PMID- 25712904
OWN - NLM
STAT- MEDLINE
DCOM- 20160301
LR  - 20150527
IS  - 1365-2826 (Electronic)
IS  - 0953-8194 (Linking)
VI  - 27
IP  - 6
DP  - 2015 Jun
TI  - Mechanical basis of osmosensory transduction in magnocellular neurosecretory 
      neurones of the rat supraoptic nucleus.
PG  - 507-15
LID - 10.1111/jne.12270 [doi]
AB  - Rat magnocellular neurosecretory cells (MNCs) release vasopressin and oxytocin to 
      promote antidiuresis and natriuresis at the kidney. The osmotic control of 
      oxytocin and vasopressin release at the neurohypophysis is required for 
      osmoregulation in these animals, and this release is mediated by a modulation of 
      the action potential firing rate by the MNCs. Under basal (isotonic) conditions, 
      MNCs fire action potentials at a slow rate, and this activity is inhibited by 
      hypo-osmotic conditions and enhanced by hypertonicity. The effects of changes in 
      osmolality on MNCs are mediated by a number of different factors, including the 
      involvement of synaptic inputs, the release of taurine by local glial cells and 
      regulation of ion channels expressed within the neurosecretory neurones 
      themselves. We review recent findings that have clarified our understanding of 
      how osmotic stimuli modulate the activity of nonselective cation channels in 
      MNCs. Previous studies have shown that osmotically-evoked changes in membrane 
      potential and action potential firing rate in acutely isolated MNCs are provoked 
      mainly by a modulation of nonselective cation channels. Notably, the excitation 
      of isolated MNCs during hypertonicity is mediated by the activation of a 
      capsaicin-insensitive cation channel that MNCs express as an N-terminal variant 
      of the transient receptor potential vanilloid 1 (Trpv1) channel. The activation 
      of this channel during hypertonicity is a mechanical process associated with cell 
      shrinking. The effectiveness of this mechanical process depends on the presence 
      of a thin layer of actin filaments (F-actin) beneath the plasma membrane, as well 
      as a densely interweaved network of microtubules (MTs) occupying the bulk of the 
      cytoplasm of MNCs. Although the mechanism by which F-actin contributes to Trpv1 
      activation remains unknown, recent data have shown that MTs interact with Trpv1 
      channels via binding sites on the C-terminus, and that the force mediated through 
      this complex is required for channel gating during osmosensory transduction. 
      Indeed, displacement of this interaction prevents channel activation during 
      shrinking, whereas increasing the density of these interaction sites potentiates 
      shrinking-induced activation of Trpv1. Therefore, the gain of the osmosensory 
      transduction process can be regulated bi-directionally through changes in the 
      organisation of F-actin and MTs.
CI  - (c) 2015 British Society for Neuroendocrinology.
FAU - Prager-Khoutorsky, M
AU  - Prager-Khoutorsky M
AD  - Centre for Research in Neuroscience, Research Institute of the McGill University 
      Health Centre, Montreal General Hospital, Montreal, Quebec, Canada.
FAU - Bourque, C W
AU  - Bourque CW
AD  - Centre for Research in Neuroscience, Research Institute of the McGill University 
      Health Centre, Montreal General Hospital, Montreal, Quebec, Canada.
LA  - eng
GR  - FRN82818/Canadian Institutes of Health Research/Canada
GR  - MOP9939/Canadian Institutes of Health Research/Canada
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - J Neuroendocrinol
JT  - Journal of neuroendocrinology
JID - 8913461
RN  - 11000-17-2 (Vasopressins)
SB  - IM
MH  - Animals
MH  - Neurons/cytology/*metabolism
MH  - Osmosis
MH  - Rats
MH  - *Signal Transduction
MH  - Supraoptic Nucleus/cytology/*metabolism
MH  - Vasopressins/*metabolism
OTO - NOTNLM
OT  - microtubule
OT  - osmoregulation
OT  - supraoptic nucleus
OT  - transient receptor potential vanilloid type-1 (Trpv1)
OT  - vasopressin
EDAT- 2015/02/26 06:00
MHDA- 2016/03/02 06:00
CRDT- 2015/02/26 06:00
PHST- 2014/12/09 00:00 [received]
PHST- 2015/02/19 00:00 [revised]
PHST- 2015/02/22 00:00 [accepted]
PHST- 2015/02/26 06:00 [entrez]
PHST- 2015/02/26 06:00 [pubmed]
PHST- 2016/03/02 06:00 [medline]
AID - 10.1111/jne.12270 [doi]
PST - ppublish
SO  - J Neuroendocrinol. 2015 Jun;27(6):507-15. doi: 10.1111/jne.12270.