Mechanisms underlying the synaptic trafficking of the glutamate delta receptor GluD1

To study the effect of endorphins on metabolic rate and on the relationship between O2 consumption (VO2) and ventilation, we administered enkephalin analogues (relatively selective delta-receptor agonists) and a morphiceptin analogue (a highly selective mu-receptor agonist) intracisternally in nine unanesthetized chronically instrumented adult dogs. Both delta- and mu-agonists decreased VO2 by 40–60%. delta-Agonists induced a dose-dependent decrease in mean instantaneous minute ventilation (VT/TT) associated with periodic breathing. The decrease in VT/TT started and resolved prior to the decrease and returned to baseline of VO2, respectively. In contrast, the mu-agonists induced an increase in VT/TT associated with rapid shallow breathing. Arterial PCO2 increased and arterial PO2 decreased after both delta- and mu-agonists. Low doses of intracisternal naloxone (0.002–2.0 micrograms/kg) reversed the opioid effect on VT/TT but not on VO2; higher doses of naloxone (5–25 micrograms/kg) reversed both. Naloxone administered alone had no effect on VT/TT or VO2. These data suggest that 1) both delta- and mu-agonists induce alveolar hypoventilation despite a decrease in VO2, 2) this hypoventilation results from a decrease in VT/TT after delta-agonists but an increase in dead space ventilation after mu-agonists, and 3) endorphins do not modulate ventilation and metabolic rate tonically, but we speculate that they may do so in response to stressful stimulation.

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Development of a Model for the .delta. Opioid Receptor Pharmacophore. 2. Conformationally Restricted Phe3 Replacements in the Cyclic .delta. Receptor Selective Tetrapeptide Tyr-c[D-Cys-Phe-D-Pen]OH (JOM-13)

Journal of Medicinal Chemistry ◽

10.1021/jm00051a016 ◽

1994 ◽

Vol 37 (25) ◽

pp. 4384-4391 ◽

Cited By ~ 44

Author(s):

Henry I. Mosberg ◽

John R. Omnaas ◽

Andrei Lomize ◽

Deborah L. Heyl ◽

Ian Nordan ◽

...

Keyword(s):

Opioid Receptor ◽

Delta Opioid Receptor ◽

Conformationally Restricted ◽

Delta Receptor

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Abstract 100: Delta Opioid Receptor Blockade Abolishes Exercise-Induced Cardioprotection Against Ischemia-Reperfusion Injury In Vivo

Circulation Research ◽

10.1161/res.113.suppl_1.a100 ◽

2013 ◽

Vol 113 (suppl_1) ◽

Author(s):

Juliana P Borges ◽

Marina Tristao ◽

Eduardo V Tibiriçá ◽

Marcos A Lessa

Keyword(s):

Receptor Antagonist ◽

Opioid Receptor ◽

Acute Exercise ◽

Ischemia Reperfusion ◽

Control Group ◽

Receptor Subtype ◽

Kappa Receptor ◽

Exercise Induced ◽

Delta Receptor ◽

And Control

Introduction: Recent studies showed that exercise enhances myocardial tolerance to ischemia-reperfusion (I-R) injury via an opioid receptor-dependent mechanism. However, the specific subtype of opioid receptor involved in this response remains to be determined. Methods: Male Wistar rats were first divided into 2 groups: exercised and control. The exercised group underwent 4 consecutive days of treadmill training (60 min at 70% of maximal oxygen consumption). The exercised group was then divided into 4 subgroups: exercised (Exe; n = 10); exercised + kappa receptor antagonist (Exe + K; n=4); exercised + delta receptor antagonist (Exe + D; n=4); exercised + mu receptor antagonist (Exe + M; n=4). Control group was also divided into 2 groups: control (Ctr; n = 10) and control sham (Sham; n = 10). To induce I-R injury, anesthetized animals were submitted to a left thoracotomy and a 30 min interventricular coronary occlusion followed by 60 min of reperfusion. The hemodynamic parameters were recorded and infarct size was post-mortem determined by double staining using TTC/Evans blue and expressed as a percentage of the area at risk. Results: As shown in the figure, Sham group showed no infarct, Exe group showed a significant reduction in the infarcted area (27.6%) when compared to Ctr group (42.0%). The pretreatment with mu and kappa receptor antagonist did not alter the cardioprotective effect of exercise. However, the pretreatment with delta receptor antagonist prevented the exercise-induced cardioprotection. Conclusions: Endogenous opioid system is involved in cardioprotection conferred by acute exercise, and delta receptor subtype seems to play an important role in this response.

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Role of enkephalins in regulation of basal intestinal water and ion absorption in the rat

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1984.246.4.g386 ◽

1984 ◽

Vol 246 (4) ◽

pp. G386-G392

Author(s):

R. Fogel ◽

R. B. Kaplan

Keyword(s):

Receptor Antagonist ◽

Water Transport ◽

Opiate Receptor ◽

Ion Absorption ◽

Mu Receptors ◽

Induced Changes ◽

Delta Receptor ◽

Mu Opiate Receptor

Intraluminal administration of naloxone (10(-4) M), a mu-opiate receptor antagonist, or diprenorphine (10(-6) M), an opiate receptor antagonist with high affinity for both delta- and mu-receptors, decreased basal in vivo water and electrolyte absorption in the jejunum and ileum but not the colon of the rat. Diprenorphine (10(-5) M) decreased basal colonic water transport. These changes were not due to a reduction in mucosal Na-K-ATPase activity. Intravenous atropine prevented as well as abolished the changes in water transport due to naloxone. The diprenorphine-induced changes were not altered by atropine. Naloxone and diprenorphine acted by different receptors. Pretreatment with naloxone (10(-4) M) prevented the increase in water transport due to morphine, a mu-agonist, whereas a higher concentration of naloxone (10(-3) M) was required to inhibit the increase due to D-Ala-methionine-enkephalinamide, a delta-receptor agonist. In contrast, diprenorphine (10(-6) M) abolished the absorption caused by morphine and D-Ala-methionine-enkephalinamide. Diprenorphine (3 X 10(-7) M) partially prevented the morphine-induced increase in water absorption.(ABSTRACT TRUNCATED AT 250 WORDS)

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