Autoradiographic mapping of μ opioid receptor changes in rat brain after long-term haloperidol treatment: relationship to the development of vacuous chewing movements

1996 ◽  
Vol 128 (1) ◽  
pp. 97-104 ◽  
Author(s):  
Tsukasa Sasaki ◽  
James L. Kennedy ◽  
José N. Nobrega
Keyword(s):  
Rat Brain ◽  
Opioid Receptor ◽  
Vacuous Chewing Movements ◽  
Treatment Relationship ◽  
Μ Opioid Receptor ◽  
Haloperidol Treatment ◽  
Vacuous Chewing

scholarly journals Long-Term Morphine Treatment Decreases the Association of μ-Opioid Receptor (MOR1) mRNA with Polysomes through miRNA23b

2009 ◽  
Vol 75 (4) ◽  
pp. 744-750 ◽  
Author(s):  
Qifang Wu ◽  
Lei Zhang ◽  
Ping-Yee Law ◽  
Li-Na Wei ◽  
Horace H. Loh
Keyword(s):  
Opioid Receptor ◽  
Morphine Treatment ◽  
Μ Opioid Receptor

Neuroleptic-induced vacuous chewing movements in rodents: incidence and effects of long-term increases in haloperidol dose

1995 ◽  
Vol 117 (1) ◽  
pp. 74-81 ◽  
Author(s):  
Michael F. Egan ◽  
Richard Jed Wyatt ◽  
Thomas M. Hyde ◽  
Joel E. Kleinman
Keyword(s):  
Vacuous Chewing Movements ◽  
Haloperidol Dose ◽  
Vacuous Chewing

Harpagophytum Procumbens Ethyl Acetate Fraction Reduces Fluphenazine-Induced Vacuous Chewing Movements and Oxidative Stress in Rat Brain

2016 ◽  
Vol 41 (5) ◽  
pp. 1170-1184 ◽  
Author(s):  
Larissa Finger Schaffer ◽  
Catiuscia Molz de Freitas ◽  
Ana Paula Chiapinotto Ceretta ◽  
Luis Ricardo Peroza ◽  
Elizete de Moraes Reis ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ethyl Acetate ◽  
Rat Brain ◽  
Ethyl Acetate Fraction ◽  
Vacuous Chewing Movements ◽  
Harpagophytum Procumbens ◽  
Vacuous Chewing ◽  
And Oxidative Stress

Inflammation-reactive astrocytes can be restored with a three drug combination

2014 ◽  
Vol 5 (3) ◽  
pp. 209-209
Author(s):  
E. Hansson ◽  
L. Block ◽  
U. Björklund ◽  
B. Biber
Keyword(s):  
Opioid Receptor ◽  
Primary Cultures ◽  
Reactive Astrocytes ◽  
Opioid Antagonist ◽  
Opioid Agonist ◽  
Cell Parameters ◽  
Ultralow Concentrations ◽  
Inflammatory State ◽  
Μ Opioid Receptor

Abstract Aims In inflammation-reactive astrocytes the cell parameters, Ca2+ signalling, Na+ transporters, cytoskeleton, and release of proinflammatory cytokines are affected. We want to re-establish these parameters with agents, which might have a potential to restore the cells back to a normal non-inflammatory level. Methods Astrocytes in primary cultures were incubated with lipopolysaccharide (LPS) (10 ng/ml) for 24 h to become inflammation-reactive. Different parameters were analysed to verify this inflammation: Ca2+ signalling, Na+/K+-ATPase expression, actin filament organization, and interleukin-1beta release (IL-1β). Results We have used an opioid agonist, endomorphin-1, that stimulates the Gi/o protein of the μ-opioid receptor, an opioid antagonist, naloxone, that inhibits the Gs protein of the μ-opioid receptor in ultralow concentrations, and an anti-epileptic agent, levetiracetam, that counteracts the release of IL-1β. The combination of these three agents managed to activate the Gi/o protein and Na+/K+-ATPase activity, inhibit the Gs protein, and decrease the release of IL-1β. The disorganized actin filaments were restored. Conclusions The findings that the important cell parameters in astrocytes were restored back to their normal non-inflammatory state after the cells were treated with the inflammatory agent LPS could be of clinical significance. It may be useful for the treatment of neuroinflammation and also maybe of long-term pain. The astrocyte networks play a significant role and therefore a well-working intercellular Ca2+ signalling is of utmost importance. Significance These findings put new potential drug regimens towards treatment of neuroinflammation and long-term pain into focus.

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