PMID- 11573973
OWN - NLM
STAT- MEDLINE
DCOM- 20011205
LR  - 20061115
IS  - 0014-4886 (Print)
IS  - 0014-4886 (Linking)
VI  - 171
IP  - 2
DP  - 2001 Oct
TI  - Peptidergic excitation of supraoptic nucleus neurons: involvement of 
      stretch-inactivated cation channels.
PG  - 210-8
AB  - Although the primary stimulus regulating vasopressin (VP) release is a change in 
      systemic osmolality, other physiological parameters are known to affect VP 
      secretion or modulate the osmotic control over its release. Neuropeptides feature 
      prominently in afferents underlying the central regulation of the VP-releasing 
      magnocellular neurosecretory cells (MNCs). Although little is yet known of the 
      circumstances under which peptides are released onto MNCs, previous studies have 
      shown that a common response profile to exogenous peptide application is a slow 
      excitation that seems to result from the activation of a nonselective cation 
      conductance. In this paper we review the basis for the excitatory effects of 
      angiotensin II, cholecystokinin, and neurotensin in MNCs acutely isolated from 
      the supraoptic nucleus of adult rats. Saturating concentrations of these three 
      peptides evoked nonadditive increases in macroscopic cation conductance. During 
      single-channel recordings Ang II, CCK, and NT caused kinetically identical 
      increases in the probability of opening of 35-pS nonselective cation channels. 
      Patches containing only one channel further revealed that the activity of single 
      channels could be regulated by separate applications of all three peptides. 
      Peptide-stimulated channels were also found to be inactivated by increases in 
      membrane stretch and to be blocked by low concentrations of gadolinium (Gd(3+)). 
      It is concluded that many excitatory peptides depolarize MNCs by stimulating the 
      stretch-inactivated cation channels underlying osmoreception. Convergent 
      regulation of these channels provides a potentially powerful mechanism for 
      integrating signals derived from the various afferents involved in the regulation 
      of MNCs.
CI  - Copyright 2001 Academic Press.
FAU - Chakfe, Y
AU  - Chakfe Y
AD  - Centre for Research in Neuroscience, Montreal General Hospital and McGill 
      University, 1650 Cedar Avenue, Montreal, QC, H3G 1A4, Canada.
FAU - Bourque, C W
AU  - Bourque CW
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Exp Neurol
JT  - Experimental neurology
JID - 0370712
RN  - 0 (Ion Channels)
RN  - 0 (Neuropeptides)
RN  - 11000-17-2 (Vasopressins)
RN  - 11128-99-7 (Angiotensin II)
RN  - 39379-15-2 (Neurotensin)
RN  - 9011-97-6 (Cholecystokinin)
SB  - IM
MH  - Angiotensin II/pharmacology
MH  - Animals
MH  - Cholecystokinin/pharmacology
MH  - Ion Channels/antagonists & inhibitors/*physiology
MH  - Neurons/drug effects/*physiology
MH  - Neuropeptides/*physiology
MH  - Neurotensin/pharmacology
MH  - Supraoptic Nucleus/drug effects/*physiology
MH  - Vasopressins/physiology
RF  - 57
EDAT- 2001/09/28 10:00
MHDA- 2002/01/05 10:01
CRDT- 2001/09/28 10:00
PHST- 2001/09/28 10:00 [pubmed]
PHST- 2002/01/05 10:01 [medline]
PHST- 2001/09/28 10:00 [entrez]
AID - S0014-4886(01)97780-5 [pii]
AID - 10.1006/exnr.2001.7780 [doi]
PST - ppublish
SO  - Exp Neurol. 2001 Oct;171(2):210-8. doi: 10.1006/exnr.2001.7780.