Neuronal Gap Junction Coupling Is Regulated by Glutamate and Plays Critical Role in Cell Death during Neuronal Injury

(Downloading may take up to 30 seconds. If the slide opens in your browser, select File -> Save As to save it.)

Click on image to view larger version.

Figure 7.
Figure 7.

The regulation by group II mGluRs is specific for Cx36-containing gap junctions. A, B, Electrotonic coupling experiments in Cx36 knock-out (Cx36 KO) mouse mature neuronal somatosensory cortical cultures reveal no coupling between the neurons. Statistical data for the incidence of electrotonic coupling and the coupling coefficient (A, B, respectively) are presented (see Table 1 for the number of samples). For comparison, data from the OGD group in wild-type (WT) neuronal cultures from Figure 2, A and B, are included in the boxes. C–E, Cx43 expression. Statistical data and representative blots (c1–e1) from Western blot experiments in the primary somatosensory cortex obtained from adult wild-type mice (C) and in wild-type mouse mature purified glial cortical cultures (D, E) are shown. Statistical analysis was as follows: ANOVA with post hoc Tukey; n = 8 (C), 8–13 (D), and 7–10 (E) per group; data are shown as mean ± SEM. Optical density signals are normalized relative to tubulin, and normalized values are compared with the nonischemic saline (C) and control (D, E), set at 1.0. Experimental conditions and drug concentrations are the same as in Cx36 experiments (see Figs. 2, 4). In C, all measurements of Cx43 expression were done in the right (ipsilateral) cortex.

  1. The Journal of Neuroscience vol. 32 no. 2 713-725
Responses to This Article
Be the first to respond to this article
View Similar Articles
Similar articles in this journal»
    Advertisement