Possible roles of gap junctions in network activity during Parkinson´s disease

    Research output: Chapter in Book/Report/Conference proceedingConference contributionAcademic

    Abstract

    Methods: Using immunohistochemistry and confocal imaging, we reconstructed the distribution of Cx36, the major neural connexin, in human post-mortem tissue of the STN, GPe and GPi. Our preliminary analysis included tissue from 6 subjects (2x STN control, 2x STN PD, 1x GPi/e control, 1x GPi/e PD). Assuming that at least a part of the detected Cx36 indicates functional gap junctions, we implemented gap junctions in an existing computational model of the basal ganglia, the Rubin-Terman model including the STN, GPe and GPi. Results: Control tissue from the GPe/i showed punctuate Cx36 labeling, which was absent in a negative control leaving out the primary antibody. PD tissue additionally showed clusters of cells highly expressing Cx36. In the STN, only few spots of Cx36 were visible in control tissues. Their occurrence did not significantly increase in PD tissue. In the Rubin-Terman model (2002/2004) including STN, GPe and GPi, homogeneous gap junction coupling between nearest neighbors inside the GPe/i only slightly influenced the network behavior, unless the gap junction conductance was very high. However, clusters of cells in the GPi/e coupled via gap junctions led to bursting and synchronization, even if the gap junction conductance was comparably low. Conclusions: Clusters of cells coupled via gap junctions seen in the GPi/e of the PD patient could explain the occurrence of bursting and synchronization in the basal ganglia. The modulation of gap junctions by dopamine might be a candidate for the remodeling of neural activity. Our experiments do not provide evidence for the functionality of the detected gap junctions.
    Original languageUndefined
    Title of host publicationInternational Basal Ganglia Society Meeting 2013
    PublisherIBAGS
    Pages29
    Number of pages1
    ISBN (Print)not assigned
    Publication statusPublished - 2013

    Publication series

    Name
    PublisherIBAGS

    Keywords

    • EWI-24269
    • IR-89153
    • METIS-302621

    Cite this

    Schwab, B. C., van Gils, S. A., Zhao, Y., Heida, T., & van Wezel, R. J. A. (2013). Possible roles of gap junctions in network activity during Parkinson´s disease. In International Basal Ganglia Society Meeting 2013 (pp. 29). IBAGS.
    @inproceedings{08adf5cbf2d845c8b582e1c32135315d,
    title = "Possible roles of gap junctions in network activity during Parkinson´s disease",
    abstract = "Methods: Using immunohistochemistry and confocal imaging, we reconstructed the distribution of Cx36, the major neural connexin, in human post-mortem tissue of the STN, GPe and GPi. Our preliminary analysis included tissue from 6 subjects (2x STN control, 2x STN PD, 1x GPi/e control, 1x GPi/e PD). Assuming that at least a part of the detected Cx36 indicates functional gap junctions, we implemented gap junctions in an existing computational model of the basal ganglia, the Rubin-Terman model including the STN, GPe and GPi. Results: Control tissue from the GPe/i showed punctuate Cx36 labeling, which was absent in a negative control leaving out the primary antibody. PD tissue additionally showed clusters of cells highly expressing Cx36. In the STN, only few spots of Cx36 were visible in control tissues. Their occurrence did not significantly increase in PD tissue. In the Rubin-Terman model (2002/2004) including STN, GPe and GPi, homogeneous gap junction coupling between nearest neighbors inside the GPe/i only slightly influenced the network behavior, unless the gap junction conductance was very high. However, clusters of cells in the GPi/e coupled via gap junctions led to bursting and synchronization, even if the gap junction conductance was comparably low. Conclusions: Clusters of cells coupled via gap junctions seen in the GPi/e of the PD patient could explain the occurrence of bursting and synchronization in the basal ganglia. The modulation of gap junctions by dopamine might be a candidate for the remodeling of neural activity. Our experiments do not provide evidence for the functionality of the detected gap junctions.",
    keywords = "EWI-24269, IR-89153, METIS-302621",
    author = "B.C. Schwab and {van Gils}, {Stephanus A.} and Yan Zhao and Tjitske Heida and {van Wezel}, {Richard Jack Anton}",
    year = "2013",
    language = "Undefined",
    isbn = "not assigned",
    publisher = "IBAGS",
    pages = "29",
    booktitle = "International Basal Ganglia Society Meeting 2013",

    }

    Schwab, BC, van Gils, SA, Zhao, Y, Heida, T & van Wezel, RJA 2013, Possible roles of gap junctions in network activity during Parkinson´s disease. in International Basal Ganglia Society Meeting 2013. IBAGS, pp. 29.

