PMID- 19732292
OWN - NLM
STAT- MEDLINE
DCOM- 20100121
LR  - 20141120
IS  - 1365-2826 (Electronic)
IS  - 0953-8194 (Linking)
VI  - 21
IP  - 11
DP  - 2009 Nov
TI  - Ghrelin potentiates miniature excitatory postsynaptic currents in supraoptic 
      magnocellular neurones.
PG  - 910-20
LID - 10.1111/j.1365-2826.2009.01911.x [doi]
AB  - Ghrelin is an orexigenic peptide discovered in the stomach as a ligand of the 
      orphan G-protein coupled receptor, and participates in the regulation of growth 
      hormone (GH) release. Previous studies have demonstrated that ghrelin suppressed 
      water intake and stimulated the secretion of arginine vasopressin in rats. We 
      examined the effect of ghrelin on the excitatory synaptic inputs to the 
      magnocellular neurosecretory cells (MNCs) in the supraoptic nucleus (SON) using 
      whole-cell patch-clamp recordings in in vitro rat and mouse brain slice 
      preparations. The application of ghrelin (10(-7) approximately 10(-6) m) caused a 
      significant increase in the frequency of the miniature excitatory postsynaptic 
      currents (mEPSCs) in a dose-related manner without affecting the amplitude. The 
      increased frequency of the spontaneous EPSCs persisted in the presence of 
      tetrodotoxin (1 microM). Des-n-octanoyl ghrelin (10(-6) m) did not have a 
      significant effect on the mEPSCs. The ghrelin-induced potentiation of the mEPSCs 
      was significantly suppressed by previous exposure to the transient receptor 
      potential vanilloid (TRPV) blocker, ruthenium red (10 microM) and GH 
      secretagougue type 1a receptor selective antagonist, BIM28163 (10 microM). The 
      effects of ghrelin on the supraoptic MNCs in trpv1 knockout mice were 
      significantly attenuated compared to those in wild-type mice counterparts. These 
      results suggest that ghrelin participates in the regulation of synaptic inputs to 
      the MNCs in the SON via interaction with the GH secretagogue type 1a receptor, 
      and that the TRPV1 channel may be involved in ghrelin-induced potentiation of 
      mEPSCs to the MNCs in the SON.
FAU - Yokoyama, T
AU  - Yokoyama T
AD  - Department of Physiology, School of Medicine, University of Occupational and 
      Environmental Health, Kitakyushu, Japan.
FAU - Saito, T
AU  - Saito T
FAU - Ohbuchi, T
AU  - Ohbuchi T
FAU - Suzuki, H
AU  - Suzuki H
FAU - Otsubo, H
AU  - Otsubo H
FAU - Okamoto, T
AU  - Okamoto T
FAU - Fujihara, H
AU  - Fujihara H
FAU - Nagatomo, T
AU  - Nagatomo T
FAU - Ueta, Y
AU  - Ueta Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090901
PL  - United States
TA  - J Neuroendocrinol
JT  - Journal of neuroendocrinology
JID - 8913461
RN  - 0 (Ghrelin)
SB  - IM
MH  - Animals
MH  - Dose-Response Relationship, Drug
MH  - Excitatory Postsynaptic Potentials/*drug effects
MH  - Ghrelin/*pharmacology
MH  - In Vitro Techniques
MH  - Mice
MH  - Neurons/*drug effects
MH  - Rats
MH  - Supraoptic Nucleus/cytology/*drug effects
EDAT- 2009/09/08 06:00
MHDA- 2010/01/22 06:00
CRDT- 2009/09/08 06:00
PHST- 2009/09/08 06:00 [entrez]
PHST- 2009/09/08 06:00 [pubmed]
PHST- 2010/01/22 06:00 [medline]
AID - JNE1911 [pii]
AID - 10.1111/j.1365-2826.2009.01911.x [doi]
PST - ppublish
SO  - J Neuroendocrinol. 2009 Nov;21(11):910-20. doi: 10.1111/j.1365-2826.2009.01911.x. 
      Epub 2009 Sep 1.