Modulation by endogenous opioid peptides of the secretion of LHRH from cockerel (Gallus domesticus) mediobasal hypothalamic tissue

1987 ◽  
Vol 114 (1) ◽  
pp. 103-110 ◽  
Author(s):  
S. C. Stansfield ◽  
F. J. Cunningham
Keyword(s):  
Opioid Peptides ◽  
Inhibitory Influence ◽  
Mediobasal Hypothalamus ◽  
Endogenous Opioid Peptides ◽  
Endogenous Opioid ◽  
Superfusion System ◽  
In Vitro Superfusion ◽  
Basal Release ◽  
Hypothalamic Tissue

ABSTRACT An in-vitro superfusion system was used to study the effects of the endogenous opioid peptides [Met]-enkephalin (and its long-lasting analogue [d-Ala2, Met]-enkephalinamide), [Leu]-enkephalin and β-endorphin and of the opiate antagonist naloxone, on the secretion of LHRH from the mediobasal hypothalamus of the cockerel. The effects of the compounds on both basal release of LHRH and on release stimulated by a depolarizing pulse of increased extra-cellular potassium ion (64 mmol/l) were investigated. None of the endogenous opioid peptides altered basal release of LHRH; however, both [Met]-enkephalin (10 μmol/l) and [d-Ala2,Met]-enkephalinamide (1 μmol/l) significantly (P<0·05) reduced the response to depolarization. Neither [Leu]-enkephalin nor β-endorphin (0·1–10 μmol/l) were effective. Naloxone (1 μmol/l) administered alone significantly (P<0·05) increased basal release of LHRH and abolished the inhibitory effects of [Met]-enkephalin and [d-Ala2,Met]-enkephalinamide on depolarization-induced release. These results suggest that the endogenous opioid peptides exert a tonic inhibitory influence on LHRH secretion by the mediobasal hypothalamus of the cockerel. J. Endocr. (1987) 114, 103–110

Involvement of opiate receptor subtypes in the modulation of LHRH secretion by the cockerel (Gallus domesticus) mediobasal hypothalamus in vitro

1987 ◽  
Vol 114 (1) ◽  
pp. 111-117 ◽  
Author(s):  
S. C. Stansfield ◽  
F. J. Cunningham
Keyword(s):  
Opiate Receptor ◽  
Ion Concentration ◽  
Receptor Subtypes ◽  
Mediobasal Hypothalamus ◽  
Superfusion System ◽  
In Vitro Superfusion ◽  
Basal Release ◽  
Specific Antagonist ◽  
Μ Receptor

ABSTRACT Using an in-vitro superfusion system, the relative importance of three distinct subtypes of the opiate receptor in the control of the secretion of LHRH from the mediobasal hypothalamus of the cockerel was investigated. Basal release of LHRH was increased by the antagonist naloxone, which shows some μ-receptor selectivity, in a manner which was reversed by the μ-receptor specific agonist [d-Ala2, N-Phe4-Gly-ol5]-enkephalin (DAGO) and the μ- and δ-specific agonist [d-Ala2,N-Phe4,Met(0)ol5]-enkephalin (FK 33–824). The †-specific agonist [d-Thr2,l-Leu5]-enkephalyl-Thr (DTLET) and the κ-specific agonist 1-methyl-2(3-thienylcarbonyl)-aminomethyl-5-(2-fluorophenyl)-H-2,3-dihydro-1,4-benzodiazepine (KC 6128; (+)-titfluadom) did not reverse the effect of naloxone. The δ-specific antagonist N,N-diallyl-Tyr-α-aminoisobutyricacid-Phe-Leu-OH (ICI 174,864) failed to influence basal release. Release of LHRH stimulated by increasing the potassium ion concentration of the superfusate to 48 mmol/l was reduced by DAGO in a manner which was reversed by naloxone, and by FK 33–824 in a manner which was reversed by both naloxone and ICI 174,864. The agonists DTLET and titfluadom did not affect stimulated release of LHRH. These results support the proposal that spontaneous release of LHRH is tonically inhibited by agonists acting through the μ-receptor whilst, in response to a stimulus, the δ-receptor, in addition to the δ-receptor, may be involved. J. Endocr. (1987) 114,111–117

