scholarly journals Opiate Drugs with Abuse Liability Hijack the Endogenous Opioid System to Disrupt Neuronal and Glial Maturation in the Central Nervous System

2018 ◽  
Vol 5 ◽  
Author(s):  
Kurt F. Hauser ◽  
Pamela E. Knapp
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Abuse Liability ◽  
Opioid System ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Opiate Drugs ◽  
The Central Nervous System

Centrally administered naloxone blocks reflex natriuresis after acute unilateral nephrectomy

1985 ◽  
Vol 249 (3) ◽  
pp. F390-F395 ◽  
Author(s):  
S. Y. Lin ◽  
M. H. Humphreys
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Opiate Receptors ◽  
Opiate Receptor ◽  
Unilateral Nephrectomy ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Arterial Blood ◽  
Artificial Cerebrospinal Fluid ◽  
The Central Nervous System

Acute unilateral nephrectomy (AUN) leads to a natriuresis and kaliuresis by the remaining kidney through reflex mechanisms involving opiate receptors. To determine whether the opiate receptors mediating these responses are located in the central nervous system, we carried out AUN in anesthetized rats undergoing continuous ventriculocisternal perfusion (VCP) with artificial cerebrospinal fluid (CSF). AUN caused large increases in both Na (UNaV) and K (UKV) excretion without changes in glomerular filtration rate or arterial blood pressure. When the opiate receptor antagonist naloxone was added to the perfusate to achieve a perfusion rate of 32 micrograms X kg-1 X h-1, AUN failed to increase either UNaV or UKV by the remaining kidney. This dose of naloxone, however, was without effect when infused intravenously. Addition of thyrotropin-releasing hormone (TRH) to the artificial CSF to achieve a VCP rate of 50 micrograms X kg-1 X h-1 also blocked the expected increase in UNaV and UKV by the remaining kidney after AUN. Infusion of TRH intravenously at the same rate did not interfere with the postnephrectomy natriuresis or kaliuresis. Higher intravenous infusion rates of TRH (1 and 2 mg X kg-1h-1) prevented the postnephrectomy natriuresis without affecting the kaliuresis. These results indicate that the effect of naloxone to block the reflex natriuresis and kaliuresis after AUN resides largely in the central nervous system. The blockade by naloxone of the postnephrectomy natriuresis is duplicated by centrally administered TRH, providing another example of the interaction of this hormone with the endogenous opioid system. Large intravenous infusions of TRH also block the postnephrectomy natriuresis but not the kaliuresis.

scholarly journals Formation of fetal opioid system

2016 ◽  
Vol 65 (2) ◽  
pp. 64-69 ◽  
Author(s):  
Anastasia A Yakovleva
Keyword(s):  
Growth Hormone ◽  
Opioid Peptides ◽  
Opioid System ◽  
Endogenous Opioid Peptides ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Placental Lactogens ◽  
Functional Development ◽  
The Central Nervous System ◽  
Different Tissues

The article presented literature review about of endogenous opioid system (EOS) formation consist of opioid receptors complex and its ligands (endogenous opioid peptides) in different tissues including placenta. It was shown that formation of fetal EOS is going with anatomic and functional development of the central nervous system and EOS expression begins in the placental tissues as soon as implantation and starts till the end of the pregnancy. Influence of opioid peptides on secretion progesterone, prolactin family peptides, growth hormone, placental lactogens and prolypherine from the trophoblast tissue is discussed.

Endogenous Opioid and Cannabinoid Mechanisms Are Involved in the Analgesic Effects of Celecoxib in the Central Nervous System

Pharmacology ◽  
2012 ◽  
Vol 89 (3-4) ◽  
pp. 127-136 ◽  
Author(s):  
R.M. Rezende ◽  
P. Paiva-Lima ◽  
W.G.P. Dos Reis ◽  
V.M. Camêlo ◽  
A. Faraco ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Endogenous Opioid ◽  
Analgesic Effects ◽  
The Central Nervous System

scholarly journals Multiple Sclerosis and the Endogenous Opioid System

2021 ◽  
Vol 15 ◽  
Author(s):  
Zoë Dworsky-Fried ◽  
Caylin I. Chadwick ◽  
Bradley J. Kerr ◽  
Anna M. W. Taylor
Keyword(s):  
Multiple Sclerosis ◽  
Neuronal Degeneration ◽  
Opioid System ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Autoimmune Encephalomyelitis ◽  
Clinical Observations ◽  
Demyelinating Lesions ◽  
Current Therapies ◽  
The Central Nervous System