    Possible roles of gap junctions in network activity during Parkinson´s disease. / Schwab, B.C.; van Gils, Stephanus A.; Zhao, Yan; Heida, Tjitske; van Wezel, Richard Jack Anton.

    International Basal Ganglia Society Meeting 2013. IBAGS, 2013. p. 29.

    Research output: Chapter in Book/Report/Conference proceedingConference contributionAcademic

    TY - GEN

    T1 - Possible roles of gap junctions in network activity during Parkinson´s disease

    AU - Schwab, B.C.

    AU - van Gils, Stephanus A.

    AU - Zhao, Yan

    AU - Heida, Tjitske

    AU - van Wezel, Richard Jack Anton

    PY - 2013

    Y1 - 2013

    N2 - Methods: Using immunohistochemistry and confocal imaging, we reconstructed the distribution of Cx36, the major neural connexin, in human post-mortem tissue of the STN, GPe and GPi. Our preliminary analysis included tissue from 6 subjects (2x STN control, 2x STN PD, 1x GPi/e control, 1x GPi/e PD). Assuming that at least a part of the detected Cx36 indicates functional gap junctions, we implemented gap junctions in an existing computational model of the basal ganglia, the Rubin-Terman model including the STN, GPe and GPi. Results: Control tissue from the GPe/i showed punctuate Cx36 labeling, which was absent in a negative control leaving out the primary antibody. PD tissue additionally showed clusters of cells highly expressing Cx36. In the STN, only few spots of Cx36 were visible in control tissues. Their occurrence did not significantly increase in PD tissue. In the Rubin-Terman model (2002/2004) including STN, GPe and GPi, homogeneous gap junction coupling between nearest neighbors inside the GPe/i only slightly influenced the network behavior, unless the gap junction conductance was very high. However, clusters of cells in the GPi/e coupled via gap junctions led to bursting and synchronization, even if the gap junction conductance was comparably low. Conclusions: Clusters of cells coupled via gap junctions seen in the GPi/e of the PD patient could explain the occurrence of bursting and synchronization in the basal ganglia. The modulation of gap junctions by dopamine might be a candidate for the remodeling of neural activity. Our experiments do not provide evidence for the functionality of the detected gap junctions.

    AB - Methods: Using immunohistochemistry and confocal imaging, we reconstructed the distribution of Cx36, the major neural connexin, in human post-mortem tissue of the STN, GPe and GPi. Our preliminary analysis included tissue from 6 subjects (2x STN control, 2x STN PD, 1x GPi/e control, 1x GPi/e PD). Assuming that at least a part of the detected Cx36 indicates functional gap junctions, we implemented gap junctions in an existing computational model of the basal ganglia, the Rubin-Terman model including the STN, GPe and GPi. Results: Control tissue from the GPe/i showed punctuate Cx36 labeling, which was absent in a negative control leaving out the primary antibody. PD tissue additionally showed clusters of cells highly expressing Cx36. In the STN, only few spots of Cx36 were visible in control tissues. Their occurrence did not significantly increase in PD tissue. In the Rubin-Terman model (2002/2004) including STN, GPe and GPi, homogeneous gap junction coupling between nearest neighbors inside the GPe/i only slightly influenced the network behavior, unless the gap junction conductance was very high. However, clusters of cells in the GPi/e coupled via gap junctions led to bursting and synchronization, even if the gap junction conductance was comparably low. Conclusions: Clusters of cells coupled via gap junctions seen in the GPi/e of the PD patient could explain the occurrence of bursting and synchronization in the basal ganglia. The modulation of gap junctions by dopamine might be a candidate for the remodeling of neural activity. Our experiments do not provide evidence for the functionality of the detected gap junctions.

    KW - EWI-24269

    KW - IR-89153

    KW - METIS-302621

    M3 - Conference contribution

    SN - not assigned

    SP - 29

    BT - International Basal Ganglia Society Meeting 2013

    PB - IBAGS

    ER -

    Schwab BC, van Gils SA, Zhao Y, Heida T, van Wezel RJA. Possible roles of gap junctions in network activity during Parkinson´s disease. In International Basal Ganglia Society Meeting 2013. IBAGS. 2013. p. 29