Effects of porcine relaxin on oxytocin release from the neurohypophysis in the anaesthetized lactating rat

1986 ◽  
Vol 109 (3) ◽  
pp. 393-397 ◽  
Author(s):  
K. T. O'Byrne ◽  
L. Eltringham ◽  
G. Clarke ◽  
A. J. S. Summerlee
Keyword(s):  
Opioid Peptides ◽  
Inhibitory Effect ◽  
Opioid Antagonist ◽  
Dependent Manner ◽  
Endogenous Opioid Peptides ◽  
Endogenous Opioid ◽  
Oxytocin Release ◽  
Relaxin 2

ABSTRACT The effect of relaxin on electrically evoked release of oxytocin from the posterior pituitary was examined by monitoring changes in intramammary pressure in the anaesthetized lactating rat. The amount of oxytocin released by electrical stimulation of the neurohypophysis in vivo was dramatically reduced following i.v. injection of highly purified porcine relaxin (2·5–10 μg/rat). Relaxin inhibited oxytocin release in a dose-dependent manner and the onset of inhibition occurred within 6–10 min and lasted for 10–60 min. No effect on the sensitivity of the mammary gland to exogenous oxytocin was observed after relaxin treatment. During the period of inhibition, i.v. injection of the opioid antagonist naloxone chloride (1 mg/kg) completely and immediately restored electrically evoked oxytocin release. The neurohypophysis is known to contain endogenous opioid peptides, therefore the effect of relaxin on electrically stimulated release of oxytocin from the rat isolated neural lobe in vitro was examined. Relaxin (500–2000 ng/ml) failed to inhibit oxytocin release in vitro. The results suggest that relaxin can inhibit the release of oxytocin from terminals in the neurohypophysis, but by an indirect mechanism. This action appears to be mediated through endogenous opioid peptides whose source is not clear. They are unlikely to be of neurohypophysial origin and may probably come from the adrenal medulla, since acute adrenalectomy negated the inhibitory effect of relaxin on oxytocin release. J. Endocr. (1986) 109, 393–397

Do Endogenous Opioid Peptides Cause Hepatic Encephalopathy?

1987 ◽  
Vol 72 (s16) ◽  
pp. 90P-91P
Author(s):  
J.R. Thornton ◽  
M.S. Losowsky
Keyword(s):  
Hepatic Encephalopathy ◽  
Opioid Peptides ◽  
Endogenous Opioid Peptides ◽  
Endogenous Opioid

Met5-enkephalin protects isolated adult rabbit cardiomyocytes via δ-opioid receptors

1999 ◽  
Vol 277 (6) ◽  
pp. H2442-H2450 ◽  
Author(s):  
Yasushi Takasaki ◽  
Roger A. Wolff ◽  
Grace L. Chien ◽  
Donna M. van Winkle
Keyword(s):  
Cell Death ◽  
Opioid Receptors ◽  
Ischemic Preconditioning ◽  
Opioid Peptides ◽  
Trypan Blue ◽  
Adult Rabbit ◽  
Endogenous Opioid Peptides ◽  
Endogenous Opioid ◽  
Simulated Ischemia ◽  
Hypoxic Incubation

In rats and rabbits, endogenous opioid peptides participate in ischemic preconditioning. However, it is not known which endogenous opioid(s) can trigger cardioprotection. We examined preconditioning-induced and opioid-induced limitation of cell death in isolated, calcium-tolerant, adult rabbit cardiomyocytes. Cells were subjected to simulated ischemia by pelleting and normothermic hypoxic incubation. Preconditioning was elicited with 15 min of simulated ischemia followed by 15 min of resuspension and reoxygenation. All cells underwent 180 min of simulated ischemia. Cell death was assessed by trypan blue permeability. Morphine protected cells, as did preconditioning; naloxone blocked the preconditioning-induced protection. Exogenous Met5-enkephalin (ME) induced protection, but exogenous β-endorphin did not. ME-induced protection was blocked by the δ-selective antagonist naltrindole. Additionally, two other proenkephalin products, Leu5-enkephalin and Met5-enkephalin-Arg-Phe, provided protection equipotent to ME. These data suggest that one or more proenkephalin products interact with δ-opioid receptors to endogenously trigger opioid-mediated protection.

Sign in / Sign up

Export Citation Format

Share Document