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 4.
Figure 4.

Increase in Cx36 expression after photothrombotic focal cerebral ischemia is regulated by group II mGluRs. Data from Western blot experiments in the primary somatosensory cortex of adult wild-type mice are presented. A–C, Statistical data and representative blots (a1–c2) are shown. In A, “C” indicates contralateral cortex (left hemisphere), and “I” indicates ipsilateral cortex (right hemisphere), which also is ischemic. In B and C, all data are from the ipsilateral cortex: nonischemic (B) and ischemic (C). In all experiments, optical density signals are normalized relative to tubulin and compared with the control: contralateral cortex (A), saline ipsilateral (B), and saline contralateral (C; not shown); set at 1.0. Statistical analysis was as follows: Student's t test; shown relative to the contralateral cortex (A) and saline ipsilateral (B, C); n = 6–10 per group; data are shown as mean ± SEM. Injections were as follows: saline (100 μl), LY379268 (10 mg/kg; in 100 μl of saline), LY341495 (5 mg/kg; in 100 μl of saline); in B, each injection was single; in C, two injections were done (immediately before and immediately after the induction of ischemia).

  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