PMID- 30943041
OWN - NLM
STAT- MEDLINE
DCOM- 20200219
LR  - 20200930
IS  - 1522-1490 (Electronic)
IS  - 0363-6119 (Linking)
VI  - 316
IP  - 6
DP  - 2019 Jun 1
TI  - Endogenous amylin contributes to birth of microglial cells in arcuate nucleus of 
      hypothalamus and area postrema during fetal development.
PG  - R791-R801
LID - 10.1152/ajpregu.00004.2019 [doi]
AB  - Amylin acts in the area postrema (AP) and arcuate nucleus (ARC) to control food 
      intake. Amylin also increases axonal fiber outgrowth from the AP-->nucleus tractus 
      solitarius and from ARC-->hypothalamic paraventricular nucleus. More recently, 
      exogenous amylin infusion for 4 wk was shown to increase neurogenesis in adult 
      rats in the AP. Furthermore, amylin has been shown to enhance leptin signaling in 
      the ARC and ventromedial nucleus of the hypothalamus (VMN). Thus, we hypothesized 
      that endogenous amylin could be a critical factor in regulating cell birth in the 
      ARC and AP and that amylin could also be involved in the birth of 
      leptin-sensitive neurons. Amylin(+/-) dams were injected with BrdU at embryonic 
      day 12 and at postnatalday 2; BrdU+ cells were quantified in wild-type (WT) and 
      amylin knockout (KO) mice. The number of BrdU+HuC/D+ neurons was similar in ARC 
      and AP, but the number of BrdU+Iba1+ microglia was significantly decreased in 
      both nuclei. Five-week-old WT and KO littermates were injected with leptin to 
      test whether amylin is involved in the birth of leptin-sensitive neurons. 
      Although there was no difference in the number of BrdU+c-Fos+ neurons in the ARC 
      and dorsomedial nucleus, an increase in BrdU+c-Fos+ neurons was seen in VMN and 
      lateral hypothalamus (LH) in amylin KO mice. In conclusion, these data suggest 
      that during fetal development, endogenous amylin favors the birth of microglial 
      cells in the ARC and AP and that it decreases the birth of leptin-sensitive 
      neurons in the VMN and LH.
FAU - Lutz, Thomas A
AU  - Lutz TA
AUID- ORCID: 0000-0002-5056-8548
AD  - Institute of Veterinary Physiology, Vetsuisse Faculty, University of Zurich , 
      Zurich , Switzerland.
FAU - Le Foll, Christelle
AU  - Le Foll C
AUID- ORCID: 0000-0002-6677-5488
AD  - Institute of Veterinary Physiology, Vetsuisse Faculty, University of Zurich , 
      Zurich , Switzerland.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190403
PL  - United States
TA  - Am J Physiol Regul Integr Comp Physiol
JT  - American journal of physiology. Regulatory, integrative and comparative 
      physiology
JID - 100901230
RN  - 0 (Islet Amyloid Polypeptide)
RN  - 0 (Leptin)
RN  - 0 (Proto-Oncogene Proteins c-fos)
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Arcuate Nucleus of Hypothalamus/embryology/*metabolism
MH  - Area Postrema/embryology/*metabolism
MH  - *Cell Lineage
MH  - Female
MH  - Gene Expression Regulation, Developmental
MH  - Gestational Age
MH  - Hypothalamic Area, Lateral/embryology/metabolism
MH  - Islet Amyloid Polypeptide/genetics/*metabolism
MH  - Leptin/metabolism
MH  - Male
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Microglia/*metabolism
MH  - Neurons/metabolism
MH  - Phenotype
MH  - Pregnancy
MH  - Proto-Oncogene Proteins c-fos/metabolism
MH  - Ventromedial Hypothalamic Nucleus/embryology/metabolism
OTO - NOTNLM
OT  - amylin
OT  - fetal development
OT  - hindbrain
OT  - hypothalamus
OT  - microglia
EDAT- 2019/04/04 06:00
MHDA- 2020/02/20 06:00
CRDT- 2019/04/04 06:00
PHST- 2019/04/04 06:00 [pubmed]
PHST- 2020/02/20 06:00 [medline]
PHST- 2019/04/04 06:00 [entrez]
AID - 10.1152/ajpregu.00004.2019 [doi]
PST - ppublish
SO  - Am J Physiol Regul Integr Comp Physiol. 2019 Jun 1;316(6):R791-R801. doi: 
      10.1152/ajpregu.00004.2019. Epub 2019 Apr 3.