004;Bruzzone and...

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“…Within gap junctions, P-face connexon IMPs are of uniform 9-nm diameter, which is noticeably larger than virtually all other IMPs in the nearby plasma membrane P-face. Connexon E-face pits are equally distinct, making even small clusters of connexon P-face particles and E-face pits easily identifiable by their size and 10-nm center-to-center spacing (Gilula et al, 1972;Raviola and Gilula, 1975;Raviola et al, 1980;Rash et al, 1996;Meier et al, 2004). …”

mentioning

confidence: 99%

Connexin36 vs. connexin32, “miniature” neuronal gap junctions, and limited electrotonic coupling in rodent suprachiasmatic nucleus

et al. 2007

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Suprachiasmatic nucleus (SCN) neurons generate circadian rhythms, and these neurons normally exhibit loosely-synchronized action potentials. Although electrotonic coupling has long been proposed to mediate this neuronal synchrony, ultrastructural studies have failed to detect gap junctions between SCN neurons. Nevertheless, it has been proposed that neuronal gap junctions exist in the SCN; that they consist of connexin32 or, alternatively, connexin36; and that connexin36 knockout eliminates neuronal coupling between SCN neurons and disrupts circadian rhythms. We used confocal immunofluorescence microscopy and freeze-fracture replica immunogold labeling to examine the distributions of connexin30, connexin32, connexin36, and connexin43 in rat and mouse SCN and used whole-cell recordings to re-assess electrotonic and tracer coupling. Connexin32-immunofluorescent puncta were essentially absent in SCN but connexin36 was relatively abundant. Fifteen neuronal gap junctions were identified ultrastructurally, all of which contained connexin36 but not connexin32, whereas nearby oligodendrocyte gap junctions contained connexin32. In adult SCN, one neuronal gap junction was >600 connexons, whereas 75% were smaller than 50 connexons, which may be below the limit of detectability by fluorescence microscopy and thin-section electron microscopy. Whole-cell recordings in hypothalamic slices revealed tracer coupling with Neurobiotin in <5% of SCN neurons, and paired recordings (>40 pairs) did not reveal obvious electrotonic coupling or synchronized action potentials, consistent with few neurons possessing large gap junctions. However, most neurons had partial spikes or spikelets (often <1 mV), which remained after QX-314 had blocked sodium-mediated action potentials within the recorded neuron, consistent with spikelet transmission via small gap junctions. Thus, a few "miniature" gap junctions on most SCN neurons appear to mediate weak electrotonic coupling between limited numbers of neuron pairs, Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2008 February 15. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript thus accounting for frequent detection of partial spikes and hypothetically providing the basis for "loose" electrical or metabolic synchronization of electrical activity commonly observed in SCN neuronal populations during circadian rhythms. Keywordsimmunocytochemistry; electrical synapse; freeze-fracture replica immunogold labeling; spikelet; metabolic coupling; syn...

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Metabolic Coupling, Ionic Coupling and Cell Contacts

Cited by 639 publications

References 19 publications

Long-term connexin-mediated bystander effect in highly tumorigenic human cells in vivo in herpes simplex virus thymidine kinase/ganciclovir gene therapy

Long-term connexin-mediated bystander effect in highly tumorigenic human cells in vivo in herpes simplex virus thymidine kinase/ganciclovir gene therapy

Identification of connexin36 in gap junctions between neurons in rodent locus coeruleus

Connexin36 vs. connexin32, “miniature” neuronal gap junctions, and limited electrotonic coupling in rodent suprachiasmatic nucleus

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