PMID- 11058221
OWN - NLM
STAT- MEDLINE
DCOM- 20001222
LR  - 20190906
IS  - 0021-9967 (Print)
IS  - 0021-9967 (Linking)
VI  - 428
IP  - 1
DP  - 2000 Dec 4
TI  - Distribution of the EP3 prostaglandin E(2) receptor subtype in the rat brain: 
      relationship to sites of interleukin-1-induced cellular responsiveness.
PG  - 5-20
AB  - The activation of neurosecretory neurons that express corticotropin-releasing 
      hormone (CRH) in response to increased circulating levels of interleukin-1beta 
      (IL-1beta) depends on prostaglandin E(2) (PGE(2)) acting locally within the brain 
      parenchyma. To identify potential central targets for PGE(2) relevant to 
      pituitary-adrenal control, the distribution of mRNA encoding the PGE(2) receptor 
      subtype EP3 (EP3R) was analyzed in rat brain. Hybridization histochemistry 
      revealed prominent labeling of cells in discrete portions of the olfactory 
      system, iso- and hippocampal cortices, and subcortical telencephalic structures 
      in the septal region and amygdala. Labeling over the midline, intralaminar, and 
      anterior thalamic groups was particularly prominent. EP3R expression was enriched 
      in the median preoptic nucleus and adjoining aspects of the medial preoptic area 
      (MPO) implicated in thermoregulatory/febrile responses and sleep induction. 
      EP3R-expressing cells were also prominent in brainstem cell groups involved in 
      nociceptive information processing/modulation (periaqueductal gray, locus 
      coeruleus (LC), parabrachial nucleus (PB), caudal raphe nuclei), arousal and 
      wakefulness (LC, midbrain raphe and tuberomammillary nuclei); and in conveying 
      interoceptive input, including systemic IL-1 signals, to the endocrine 
      hypothalamus (nucleus of the solitary tract (NTS) and rostral ventrolateral 
      medulla [VLM]). Combined hybridization histochemical detection of EP3R mRNA with 
      immunolocalization of IL-1beta-induced Fos protein expression identified 
      cytokine-sensitive, EP3R-positive cells in the medial NTS, rostral VLM, and, to a 
      lesser extent, aspects of the MPO. These findings are consistent with the view 
      that increased circulating IL-1 may stimulate central neural mechanisms, 
      including hypothalamic CRH neurons, through an EP3R-dependent mechanism involving 
      PGE(2)-mediated activation of cells in the caudal medulla and/or preoptic region.
CI  - Copyright 2000 Wiley-Liss, Inc.
FAU - Ek, M
AU  - Ek M
AD  - Department of Medicine, Unit of Rheumatology, The Karolinska Institute, S-171 76, 
      Stockholm, Sweden. Monica.Ek@cmm.ki.se
FAU - Arias, C
AU  - Arias C
FAU - Sawchenko, P
AU  - Sawchenko P
FAU - Ericsson-Dahlstrand, A
AU  - Ericsson-Dahlstrand A
LA  - eng
GR  - NS21182/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Comp Neurol
JT  - The Journal of comparative neurology
JID - 0406041
RN  - 0 (Interleukin-1)
RN  - 0 (Ptger3 protein, rat)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Prostaglandin E)
RN  - 0 (Receptors, Prostaglandin E, EP3 Subtype)
RN  - K7Q1JQR04M (Dinoprostone)
SB  - IM
MH  - Animals
MH  - Brain/cytology/*metabolism
MH  - Dinoprostone/*metabolism
MH  - Interleukin-1/*metabolism/pharmacology
MH  - Male
MH  - Neurons/cytology/*metabolism
MH  - Pituitary Gland/cytology/metabolism
MH  - Pituitary-Adrenal System/cytology/*metabolism
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Prostaglandin E/drug effects/*genetics
MH  - Receptors, Prostaglandin E, EP3 Subtype
EDAT- 2000/11/01 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/11/01 11:00
PHST- 2000/11/01 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/11/01 11:00 [entrez]
AID - 10.1002/1096-9861(20001204)428:1<5::AID-CNE2>3.0.CO;2-M [pii]
AID - 10.1002/1096-9861(20001204)428:1<5::aid-cne2>3.0.co;2-m [doi]
PST - ppublish
SO  - J Comp Neurol. 2000 Dec 4;428(1):5-20. doi: 
      10.1002/1096-9861(20001204)428:1<5::aid-cne2>3.0.co;2-m.