Faculty Opinions recommendation of Additive wake-promoting actions of medial basal forebrain noradrenergic alpha1- and beta-receptor stimulation.

Author(s):  
Gary Aston-Jones
1987 ◽  
Vol 253 (4) ◽  
pp. F636-F641
Author(s):  
N. S. Morgunov

Electrophysiological response to isoproterenol stimulation was studied in isolated perfused salamander proximal tubules. The addition of 10(-5) M isoproterenol to the bath superfusate depolarized both the cell membrane, and transepithelial potentials by 2.2 +/- 0.2 and 0.31 +/- 0.04 mV, respectively (P less than 0.01, n = 35) and significantly reduced the apical-to-basolateral membrane resistance ratio by 30% (P less than 0.01, n = 7) from a control value of 3.7 +/- 0.6. These responses were blocked by 10(-6) M propranolol but not mimicked by 10(-4) M adenosine 3',5'-cyclic monophosphate. Qualitatively similar effects were observed with 10(-3) and 10(-7) M isoproterenol. Further characterization of the 10(-5) M isoproterenol response revealed 1) a 50% reduction in the response following the removal of organic substrates from the luminal perfusate, 2) an absolute requirement for sodium, and 3) an absolute requirement for a functioning basolateral Na+-K+-ATPase. The data suggest that beta-receptor stimulation may increase sodium reabsorption by activating sodium cotransport systems.


2005 ◽  
Vol 289 (6) ◽  
pp. R1715-R1723 ◽  
Author(s):  
Melvi M. Methippara ◽  
Sunil Kumar ◽  
Md. Noor Alam ◽  
Ronald Szymusiak ◽  
Dennis McGinty

Evidence suggests that adenosine (AD) is an endogenous sleep factor. The hypnogenic action of AD is mediated through its inhibitory A1 and excitatory A2A receptors. Although AD is thought to be predominantly active in the wake-active region of the basal forebrain (BF), a hypnogenic action of AD has been demonstrated in several other brain areas, including the preoptic area. We hypothesized that in lateral preoptic area (LPOA), a region with an abundance of sleep-active neurons, AD acting via A1 receptors would induce waking by inhibition of sleep-active neurons and that AD acting via A2A receptors would promote sleep by stimulating the sleep-active neurons. To this end, we studied the effects on sleep of an AD transport inhibitor, nitrobenzyl-thio-inosine (NBTI) and A1 and A2A receptor agonists/antagonists by microdialyzing them into the LPOA. The results showed that, in the sleep-promoting area of LPOA: 1) A1 receptor stimulation or inhibition of AD transport by NBTI induced waking and 2) A2A receptor stimulation induced sleep. We also confirmed that NBTI administration in the wake promoting area of the BF increased sleep. The effects of AD could be mediated either directly or indirectly via interaction with other neurotransmitter systems. These observations support a hypothesis that AD mediated effects on sleep-wake cycles are site and receptor dependent.


1987 ◽  
Vol 21 (2-3) ◽  
pp. 256
Author(s):  
Takeshi Ishide ◽  
Toshihiro Saito ◽  
Kazuo Noda ◽  
Masashi Takahashi ◽  
Akira Nakayama ◽  
...  

2005 ◽  
Vol 119 (3) ◽  
pp. 743-751 ◽  
Author(s):  
C. W. Berridge ◽  
R. L. Stellick ◽  
B. E. Schmeichel

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