Multiple sclerosis (MS) is an autoimmune disease characterized by chronic inflammation, neuronal degeneration and demyelinating lesions within the central nervous system. The mechanisms that underlie the pathogenesis and progression of MS are not fully known and current therapies have limited efficacy. Preclinical investigations using the murine experimental autoimmune encephalomyelitis (EAE) model of MS, as well as clinical observations in patients with MS, provide converging lines of evidence implicating the endogenous opioid system in the pathogenesis of this disease. In recent years, it has become increasingly clear that endogenous opioid peptides, binding μ- (MOR), κ- (KOR) and δ-opioid receptors (DOR), function as immunomodulatory molecules within both the immune and nervous systems. The endogenous opioid system is also well known to play a role in the development of chronic pain and negative affect, both of which are common comorbidities in MS. As such, dysregulation of the opioid system may be a mechanism that contributes to the pathogenesis of MS and associated symptoms. Here, we review the evidence for a connection between the endogenous opioid system and MS. We further explore the mechanisms by which opioidergic signaling might contribute to the pathophysiology and symptomatology of MS.

Effects of Hyperoxia on Lung Utrastructure

1970 ◽  
Vol 28 ◽  
pp. 26-27
Author(s):  
Gladys Harrison
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Light Microscopy ◽  
Oxygen Effects ◽  
Age Dependent ◽  
The Central Nervous System ◽  
The Subject ◽  
Space Age ◽  
Alveolar Septa ◽  
Extensive Damage

With the advent of the space age and the need to determine the requirements for a space cabin atmosphere, oxygen effects came into increased importance, even though these effects have been the subject of continuous research for many years. In fact, Priestly initiated oxygen research when in 1775 he published his results of isolating oxygen and described the effects of breathing it on himself and two mice, the only creatures to have had the “privilege” of breathing this “pure air”.Early studies had demonstrated the central nervous system effects at pressures above one atmosphere. Light microscopy revealed extensive damage to the lungs at one atmosphere. These changes which included perivascular and peribronchial edema, focal hemorrhage, rupture of the alveolar septa, and widespread edema, resulted in death of the animal in less than one week. The severity of the symptoms differed between species and was age dependent, with young animals being more resistant.

Emigration of neutrophils in the central nervous system

1983 ◽  
Vol 41 ◽  
pp. 788-789
Author(s):  
John L.Beggs ◽  
John D. Waggener ◽  
Wanda Miller ◽  
Jane Watkins
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Osmium Tetroxide ◽  
White Blood Cells ◽  
Arterial Perfusion ◽  
E Coli ◽  
Intracisternal Injection ◽  
The Central Nervous System ◽  
Brain And Spinal Cord ◽  
Interendothelial Junctions

Studies using mesenteric and ear chamber preparations have shown that interendothelial junctions provide the route for neutrophil emigration during inflammation. The term emigration refers to the passage of white blood cells across the endothelium from the vascular lumen. Although the precise pathway of transendo- thelial emigration in the central nervous system (CNS) has not been resolved, the presence of different physiological and morphological (tight junctions) properties of CNS endothelium may dictate alternate emigration pathways.To study neutrophil emigration in the CNS, we induced meningitis in guinea pigs by intracisternal injection of E. coli bacteria.In this model, leptomeningeal inflammation is well developed by 3 hr. After 3 1/2 hr, animals were sacrificed by arterial perfusion with 3% phosphate buffered glutaraldehyde. Tissues from brain and spinal cord were post-fixed in 1% osmium tetroxide, dehydrated in alcohols and propylene oxide, and embedded in Epon. Thin serial sections were cut with diamond knives and examined in a Philips 300 electron microscope.

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