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Parallèlement au développement d’un capitalisme financier et de l’extension du marché à tous les domaines de la vie, induisant par conséquent un recul de la protection sociale et des services publics en général, des formes de coopération émergent en marge des systèmes classiques privilégiant soit le marché soit l’État comme vecteurs principaux du lien social. Ces formes de coopération, qui ont connu une existence pratique avant leur formulation théorique, s’inscrivent dans le mouvement des communs, qui connaît aujourd’hui un essor grandissant malgré les obstacles économiques et institutionnels. Édouard Jourdain est docteur en philosophie et en science politique, chercheur associé au CESPRA (EHESS) et post-doctorant à Polytechnique. Il enseigne la théorie politique à l’Université Versailles Saint Quentin et travaille avec l’Agence nationale de la cohésion des territoires (ANCT) sur les relations entre communs et intérêt général. Emmanuel Dupont est responsable de la recherche et de l’innovation à l’ANCT.

Parallèlement au développement d’un capitalisme financier et de l’extension du marché à tous les domaines de la vie, induisant par conséquent un recul de la protection sociale et des services publics en général, des formes de coopération émergent en marge des systèmes classiques privilégiant soit le marché soit l’État comme vecteurs principaux du lien social. Ces formes de coopération, qui ont connu une existence pratique avant leur formulation théorique, s’inscrivent dans le mouvement des communs, qui connaît aujourd’hui un essor grandissant malgré les obstacles économiques et institutionnels. Édouard Jourdain est docteur en philosophie et en science politique, chercheur associé au CESPRA (EHESS) et post-doctorant à Polytechnique. Il enseigne la théorie politique à l’Université Versailles Saint Quentin et travaille avec l’Agence nationale de la cohésion des territoires (ANCT) sur les relations entre communs et intérêt général. Emmanuel Dupont est responsable de la recherche et de l’innovation à l’ANCT.

The role of gap junction channels on cardiac impulse propagation is complex. This review focuses on the differential expression of connexins in the heart and the biophysical properties of gap junction channels under normal and disease conditions. Structural determinants of impulse propagation have been gained from biochemical and immunocytochemical studies performed on tissue extracts and intact cardiac tissue. These have defined the distinctive connexin coexpression patterns and relative levels in different cardiac tissues. Functional determinants of impulse propagation have emerged from electrophysiological experiments carried out on cell pairs. The static properties (channel number and conductance) limit the current flow between adjacent cardiomyocytes and thus set the basic conduction velocity. The dynamic properties (voltage-sensitive gating and kinetics of channels) are responsible for a modulation of the conduction velocity during propagated action potentials. The effect is moderate and depends on the type of Cx and channel. For homomeric-homotypic channels, the influence is small to medium; for homomeric-heterotypic channels, it is medium to strong. Since no data are currently available on heteromeric channels, their influence on impulse propagation is speculative. The modulation by gap junction channels is most prominent in tissues at the boundaries between cardiac tissues such as sinoatrial node-atrial muscle, atrioventricular node-His bundle, His bundle-bundle branch and Purkinje fibers-ventricular muscle. The data predict facilitation of orthodromic propagation

HeLa cells expressing rat connexin43 (Cx43) and/or mouse Cx45 were studied with the dual voltage-clamp technique. Different types of cell pairs were established and their gap junction properties determined, i.e. the dependence of the instantaneous and steady-state conductances (g j,inst, g j,ss) on the transjunctional voltage (V j) and the kinetics of inactivation of the gap junction current (I j). Pairs of singly transfected cells showed homogeneous behaviour at both V j polarities. Homotypic Cx43-Cx43 and Cx45-Cx45 cell pairs yielded distinct symmetrical functions g j,inst=f(V j) and g j,ss=f(V j). Heterotypic Cx43-Cx45 preparations exhibited asymmetric functions g j,inst=f(V j) and g j,ss=f(V j) suggesting that connexons Cx43 and Cx45 gate with positive and negative V j, respectively. Preparations containing a singly (Cx43 or Cx45) or doubly (Cx43/45) transfected cell showed quasi-homogeneous behaviour at one V j polarity and heterogeneous behaviour at the other polarity. The former yielded Boltzmann parameters intermediate between those of Cx43-Cx43, Cx45-Cx45 and Cx43-Cx45 preparations; the latter could not be explained by homotypic and heterotypic combinations of homomeric connexons. Each pair of doubly transfected cells (Cx43/Cx45) yielded unique functions g j,inst=f(V j) and g j,ss=f(V j). This can not be explained by combinations of homomeric connexons. We conclude that Cx43 and Cx45 form homomeric-homotypic, homomeric-heterotypic channels as well as heteromeric-homotypic and heteromeric-heterotypic channels. This has implications for the impulse propagation in specific areas of the heart

HeLa cells expressing wild-type connexin43, connexin40 or connexin45 and connexins fused with a V5/6-His tag to the carboxyl terminus (CT) domain (Cx43-tag, Cx40-tag, Cx45-tag) were used to study connexin expression and the electrical properties of gap junction channels. Immunoblots and immunolabeling indicated that tagged connexins are synthesized and targeted to gap junctions in a similar manner to their wild-type counterparts. Voltage-clamp experiments on cell pairs revealed that tagged connexins form functional channels. Comparison of multichannel and single-channel conductances indicates that tagging reduces the number of operational channels, implying interference with hemichannel trafficking, docking and/or channel opening. Tagging provoked connexin-specific effects on multichannel and single-channel properties. The Cx43-tag was most affected and the Cx45-tag, least. The modifications included (1) V j-sensitive gating of I j (V j, gap junction voltage; I j, gap junction current), (2) contribution and (3) kinetics of I j deactivation and (4) single-channel conductance. The first three reflect alterations of fast V j gating. Hence, they may be caused by structural and/or electrical changes on the CT that interact with domains of the amino terminus and cytoplasmic loop. The fourth reflects alterations of the ion-conducting pathway. Conceivably, mutations at sites remote from the channel pore, e.g., 6-His-tagged CT, affect protein conformation and thus modify channel properties indirectly. Hence, V5/6-His tagging of connexins is a useful tool for expression studies in vivo. However, it should not be ignored that it introduces connexin-dependent changes in both expression level and electrophysiological properties