Reciprocal interactions between α2-adrenoceptor agonist and neuropeptide Y binding sites in the nucleus tractus solitarius of the rat

1989 ◽  
Vol 75 (2) ◽  
pp. 83-99 ◽  
Author(s):  
A. Härfstrand ◽  
K. Fuxe ◽  
L. Agnati ◽  
B. Fredholm
1994 ◽  
Vol 115 (1-2) ◽  
pp. 135-140 ◽  
Author(s):  
Ane M. Gabilondo ◽  
J. Javier Meana ◽  
Fernando Barturen ◽  
Magdalena Sastre ◽  
Jesús A. García-Sevilla

1986 ◽  
Vol 70 (2) ◽  
pp. 147-153 ◽  
Author(s):  
C. R. Jones ◽  
M. Giembcyz ◽  
C. A. Hamilton ◽  
I. W. Rodger ◽  
K. Whyte ◽  
...  

1. The effect of intravenous infusion of catecholamines and related drugs on human platelet α2-adrenoceptor number and function was investgated. 2. Short (60–120 min) infusions of catecholamines with α2 agonist activity in vivo produced attenuation of the platelet responses to adrenaline in vitro. This desensitization was specific for the adrenaline induced aggregatory response. 3. The maximum number of [3H]yohimbine binding sites on platelets was not altered by adrenaline infusion. 4. The ability of adrenaline to reduce platelet cyclic AMP levels was significantly reduced after the infusions. 5. Acute infusions of α2-adrenoceptor agonists may alter the coupling of the platelet α2-adrenoceptor to adenylate cyclase.


2002 ◽  
Vol 63 (1) ◽  
pp. 256-265 ◽  
Author(s):  
Antonio M. González ◽  
Julio Pascual ◽  
J. Javier Meana ◽  
Fernando Barturen ◽  
Carmen Del Arco ◽  
...  

1997 ◽  
Vol 35 (6) ◽  
pp. 561-568
Author(s):  
GYÖNGI HORVÁTH ◽  
ILDIKÓ DOBOS ◽  
PÉTER LISZLI ◽  
WALTER KLIMSCHA ◽  
MARGIT SZIKSZAY ◽  
...  

2001 ◽  
Vol 105 (2) ◽  
pp. 159-166 ◽  
Author(s):  
David B Bylund ◽  
Moira E Gerety ◽  
H.Kevin Happe ◽  
L.Charles Murrin

Author(s):  
R. Quirion ◽  
J.C. Martel ◽  
Y. Robitaille ◽  
P. Etienne ◽  
P. Wood ◽  
...  

Abstract:Multiple neurotransmitter systems are affected in senile dementia of the Alzheimer's type (SDAT). Among them, acetylcholine has been most studied. It is now well accepted that the activity of the enzyme, choline acetyltransferase (ChAT) is much decreased in various brain regions including the frontal and temporal cortices, hippocampus and nucleus basalis of Meynert (nbm) in SDAT. Cortical M2-muscarinic and nicotinic cholinergic receptors are also decreased but only in a certain proportion (30-40%) of SDAT patients. For other systems, it appears that cortical serotonin (5-HT)-type 2 receptor binding sites are decreased in SDAT. This diminution in 5-HT2 receptors correlates well with the decreased levels of somatostatin-like immunoreactive materials found in the cortex of SDAT patients. Cortical somatostatin receptor binding sites are decreased in about one third of SDAT patients. Finally, neuropeptide Y and neuropeptide Y receptor binding sites are distributed in areas enriched in cholinergic cell bodies and nerve fiber terminals and it would be of interest to determine possible involvement of this peptide in SDAT. Thus, it appears that multi-drug clinical trials should be considered for the treatment of SDAT.


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