PMID- 30544226
OWN - NLM
STAT- MEDLINE
DCOM- 20191203
LR  - 20191203
IS  - 1945-7170 (Electronic)
IS  - 0013-7227 (Linking)
VI  - 160
IP  - 2
DP  - 2019 Feb 1
TI  - Somatostatin-Somatostatin Receptor 2 Signaling Mediates LH Pulse Suppression in 
      Lactating Rats.
PG  - 473-483
LID - 10.1210/en.2018-00882 [doi]
AB  - Follicular development and ovulation are profoundly suppressed during lactation 
      in mammals. This suppression is suggested to be mainly due to the 
      suckling-induced inhibition of kisspeptin gene (Kiss1) expression in the arcuate 
      nucleus (ARC) and consequent inhibition of pulsatile GnRH/LH release. We examined 
      whether central somatostatin (SST) signaling mediates the suckling-induced 
      suppression of pulsatile LH secretion. SST has been reported to be expressed in 
      the posterior intralaminar thalamic nucleus (PIL), where the suckling stimulus is 
      postulated to be relayed to the hypothalamus during lactation. SST inhibitory 
      receptors (SSTRs) are abundantly expressed in the ARC, where 
      kisspeptin/neurokinin B/dynorphin A (KNDy) neurons are located. Histological and 
      quantitative studies revealed that the suckling stimulus increased the number of 
      SST-expressing cells in the PIL, and Sstr2 expression in the ARC. Furthermore, a 
      central injection of an SSTR2 antagonist caused a significant increase in 
      pulsatile LH release in lactating rats. Double labeling of Sstr2 and the 
      neurokinin B gene, as a marker for ARC KNDy neurons, showed Sstr2 expression was 
      abundantly detected in the ARC, but few KNDy neurons coexpressed Sstr2 in 
      lactating rats. Taken together, these findings suggest the suckling-induced 
      activation of SST-SSTR2 signaling mediates, at least in part, the suppression of 
      pulsatile LH secretion during lactation in rats, probably via the indirect 
      effects of SST on KNDy neurons. These results provide a new aspect on the role of 
      central SST-SSTR signaling in understanding the mechanism underlying lactational 
      anestrus.
FAU - Sugimoto, Arisa
AU  - Sugimoto A
AD  - Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Aichi, 
      Japan.
FAU - Tsuchida, Hitomi
AU  - Tsuchida H
AD  - Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Aichi, 
      Japan.
FAU - Ieda, Nahoko
AU  - Ieda N
AD  - Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Aichi, 
      Japan.
FAU - Ikegami, Kana
AU  - Ikegami K
AD  - Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Aichi, 
      Japan.
FAU - Inoue, Naoko
AU  - Inoue N
AD  - Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Aichi, 
      Japan.
FAU - Uenoyama, Yoshihisa
AU  - Uenoyama Y
AD  - Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Aichi, 
      Japan.
FAU - Tsukamura, Hiroko
AU  - Tsukamura H
AD  - Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Aichi, 
      Japan.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Neuropeptides)
RN  - 0 (Receptors, Somatostatin)
RN  - 0 (Sstr2 protein, rat)
RN  - 0 (tuberoinfundibular peptide 39)
RN  - 51110-01-1 (Somatostatin)
RN  - 9002-67-9 (Luteinizing Hormone)
SB  - IM
MH  - Animals
MH  - Animals, Suckling
MH  - Arcuate Nucleus of Hypothalamus/*metabolism
MH  - Female
MH  - Intralaminar Thalamic Nuclei/metabolism
MH  - *Lactation
MH  - Luteinizing Hormone/*metabolism
MH  - Neuropeptides/metabolism
MH  - Rats
MH  - Receptors, Somatostatin/antagonists & inhibitors/*metabolism
MH  - Somatostatin/metabolism
EDAT- 2018/12/14 06:00
MHDA- 2019/12/04 06:00
CRDT- 2018/12/14 06:00
PHST- 2018/10/11 00:00 [received]
PHST- 2018/12/07 00:00 [accepted]
PHST- 2018/12/14 06:00 [pubmed]
PHST- 2019/12/04 06:00 [medline]
PHST- 2018/12/14 06:00 [entrez]
AID - 5239797 [pii]
AID - 10.1210/en.2018-00882 [doi]
PST - ppublish
SO  - Endocrinology. 2019 Feb 1;160(2):473-483. doi: 10.1210/en.2018-00882.