PMID- 9927698
OWN - NLM
STAT- MEDLINE
DCOM- 19990305
LR  - 20190501
IS  - 0027-8424 (Print)
IS  - 1091-6490 (Electronic)
IS  - 0027-8424 (Linking)
VI  - 96
IP  - 3
DP  - 1999 Feb 2
TI  - Molecular and functional remodeling of electrogenic membrane of hypothalamic 
      neurons in response to changes in their input.
PG  - 1088-93
AB  - Neurons respond to stimuli by integrating generator and synaptic potentials and 
      generating action potentials. However, whether the underlying electrogenic 
      machinery within neurons itself changes, in response to alterations in input, is 
      not known. To determine whether there are changes in Na+ channel expression and 
      function within neurons in response to altered input, we exposed magnocellular 
      neurosecretory cells (MNCs) in the rat supraoptic nucleus to different osmotic 
      milieus by salt-loading and studied Na+ channel mRNA and protein, and Na+ 
      currents, in these cells. In situ hybridization demonstrated significantly 
      increased mRNA levels for alpha-II, Na6, beta1 and beta2 Na+ channel subunits, 
      and immunohistochemistry/immunoblotting showed increased Na+ channel protein 
      after salt-loading. Using patch-clamp recordings to examine the deployment of 
      functional Na+ channels in the membranes of MNCs, we observed an increase in the 
      amplitude of the transient Na+ current after salt-loading and an even greater 
      increase in amplitude and density of the persistent Na+ current evoked at 
      subthreshold potentials by slow ramp depolarizations. These results demonstrate 
      that MNCs respond to salt-loading by selectively synthesizing additional, 
      functional Na+ channel subtypes whose deployment in the membrane changes its 
      electrogenic properties. Thus, neurons may respond to changes in their input not 
      only by producing different patterns of electrical activity, but also by 
      remodeling the electrogenic machinery that underlies this activity.
FAU - Tanaka, M
AU  - Tanaka M
AD  - Department of Neurology, Yale University School of Medicine, New Haven, CT 06510, 
      USA.
FAU - Cummins, T R
AU  - Cummins TR
FAU - Ishikawa, K
AU  - Ishikawa K
FAU - Black, J A
AU  - Black JA
FAU - Ibata, Y
AU  - Ibata Y
FAU - Waxman, S G
AU  - Waxman SG
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - Proc Natl Acad Sci U S A
JT  - Proceedings of the National Academy of Sciences of the United States of America
JID - 7505876
RN  - 0 (Macromolecular Substances)
RN  - 0 (RNA, Messenger)
RN  - 0 (Sodium Channels)
RN  - 9NEZ333N27 (Sodium)
SB  - IM
MH  - Animals
MH  - Cell Membrane/physiology
MH  - Hypothalamus/*physiology
MH  - In Situ Hybridization
MH  - Macromolecular Substances
MH  - Male
MH  - Membrane Potentials/physiology
MH  - Neurons/*physiology
MH  - Patch-Clamp Techniques
MH  - Pituitary Gland, Posterior/*physiology
MH  - RNA, Messenger/analysis/genetics
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sodium/metabolism
MH  - Sodium Channels/genetics/*physiology
MH  - Supraoptic Nucleus/*physiology
MH  - Transcription, Genetic
PMC - PMC15355
EDAT- 1999/02/03 00:00
MHDA- 1999/02/03 00:01
PMCR- 1999/08/02
CRDT- 1999/02/03 00:00
PHST- 1999/02/03 00:00 [pubmed]
PHST- 1999/02/03 00:01 [medline]
PHST- 1999/02/03 00:00 [entrez]
PHST- 1999/08/02 00:00 [pmc-release]
AID - 4684 [pii]
AID - 10.1073/pnas.96.3.1088 [doi]
PST - ppublish
SO  - Proc Natl Acad Sci U S A. 1999 Feb 2;96(3):1088-93. doi: 10.1073/pnas.96.3.1088.