Journal
JOURNAL OF NEUROSCIENCE
Volume 26, Issue 43, Pages 10984-10991Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0304-06.2006
Keywords
demyelination; oligodendrocyte; gap junction; connexin; potassium channel; astrocyte
Categories
Funding
- NIGMS NIH HHS [GM18974, GM37751, R01 GM018974, R01 GM037751] Funding Source: Medline
- NINDS NIH HHS [NS42878, R01 NS043560, NS43560, R01 NS042878] Funding Source: Medline
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Mice lacking the K+ channel Kir4.1 or both connexin32 (Cx32) and Cx47 exhibit myelin-associated vacuoles, raising the possibility that oligodendrocytes, and the connexins they express, contribute to recycling the K+ evolved during neuronal activity. To study this possibility, we first examined the effect of neuronal activity on the appearance of vacuoles in mice lacking both Cx32 and Cx47. The size and number of myelin vacuoles was dramatically increased when axonal activity was increased, by either a natural stimulus ( eye opening) or pharmacological treatment. Conversely, myelin vacuoles were dramatically reduced when axonal activity was suppressed. Second, we used genetic complementation to test for a relationship between the function of Kir4.1 and oligodendrocyte connexins. In a Cx32-null background, haploinsufficiency of either Cx47 or Kir4.1 did not affect myelin, but double heterozygotes developed vacuoles, consistent with the idea that oligodendrocyte connexins and Kir4.1 function in a common pathway. Together, these results implicate oligodendrocytes and their connexins as having critical roles in the buffering of K+ released during neuronal activity.
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