scholarly journals Role of the endogenous opioid system in modulation of urinary bladder activity by spinal nerve stimulation

2013 ◽  
Vol 305 (1) ◽  
pp. F52-F60 ◽  
Author(s):  
Xin Su ◽  
Angela Nickles ◽  
Dwight E. Nelson

The role of the endogenous opioid system in modulation of urinary bladder activity by spinal nerve (SN) stimulation was studied in anesthetized female rats, using the rat model of isovolumetric bladder contraction. SN stimulation at a fixed frequency of 10 Hz attenuated bladder contraction frequency; the magnitude of the inhibition was directly proportional to the current intensity. Neither the κ-opioid antagonist nor-binaltorphimine (2 mg/kg iv) nor the δ-opioid antagonist naltrindole (5 mg/kg iv) attenuated the bladder inhibitory response to SN stimulation. In contrast, the μ-opioid receptor antagonist naloxone (NLX; 0.03 mg/kg iv) blocked the inhibitory responses evoked by SN stimulation at therapeutic current intensities at ≤1 × motor threshold current (Tmot). An action at spinal and supraspinal centers was further confirmed by the ability of intrathecal or intracerebroventricular administration of NLX methiodide to attenuate the bladder inhibitory effects of 1 × Tmot SN stimulation. The magnitude of SN-mediated neuromodulation using therapeutically relevant stimulation intensity (Tmot) is equivalent to 0.16 mg/kg of systemically administered morphine, which produces 50% inhibition of bladder contraction frequency. These results suggest that the inhibitory effects of lower intensity SN stimulation may be mediated through the release of endogenous μ-opioid peptides. Additionally, these data suggest that neuromodulation may offer a mode of treating the symptoms of overactive bladder with efficacy equal to the opioid drugs but without their liability for abuse and dependence.

1988 ◽  
Vol 105 (2) ◽  
pp. 162-164 ◽  
Author(s):  
G. N. Kryzhanovskii ◽  
L. P. Bakuleva ◽  
N. L. Luzina ◽  
V. A. Vinogradov ◽  
K. N. Yarygin ◽  
...  

1994 ◽  
Vol 9 (2) ◽  
pp. 105-131 ◽  
Author(s):  
Christina Gianoulakis ◽  
Jean-Pascal de Waele

2003 ◽  
Vol 470 (1-2) ◽  
pp. 99-102 ◽  
Author(s):  
Akira Yoshida ◽  
Yasuko Sakurai-Yamashita ◽  
Kimihiro Yamashita ◽  
Nobuyuki Tanaka ◽  
Kohtaro Taniyama

2011 ◽  
Vol 56 (No. 9) ◽  
pp. 423-429 ◽  
Author(s):  
M. Golynski ◽  
W. Krumrych ◽  
K. Lutnicki

  Opium alkaloids counterparts are secreted by human and animal organisms but the role of endogenous opioid peptides in horses has not yet been fully elucidated. Endogenous opioids are involved in regulating food intake, sexual and social activity, pain relief and pain threshold regulation in horses as well as in regulating the functions of the immune system. The aim of this review is to describe the endogenous opioid system in the horse and its function during stress, illness, reproduction, and its influence on immunity and on the formation of reactive oxygen species (ROS) in horses. What is currently known concerning beta-endorphin suggests that they can be a promising diagnostic or prognostic indicator of many pathologic states in horses.


Endocrinology ◽  
2003 ◽  
Vol 144 (5) ◽  
pp. 1753-1760 ◽  
Author(s):  
Suzanne M. Appleyard ◽  
Michael Hayward ◽  
Juan I. Young ◽  
Andrew A. Butler ◽  
Roger D. Cone ◽  
...  

Proopiomelanocortin (POMC) neurons in the hypothalamus are direct targets of the adipostatic hormone leptin and contribute to energy homeostasis by integrating peripheral and central information. The melanocortin and β-endorphin neuropeptides are processed from POMC and putatively coreleased at axon terminals. Melanocortins have been shown by a combination of pharmacological and genetic methods to have inhibitory effects on appetite and body weight. In contrast, pharmacological studies have generally indicated that opioids stimulate food intake. Here we report that male mice engineered to selectively lack β-endorphin, but that retained normal melanocortin signaling, were hyperphagic and obese. Furthermore, β-endorphin mutant and wild-type mice had identical orexigenic responses to exogenous opioids and identical anorectic responses to the nonselective opioid antagonist naloxone, implicating an alternative endogenous opioid tone to β-endorphin that physiologically stimulates feeding. These genetic data indicate that β-endorphin is required for normal regulation of feeding, but, in contrast to earlier reports suggesting opposing actions of β-endorphin and melanocortins on appetite, our results suggest a more complementary interaction between the endogenously released POMC-derived peptides in the regulation of energy homeostasis.


2009 ◽  
Vol 92 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Aimee D. Eyvazzadeh ◽  
Kathryn P. Pennington ◽  
Rodica Pop-Busui ◽  
MaryFran Sowers ◽  
Jon-Kar Zubieta ◽  
...  

2005 ◽  
Vol 29 (8) ◽  
pp. 1522-1527 ◽  
Author(s):  
Carles Sanchis-Segura ◽  
Judy E. Grisel ◽  
M Foster Olive ◽  
Sandra Ghozland ◽  
George F. Koob ◽  
...  

1999 ◽  
Vol 84 (1) ◽  
pp. 64-68
Author(s):  
Gary S. Wand ◽  
Deborah Mangold ◽  
Mahmood Ali

The endogenous opioid system is part of a neural circuitry functionally related to alcohol-seeking behaviors. A family history of alcoholism is the strongest predictor of future development of alcohol dependence. This study was designed to evaluate ACTH responses to opioid receptor blockade as a function of family history for alcohol dependence. The nonselective opioid antagonist naloxone stimulates ACTH secretion by blocking opioidergic input on paraventricular corticotropin-releasing factor neurons, thereby providing a methodology for comparing hypothalamic opioid tone between study groups. Sixty nonalcoholic subjects, aged 18–25 yr, were enrolled in a protocol to measure the ACTH response to naloxone. Thirty-two subjects were offspring from families with a high density of alcohol dependence and were designated as family history-positive subjects. Twenty-eight subjects were offspring of nonalcohol-dependent parents and were designated family history-negative subjects. Subjects received naloxone (125 μg/kg) or placebo (0.9% saline) in double blind, randomized order. Plasma ACTH was monitored. Family history-positive men had increased ACTH response to naloxone compared to 1) family history-positive women, 2) family history-negative men, and 3) family history-negative women. Despite differences in plasma ACTH levels after naloxone administration, plasma naloxone concentrations did not differ between study groups. This finding suggests that nonalcoholic male offspring of alcohol-dependent men have altered endogenous opioid activity directed at hypothalamic corticotropin-releasing factor neurons.


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