Receptors for VIP and PACAP in Guinea Pig Cerebral Cortex: Effects on Cyclic AMP Synthesis and Characterization by 125I-VIP Binding

2005 ◽  
Vol 25 (3) ◽  
pp. 215-224 ◽  
Author(s):  
Jolanta B. Zawilska ◽  
Agnieszka Dejda ◽  
Pawel Niewiadomski ◽  
Illana Gozes ◽  
Jerzy Z. Nowak
1973 ◽  
Vol 132 (3) ◽  
pp. 475-482 ◽  
Author(s):  
Martin Reddington ◽  
Richard Rodnight ◽  
Michael Williams

1. The effect of various agents on the turnover of protein-bound phosphorus in respiring slices of cerebral cortex was studied. 2. Confirming previous work turnover was increased by the application of electrical pulses for 10s to the tissue. 3. Turnover was also increased by exposure of the slices for 10min to noradrenaline (0.5mm), 5-hydroxytryptamine (1μm) and histamine (0.1mm). 4. When slices were stimulated by electrical pulses in the presence of histamine the increase in turnover was the sum of the responses given by each agent above, suggesting that different phosphorylating systems were involved. 5. Tetrodotoxin (0.5μm) blocked the increased turnover due to electrical pulses, but not that due to histamine. Tetrodotoxin also prevented the increase in tissue cyclic AMP content caused by the application of electrical pulses. 6. Phosphoprotein turnover was not affected by adenosine, despite the increase in tissue cyclic AMP content given by this agent. 7. Adenosine blocked the phosphoprotein response to histamine, but did not affect the response to electrical pulses. 8. The results are discussed in relation to the hypothesis that the stimulation of protein phosphorus turnover by electrical pulses is secondary to the release of cyclic AMP in the tissue.


1977 ◽  
Vol 164 (1) ◽  
pp. 287-288
Author(s):  
C E Rowe

Certain observations reported previously from this laboratory have not proved reproducible. These are (1) the relatively rapid hydrolysis of added phosphatidylcholine by phospholipase A2 of tissue from the cerebral cortex of the guinea pig and (2) the stimulation by 10 micron-noradrenaline and by 1.0nM-cyclic AMP of the phospholipase A2-acylation system of isolated synaptic membranes.


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