scholarly journals Effects of protein kinase A inhibitor and activator on rewarding effects of SKF-82958 microinjected into nucleus accumbens shell of ad libitum fed and food-restricted rats

2011 ◽  
Vol 221 (4) ◽  
pp. 589-599
Author(s):  
Soledad Cabeza de Vaca ◽  
Xing-Xiang Peng ◽  
Seth Concors ◽  
Casey Farin ◽  
Elena Lascu ◽  
...  
2006 ◽  
Vol 84 (2) ◽  
pp. 203-211 ◽  
Author(s):  
Samuel B. Kombian ◽  
Kethireddy V.V. Ananthalakshmi ◽  
Subramanian S. Parvathy ◽  
Wandikayi C. Matowe

We recently reported that the activation of cholecystokinin-2 receptors depress evoked excitatory postsynaptic currents (EPSCs) in nucleus accumbens (NAc) indirectly through γ-aminobutyric acid (GABA) acting on γ-aminobutyric acid-B (GABAB) receptors. Here, we determined the second messenger system that couples cholecystokinin-2 receptors to the observed synaptic depression. Using in vitro forebrain slices of rats and whole-cell patch recording, we tested the hypothesis that cholecystokinin-2 receptors are coupled to cAMP and protein kinase A signaling pathway. Cholecystokinin-8S induced inward currents and depressed evoked EPSCs. Forskolin, an activator of adenylyl cyclase and rolipram that is an inhibitor of phosphodiesterase type IV, independently increased EPSC amplitude and blocked the inward current and synaptic depression induced by cholecystokinin-8S. Furthermore, the membrane-permeable cAMP analog, 8-bromo-cAMP, blocked the cholecystokinin-8S effects. H89, a protein kinase A inhibitor, also blocked cholecystokinin-8S effects. However, depression of the evoked EPSC by baclofen, a GABAB receptor agonist, was not blocked by H89 or forskolin. These findings indicate that cholecystokinin-2, but not GABAB, receptors are coupled to the adenylyl cyclase – cAMP – protein kinase A signaling pathway in the NAc to induce inward currents and cause synaptic depression.


2005 ◽  
Vol 313 (2) ◽  
pp. 594-603 ◽  
Author(s):  
Marion Wittmann ◽  
Michael J. Marino ◽  
Darrell A. Henze ◽  
Guy R. Seabrook ◽  
P. Jeffrey Conn

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