Interaction of Brain Histaminergic and Dopaminergic Systems

2016 ◽  
pp. 295-310
Author(s):  
Saara Nuutinen ◽  
Outi Salminen
Keyword(s):  
2005 ◽  
Vol 31 (5) ◽  
pp. 904-911 ◽  
Author(s):  
Theodore A Slotkin ◽  
Marisa L Kreider ◽  
Charlotte A Tate ◽  
Frederic J Seidler
Keyword(s):  

ASN NEURO ◽  
2021 ◽  
Vol 13 ◽  
pp. 175909142110097
Author(s):  
Kui Cui ◽  
Fan Yang ◽  
Turan Tufan ◽  
Muhammad U. Raza ◽  
Yanqiang Zhan ◽  
...  

Dysfunction of the central noradrenergic and dopaminergic systems is the primary neurobiological characteristic of Parkinson’s disease (PD). Importantly, neuronal loss in the locus coeruleus (LC) that occurs in early stages of PD may accelerate progressive loss of dopaminergic neurons. Therefore, restoring the activity and function of the deficient noradrenergic system may be an important therapeutic strategy for early PD. In the present study, the lentiviral constructions of transcription factors Phox2a/2b, Hand2 and Gata3, either alone or in combination, were microinjected into the LC region of the PD model VMAT2 Lo mice at 12 and 18 month age. Biochemical analysis showed that microinjection of lentiviral expression cassettes into the LC significantly increased mRNA levels of Phox2a, and Phox2b, which were accompanied by parallel increases of mRNA and proteins of dopamine β-hydroxylase (DBH) and tyrosine hydroxylase (TH) in the LC. Furthermore, there was considerable enhancement of DBH protein levels in the frontal cortex and hippocampus, as well as enhanced TH protein levels in the striatum and substantia nigra. Moreover, these manipulations profoundly increased norepinephrine and dopamine concentrations in the striatum, which was followed by a remarkable improvement of the spatial memory and locomotor behavior. These results reveal that over-expression of these transcription factors in the LC improves noradrenergic and dopaminergic activities and functions in this rodent model of PD. It provides the necessary groundwork for the development of gene therapies of PD, and expands our understanding of the link between the LC-norepinephrine and dopamine systems during the progression of PD.


1998 ◽  
Vol 30 (2) ◽  
pp. 135-144 ◽  
Author(s):  
Masayuki Watanabe ◽  
Ryo-ichi Nonaka ◽  
Yoko Hagino ◽  
Yoshio Kodama

1981 ◽  
Vol 5 (5-6) ◽  
pp. 527-530 ◽  
Author(s):  
Pardeep Ahluwalia ◽  
Darshan S. Grewaal ◽  
Radhey L. Singhal

1997 ◽  
Vol 770 (1-2) ◽  
pp. 45-52 ◽  
Author(s):  
Yuzuru Tashiro ◽  
James M Drake ◽  
Shushovan Chakrabortty ◽  
Toshiaki Hattori

Molecules ◽  
2018 ◽  
Vol 23 (8) ◽  
pp. 2072 ◽  
Author(s):  
Mustafa Barbaros ◽  
Özgür Can ◽  
Umut Üçel ◽  
Nazlı Turan Yücel ◽  
Ümide Demir Özkay

Atomoxetine is a selective noradrenaline reuptake inhibitor drug. Based on the knowledge that agents increasing monoamine levels in the central nervous system have therapeutic potential for neuropathic pain, it is planned to investigate the possible efficacy of atomoxetine on diabetes-induced hyperalgesia, in this study. Randall-Selitto (mechanical noxious stimuli) and Hargreaves (thermal noxious stimuli) tests were used to evaluate nociceptive perception of rats. Obtained data indicated that streptozotocin-induced diabetes causes significant decreases in the paw withdrawal threshold and paw withdrawal latency values of the animals, respectively. However, atomoxetine administered at 3 mg/kg/day for 7 and 14 days improved these diabetes-induced hyperalgesia responses. Furthermore, antihyperalgesic activity was antagonized with α-methyl-para-tyrosine methyl ester, phentolamine, propranolol, and sulpiride pre-treatments. The same effect was not reversed, however, by SCH 23390. These findings demonstrated, for the first time, that atomoxetine possesses significant antihyperalgesic activity on diabetes-induced neuropathic pain and this effect seems to be mediated by α- and β-adrenergic and D2/D3 dopaminergic receptors. Results of this present study seem to offer a new indication for an old drug; atomoxetine, but these preclinical data should first be confirmed with further well-designed clinical trials.


1994 ◽  
Vol 17 (6) ◽  
pp. 398-404 ◽  
Author(s):  
D. K. Lim ◽  
K. M. Lee ◽  
I. K. Ho

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