Mu-Opiate Receptor and Beta-Endorphin Expression in Nerve Endings and Keratinocytes in Human Skin

Dermatology ◽  
2004 ◽  
Vol 209 (3) ◽  
pp. 183-189 ◽  
Author(s):  
M. Bigliardi-Qi ◽  
L.T. Sumanovski ◽  
S. Büchner ◽  
T. Rufli ◽  
P.L. Bigliardi
Keyword(s):  
Human Skin ◽  
Opiate Receptor ◽  
Nerve Endings ◽  
Beta Endorphin ◽  
Mu Opiate Receptor

Changes of Epidermal Mu-Opiate Receptor Expression and Nerve Endings in Chronic Atopic Dermatitis

Dermatology ◽  
2005 ◽  
Vol 210 (2) ◽  
pp. 91-99 ◽  
Author(s):  
M. Bigliardi-Qi ◽  
B. Lipp ◽  
L.T. Sumanovski ◽  
S.A. Buechner ◽  
P.L. Bigliardi
Keyword(s):  
Atopic Dermatitis ◽  
Opiate Receptor ◽  
Receptor Expression ◽  
Nerve Endings ◽  
Mu Opiate Receptor

[MU]-opiate receptor system in skin and relationship to itch

2004 ◽  
Vol 50 (3) ◽  
pp. P29
Author(s):  
Bigliardi-Qi L Paul ◽  
Bigliardi-Qi Mei ◽  
Rufli Theo ◽  
Zhou Haiyan
Keyword(s):  
Opiate Receptor ◽  
Receptor System ◽  
Mu Opiate Receptor

scholarly journals Differentiation of delta and mu opiate receptor localizations by light microscopic autoradiography.

1980 ◽  
Vol 77 (10) ◽  
pp. 6239-6243 ◽  
Author(s):  
R. R. Goodman ◽  
S. H. Snyder ◽  
M. J. Kuhar ◽  
W. S. Young
Keyword(s):  
Opiate Receptor ◽  
Mu Opiate Receptor

Effect of opiate-receptor blockade on normoglycemic and hypoglycemic glucoregulation

1986 ◽  
Vol 250 (3) ◽  
pp. E236-E242 ◽  
Author(s):  
K. M. el-Tayeb ◽  
P. L. Brubaker ◽  
H. L. Lickley ◽  
E. Cook ◽  
M. Vranic
Keyword(s):  
Plasma Glucose ◽  
Glucose Production ◽  
Opiate Receptor ◽  
Receptor Blockade ◽  
Endogenous Opiates ◽  
Counterregulatory Hormones ◽  
Beta Endorphin ◽  
Initial Decrease ◽  
Pituitary Adrenal Axis ◽  
Naloxone Treatment

By use of the opiate antagonist naloxone, we have examined the hormonal and metabolic responses to opiate-receptor blockade under basal conditions and during insulin-induced hypoglycemia in normal dogs. Naloxone treatment had no measurable effect on glucose concentration, turnover, and norepinephrine levels, but stimulated plasma epinephrine, glucagon, and cortisol and inhibited insulin release. Insulin (7 mU X kg-1 X min-1) decreased plasma glucose to 42 +/- 4 mg/dl due to an initial decrease in glucose production and an increase in glucose disappearance. Glucose production then increased, and plasma glucose plateaued. After 50 min of insulin infusion, epinephrine levels increased 26-fold (P less than 0.05), norepinephrine and glucagon 3-fold (P less than 0.02), and cortisol 4-fold (P less than 0.01). Similarly, plasma beta-endorphin and adrenocorticotropin (ACTH) were elevated (6-fold, P less than 0.01, and 16-fold, P less than 0.05, respectively). When naloxone was given during insulin-induced hypoglycemia, there was earlier release of epinephrine, glucagon, beta-endorphin, ACTH, and cortisol as well as a greater release of glucagon (P less than 0.001) and cortisol (P less than 0.0001). This resulted in a greater increase in glucose production (P less than 0.01), thus lessening the insulin-induced hypoglycemic excursion. In conclusion, in the dog, endogenous opiates may play a small role in the regulation of basal insulin and glucagon release and can inhibit the pituitary-adrenal axis under basal conditions and during hypoglycemia. Thus increased glucose production in response to insulin-induced hypoglycemia is consistent with the excessive response of counterregulatory hormones during opiate-receptor blockade.

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

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)

Expressed mu opiate receptor couples to adenylate cyclase and phosphatidyl inositol turnover

Neuroreport ◽  
1994 ◽  
Vol 5 (4) ◽  
pp. 507-509 ◽  
Author(s):  
Peter S. Johnson ◽  
Jia Bei Wang ◽  
Wen Fei Wang ◽  
George R. Uhl
Keyword(s):  
Adenylate Cyclase ◽  
Phosphatidyl Inositol ◽  
Opiate Receptor ◽  
Mu Opiate Receptor

Intra‐epidermal nerve endings progress within keratinocyte cytoplasmic tunnels in normal human skin

2020 ◽  
Vol 29 (4) ◽  
pp. 387-392 ◽  
Author(s):  
Matthieu Talagas ◽  
Nicolas Lebonvallet ◽  
Raphael Leschiera ◽  
Philippe Elies ◽  
Pascale Marcorelles ◽  
...  
Keyword(s):  
Human Skin ◽  
Nerve Endings ◽  
Normal Human Skin ◽  
Normal Human
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