Activation of the mesocorticolimbic dopaminergic system by stimulation of muscarinic cholinergic receptors in the ventral tegmental area

2000 ◽  
Vol 147 (4) ◽  
pp. 347-355 ◽  
Author(s):  
B. Gronier ◽  
K. W. Perry ◽  
K. Rasmussen
Keyword(s):  
Ventral Tegmental Area ◽  
Dopaminergic System ◽  
Cholinergic Receptors ◽  
Muscarinic Cholinergic Receptors ◽  
Muscarinic Cholinergic ◽  
Ventral Tegmental ◽  
Mesocorticolimbic Dopaminergic System ◽  
Stimulation Of

Local heating of human skin causes hyperemia without mediation by muscarinic cholinergic receptors or prostanoids

2004 ◽  
Vol 97 (5) ◽  
pp. 1781-1786 ◽  
Author(s):  
Sandrine Golay ◽  
Christian Haeberli ◽  
Anne Delachaux ◽  
Lucas Liaudet ◽  
Paul Kucera ◽  
...  
Keyword(s):  
Surface Temperature ◽  
Human Skin ◽  
Time Course ◽  
Local Heating ◽  
Cholinergic Receptors ◽  
Antimuscarinic Agent ◽  
Muscarinic Cholinergic Receptors ◽  
Local Skin ◽  
Muscarinic Cholinergic ◽  
Stimulation Of

Local changes in surface temperature have a powerful influence on the perfusion of human skin. Heating increases local skin blood flow, but the mechanisms and mediators of this response (thermal hyperemia response) are incompletely elucidated. In the present study, we examined the possible dependence of the thermal hyperemia response on stimulation of muscarinic cholinergic receptors and on production of vasodilator prostanoids. In 13 male healthy subjects aged 20–30 yr, a temperature-controlled chamber was positioned on the volar face of one forearm and used to raise surface temperature from 34 to 41°C. The time course of the resulting thermal hyperemia response was recorded with a laser-Doppler imager. In one experiment, each of eight subjects received an intravenous bolus of the antimuscarinic agent glycopyrrolate (4 μg/kg) on one visit and saline on the other. The thermal hyperemia response was determined within the hour after the injections. Glycopyrrolate effectively inhibited the skin vasodilation induced by iontophoresis of acetylcholine but did not influence the thermal hyperemia response. In a second experiment, conducted in five other subjects, 1 g of the cyclooxygenase inhibitor aspirin administered orally totally abolished the vasodilation induced in the skin by anodal current but also failed to modify the thermal hyperemia response. The present study excludes the stimulation of muscarinic receptors and the production of vasodilator prostaglandins as essential and nonredundant mechanisms for the vasodilation induced by local heating in human forearm skin.

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