PMID- 8793890
OWN - NLM
STAT- MEDLINE
DCOM- 19961203
LR  - 20180214
IS  - 0028-3835 (Print)
IS  - 0028-3835 (Linking)
VI  - 63
IP  - 6
DP  - 1996 Jun
TI  - mu-Opioid agonists stimulate growth hormone secretion in immature rats.
PG  - 489-97
AB  - The purpose of the present study was to evaluate the opioid receptor subtype 
      mediating opioid modulation of growth hormone (GH) secretion during ontogeny. The 
      mu-agonist morphine and the kappa agonist U50,488 caused a stimulation and 
      inhibition of GH secretion, respectively, on postnatal day 10. Studies on 
      postnatal days 2, 5, 10, 15 and 20 showed that kappa-inhibition could be observed 
      as early as day 2, but substantial mu-stimulation was not observed until 
      postnatal day 10. Intracerebroventricular (i.c.v.) administration of the 
      mu-selective peptide [D-Ala2-NMe-Phe4-Gly-ol]-enkephalin (DAMGO) elicited a 
      marked rise in GH secretion, while administration of the delta-agonists 
      [D-pen2D-pen5]-enkephalin (DPDPE) or deltorphin II caused only a minor and 
      non-dose-related rise in GH secretion in neonatal rats. The relative importance 
      of mu- and delta-receptors in stimulating GH secretion was also studied in older 
      pups (day 20). i.c.v. administration of DAMGO stimulated GH secretion, while 
      neither DPDPE nor deltorphin II consistently increased GH secretion. Furthermore, 
      peripheral administration of either morphine or the highly selective mu-agonist 
      sufentanil elicited marked GH secretion on postnatal day 20, but only combined 
      administration of the mu-antagonist beta-funaltrexamine (beta-FNA) and the 
      delta-antagonist naltrindole substantially diminished these responses. These 
      results suggest that both mu- and kappa-opioid receptors are involved in the 
      regulation of GH secretion in neonatal rats. While delta-receptors do not play a 
      prominent independent role in this response, they may act synergistically with 
      mu-receptors in producing stimulation.
FAU - Eason, M G
AU  - Eason MG
AD  - Department of Pharmacology, Duke University Medical Center, Durham, N.C. 27710 
      USA.
FAU - Francis, R S
AU  - Francis RS
FAU - Kuhn, C M
AU  - Kuhn CM
LA  - eng
PT  - Journal Article
PL  - Switzerland
TA  - Neuroendocrinology
JT  - Neuroendocrinology
JID - 0035665
RN  - 0 (Analgesics)
RN  - 0 (Enkephalins)
RN  - 0 (Pyrrolidines)
RN  - 0 (Receptors, Opioid, mu)
RN  - 100929-53-1 (Enkephalin, Ala(2)-MePhe(4)-Gly(5)-)
RN  - 67198-13-4 
      (3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, 
      (trans)-Isomer)
RN  - 76I7G6D29C (Morphine)
RN  - 9002-72-6 (Growth Hormone)
SB  - IM
MH  - 3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, 
      (trans)-Isomer
MH  - Age Factors
MH  - Analgesics/*pharmacology
MH  - Animals
MH  - Dose-Response Relationship, Drug
MH  - Enkephalin, Ala(2)-MePhe(4)-Gly(5)-
MH  - Enkephalins/pharmacology
MH  - Female
MH  - Growth Hormone/*drug effects
MH  - Male
MH  - Morphine/pharmacology
MH  - Pyrrolidines/*pharmacology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Opioid, mu/*agonists
MH  - Time Factors
EDAT- 1996/06/01 00:00
MHDA- 1996/06/01 00:01
CRDT- 1996/06/01 00:00
PHST- 1996/06/01 00:00 [pubmed]
PHST- 1996/06/01 00:01 [medline]
PHST- 1996/06/01 00:00 [entrez]
AID - 10.1159/000127077 [doi]
PST - ppublish
SO  - Neuroendocrinology. 1996 Jun;63(6):489-97. doi: 10.1159/000127077.