PMID- 2903913
OWN - NLM
STAT- MEDLINE
DCOM- 19890103
LR  - 20191101
IS  - 0270-6474 (Print)
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Linking)
VI  - 8
IP  - 10
DP  - 1988 Oct
TI  - Regulation of hypothalamic magnocellular neuropeptides and their mRNAs in the 
      Brattleboro rat: coordinate responses to further osmotic challenge.
PG  - 3785-96
AB  - A paradigm was developed for the chronic osmotic stimulation of homozygous 
      diabetes insipidus rats of the Brattleboro strain, a strain that fails to 
      synthesize vasopressin. This study examines the adaptation of 2 sets of 
      coexisting peptide hormone magnocellular neurons in the 
      hypothalamoneurohypophyseal system (HNS) of Long Evans (LE), Brattleboro 
      heterozygote (HZ), and Brattleboro homozygote (DI) rats: (1) the 
      arginine8-vasopressin (AVP)/dynorphin (DYN) neurons, and (2) the oxytocin 
      (OT)/cholecystokinin (CCK8) neurons of the paraventricular and supraoptic nuclei, 
      which project to the posterior pituitary. The regimen of chronic intermittent 
      salt-loading (CISL) involved the replacement of 2% saline for normal drinking 
      water for 18 hr/d. This protocol effectively increased plasma levels of AVP and 
      OT in LE and HZ rats, oxytocin in DI rats, and maintained the posterior pituitary 
      in a state depleted of AVP, OT, CCK, and peptides derived from pro-dynorphin: DYN 
      A 1-17, DYN A 1-8, and DYN B 1-13. The ratio of pituitary DYN A 1-17 to DYN A 1-8 
      content in DI rats or in LE, HZ, and DI rats following 6 d of CISL suggests a 
      preferential release of DYN A 1-17 during periods of chronic secretory activity. 
      In response to chronic secretory activity, mRNAs for AVP, OT, DYN, and CCK 
      increased 1.5-2-fold in all 3 AVP rat strains, with mRNAs for coexisting peptide 
      hormones displaying parallel increases. Mutant AVP mRNA in the DI rat was 
      expressed at very low levels and DYN mRNA in very high levels, with each of these 
      mRNAs continuing to be regulated by CISL in a normal manner. These results 
      suggest a regulatory relationship between AVP and OT neurons, in which 
      vasopressin neurons are feedback-regulated by AVP, most likely via plasma 
      osmolarity, and that oxytocin neurons are modulated by peptides derived from 
      pro-dynorphin.
FAU - Sherman, T G
AU  - Sherman TG
AD  - Mental Health Research Institute, University of Michigan, Ann Arbor 48109.
FAU - Day, R
AU  - Day R
FAU - Civelli, O
AU  - Civelli O
FAU - Douglass, J
AU  - Douglass J
FAU - Herbert, E
AU  - Herbert E
FAU - Akil, H
AU  - Akil H
FAU - Watson, S J
AU  - Watson SJ
LA  - eng
GR  - AM 16166/AM/NIADDK NIH HHS/United States
GR  - F32MH09239/MH/NIMH NIH HHS/United States
GR  - P0I 422251/PHS 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 Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Neuropeptides)
RN  - 0 (RNA, Messenger)
RN  - 113-79-1 (Arginine Vasopressin)
RN  - 50-56-6 (Oxytocin)
RN  - 74913-18-1 (Dynorphins)
RN  - M03GIQ7Z6P (Sincalide)
SB  - IM
MH  - Animals
MH  - Arginine Vasopressin/metabolism
MH  - Diabetes Insipidus/genetics/metabolism
MH  - Dynorphins/metabolism
MH  - *Gene Expression Regulation
MH  - Hypothalamo-Hypophyseal System/*metabolism
MH  - Neuropeptides/*genetics/metabolism
MH  - Osmolar Concentration
MH  - Oxytocin/metabolism
MH  - Pituitary Gland, Posterior/metabolism
MH  - RNA, Messenger/*metabolism
MH  - Rats
MH  - Rats, Brattleboro/*metabolism
MH  - Rats, Mutant Strains/*metabolism
MH  - Sincalide/metabolism
PMC - PMC6569603
EDAT- 1988/10/01 00:00
MHDA- 1988/10/01 00:01
PMCR- 1989/04/01
CRDT- 1988/10/01 00:00
PHST- 1988/10/01 00:00 [pubmed]
PHST- 1988/10/01 00:01 [medline]
PHST- 1988/10/01 00:00 [entrez]
PHST- 1989/04/01 00:00 [pmc-release]
AID - 10.1523/JNEUROSCI.08-10-03785.1988 [doi]
PST - ppublish
SO  - J Neurosci. 1988 Oct;8(10):3785-96. doi: 10.1523/JNEUROSCI.08-10-03785.1988.