PMID- 22060896
OWN - NLM
STAT- MEDLINE
DCOM- 20120727
LR  - 20211021
IS  - 1365-2826 (Electronic)
IS  - 0953-8194 (Print)
IS  - 0953-8194 (Linking)
VI  - 24
IP  - 4
DP  - 2012 Apr
TI  - Enhanced expression of heme oxygenase-1 and carbon monoxide excitatory effects in 
      oxytocin and vasopressin neurones during water deprivation.
PG  - 653-63
LID - 10.1111/j.1365-2826.2011.02249.x [doi]
AB  - A growing body of evidence indiates that carbon monoxide (CO) acts as a gas 
      neurotransmitter within the central nervous system. Although CO has been shown to 
      affect neurohypophyseal hormone release in response to osmotic stimuli, the 
      precise sources, targets and mechanisms underlying the actions of CO within the 
      magnocellular neurosecretory system remain largely unknown. In the present study, 
      we combined immunohistochemistry and patch-clamp electrophysiology to study the 
      cellular distribution of the CO-synthase enzyme heme oxygenase type 1 (HO-1), as 
      well as the actions of CO on oxytocin (OT) and vasopressin (VP) magnocellular 
      neurosecretory cells (MNCs), in euhydrated (EU) and 48-h water-deprived rats 
      (48WD). Our results show the expression of HO-1 immunoreactivity both in OT and 
      VP neurones, as well as in a small proportion of astrocytes, both in supraoptic 
      (SON) and paraventricular (PVN) nuclei. HO-1 expression, and its colocalisation 
      with OT and VP neurones within the SON and PVN, was significantly enhanced in 
      48WD rats. Inhibition of HO activity with chromium mesoporphyrin IX chloride 
      (CrMP; 20 mum) resulted in a slight membrane hyperpolarisation in SON neurones 
      from EU rats, without significantly affecting their firing activity. In 48WD 
      rats, on the other hand, CrMP resulted in a more robust membrane 
      hyperpolarisation, significantly decreasing neuronal firing discharge. Taken 
      together, our results indicate that magnocellular SON and PVN neurones express 
      HO-1, and that CO acts as an excitatory gas neurotransmitter in this system. 
      Moreover, we found that the expression and actions of CO were enhanced in 
      water-deprived rats, suggesting that the state-dependent up-regulation of the 
      HO-1/CO signalling pathway contributes to enhance MNCs firing activity during an 
      osmotic challenge.
CI  - (c) 2011 The Authors. Journal of Neuroendocrinology (c) 2011 Blackwell Publishing 
      Ltd.
FAU - Reis, W L
AU  - Reis WL
AD  - Department of Physiology, Georgia Health Sciences University, Augusta, GA 30912, 
      USA.
FAU - Biancardi, V C
AU  - Biancardi VC
FAU - Son, S
AU  - Son S
FAU - Antunes-Rodrigues, J
AU  - Antunes-Rodrigues J
FAU - Stern, J E
AU  - Stern JE
LA  - eng
GR  - R01 HL090948/HL/NHLBI NIH HHS/United States
GR  - R01 HL090948-05/HL/NHLBI NIH HHS/United States
GR  - R21 HL113801/HL/NHLBI NIH HHS/United States
GR  - HL 090948-01/HL/NHLBI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neuroendocrinol
JT  - Journal of neuroendocrinology
JID - 8913461
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Mesoporphyrins)
RN  - 0 (chromium mesoporphyrin)
RN  - 11000-17-2 (Vasopressins)
RN  - 50-56-6 (Oxytocin)
RN  - 7U1EE4V452 (Carbon Monoxide)
RN  - EC 1.14.14.18 (Heme Oxygenase-1)
SB  - IM
MH  - Animals
MH  - Astrocytes/drug effects/metabolism
MH  - Carbon Monoxide/*physiology
MH  - Enzyme Inhibitors/pharmacology
MH  - Heme Oxygenase-1/antagonists & inhibitors/*biosynthesis
MH  - Male
MH  - Membrane Potentials/drug effects/*physiology
MH  - Mesoporphyrins/pharmacology
MH  - Neurons/metabolism/physiology
MH  - Oxytocin/*metabolism
MH  - Paraventricular Hypothalamic Nucleus/drug effects/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Supraoptic Nucleus/drug effects/metabolism
MH  - Up-Regulation/physiology
MH  - Vasopressins/*metabolism
MH  - Water Deprivation/*physiology
PMC - PMC3314108
MID - NIHMS336741
EDAT- 2011/11/09 06:00
MHDA- 2012/07/28 06:00
PMCR- 2013/04/01
CRDT- 2011/11/09 06:00
PHST- 2011/11/09 06:00 [entrez]
PHST- 2011/11/09 06:00 [pubmed]
PHST- 2012/07/28 06:00 [medline]
PHST- 2013/04/01 00:00 [pmc-release]
AID - 10.1111/j.1365-2826.2011.02249.x [doi]
PST - ppublish
SO  - J Neuroendocrinol. 2012 Apr;24(4):653-63. doi: 10.1111/j.1365-2826.2011.02249.x.