PMID- 17065440
OWN - NLM
STAT- MEDLINE
DCOM- 20061124
LR  - 20200225
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 26
IP  - 43
DP  - 2006 Oct 25
TI  - Genetic and physiological evidence that oligodendrocyte gap junctions contribute 
      to spatial buffering of potassium released during neuronal activity.
PG  - 10984-91
AB  - 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.
FAU - Menichella, Daniela M
AU  - Menichella DM
AD  - Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, 
      USA.
FAU - Majdan, Marta
AU  - Majdan M
FAU - Awatramani, Rajeshwar
AU  - Awatramani R
FAU - Goodenough, Daniel A
AU  - Goodenough DA
FAU - Sirkowski, Erich
AU  - Sirkowski E
FAU - Scherer, Steven S
AU  - Scherer SS
FAU - Paul, David L
AU  - Paul DL
LA  - eng
GR  - NS43560/NS/NINDS NIH HHS/United States
GR  - R01 NS043560/NS/NINDS NIH HHS/United States
GR  - NS42878/NS/NINDS NIH HHS/United States
GR  - GM37751/GM/NIGMS NIH HHS/United States
GR  - R01 GM018974/GM/NIGMS NIH HHS/United States
GR  - R01 GM037751/GM/NIGMS NIH HHS/United States
GR  - GM18974/GM/NIGMS NIH HHS/United States
GR  - R01 NS042878/NS/NINDS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Kcnj10 (channel))
RN  - 0 (Potassium Channels, Inwardly Rectifying)
RN  - RWP5GA015D (Potassium)
SB  - IM
MH  - Animals
MH  - Female
MH  - Gap Junctions/*genetics/*metabolism/pathology
MH  - Male
MH  - Mice
MH  - Mice, Knockout
MH  - Neurons/*metabolism/pathology
MH  - Oligodendroglia/*metabolism/pathology
MH  - Optic Nerve/metabolism/pathology
MH  - Potassium/*metabolism
MH  - Potassium Channels, Inwardly Rectifying/genetics/metabolism
PMC - PMC6674647
EDAT- 2006/10/27 09:00
MHDA- 2006/12/09 09:00
PMCR- 2007/04/25
CRDT- 2006/10/27 09:00
PHST- 2006/10/27 09:00 [pubmed]
PHST- 2006/12/09 09:00 [medline]
PHST- 2006/10/27 09:00 [entrez]
PHST- 2007/04/25 00:00 [pmc-release]
AID - 26/43/10984 [pii]
AID - 3156461 [pii]
AID - 10.1523/JNEUROSCI.0304-06.2006 [doi]
PST - ppublish
SO  - J Neurosci. 2006 Oct 25;26(43):10984-91. doi: 10.1523/JNEUROSCI.0304-06.2006.