scholarly journals Regional expression of extracellular signal-regulated kinase 1 and 2 mRNA in a morphine-induced conditioned place preference model

2014 ◽  
Vol 1543 ◽  
pp. 191-199 ◽  
Author(s):  
Jing Yuan Ma ◽  
Shan Zhi Gu ◽  
Min Meng ◽  
Yong Hui Dang ◽  
Chong Ya Huang ◽  
...  
2020 ◽  
Vol 34 (12) ◽  
pp. 1357-1370
Author(s):  
Simona Porru ◽  
Riccardo Maccioni ◽  
Valentina Bassareo ◽  
Alessandra T Peana ◽  
John D Salamone ◽  
...  

Background: Epidemiological studies indicate a rise in the combined consumption of caffeinated and alcoholic beverages, which can lead to increased risk of alcoholic-beverage overconsumption. However, the effects of the combination of caffeine and ethanol in animal models related to aspects of drug addiction are still underexplored. Aims: To characterize the pharmacological interaction between caffeine and ethanol and establish if caffeine can affect the ability of ethanol (2 g/kg) to elicit conditioned place preference and conditioned place aversion, we administered caffeine (3 or 15 mg/kg) to male CD-1 mice before saline or ethanol. Moreover, we determined if these doses of caffeine could affect ethanol (2 g/kg) elicited extracellular signal-regulated kinase phosphorylation in brain areas, nucleus accumbens, bed nucleus of stria terminalis, central nucleus of the amygdala, and basolateral amygdala, previously associated with this type of associative learning. Results: In the place-conditioning paradigm, caffeine did not have an effect on its own, whereas ethanol elicited significant conditioned-place preference and conditioned-place aversion. Caffeine (15 mg/kg) significantly prevented the acquisition of ethanol-elicited conditioned-place preference and, at both doses, also prevented the acquisition of ethanol-elicited conditioned-place aversion. Moreover, both doses of caffeine also prevented ethanol-elicited extracellular signal-regulated kinase phosphorylation expression in all brain areas examined. Conclusions: The present data indicate a functional antagonistic action of caffeine and ethanol on associative learning and extracellular signal-regulated kinase phosphorylation after an acute interaction. These results could provide exciting grounds for further studies, also in a translational perspective, of their pharmacological interaction modulating other processes involved in drug consumption and addiction.


2019 ◽  
Vol 10 (7) ◽  
pp. 3271-3283 ◽  
Author(s):  
Taleen S. Der-Ghazarian ◽  
Delaram Charmchi ◽  
Sean N. Noudali ◽  
Samantha N. Scott ◽  
Michael C. Holter ◽  
...  

2021 ◽  
Vol 12 (05) ◽  
pp. 100-108
Author(s):  
Cheyenne Moffett ◽  
Katherine J. Kost ◽  
Austen Thompson ◽  
Michael H. Ossipov ◽  
Joseph V. Pergolizzi Jr. ◽  
...  

2017 ◽  
Vol 363 (1) ◽  
pp. 66-79 ◽  
Author(s):  
A. J. Brock ◽  
S. M. G. Goody ◽  
A. N. Mead ◽  
A. Sudwarts ◽  
M.O. Parker ◽  
...  

Author(s):  
V. Şorodoc ◽  
G. Rusu-Zota ◽  
P. Nechita ◽  
C. Moraru ◽  
O. M. Manole

AbstractAgmatine (AG), idazoxan (IDZ), and efaroxan (EFR) are imidazoline receptor ligands with beneficial effects in central nervous system disorders. The present study aimed to evaluate the interaction between AG, IDZ, and EFR with an opiate, tramadol (TR), in a conditioned place preference (CPP) paradigm. In the experiment, we used five groups with 8 adult male Wistar rats each. During the condition session, on days 2, 4, 6, and 8, the rats received the drugs (saline, or TR, or IDZ and TR, or EFR and TR, or AG and TR) and were placed in their least preferred compartment. On days 1, 3, 5, and 7, the rats received saline in the preferred compartment. In the preconditioning, the preferred compartment was determined. In the postconditioning, the preference for one of the compartments was reevaluated. TR increased the time spent in the non-preferred compartment. AG decreased time spent in the TR-paired compartment. EFR, more than IDZ, reduced the time spent in the TR-paired compartment, but without statistical significance. AG reversed the TR-induced CPP, while EFR and IDZ only decreased the time spent in the TR-paired compartment, without statistical significance.


Author(s):  
GOFARANA WILAR ◽  
KOHJI FUKUNAGA

Objective: Nicotine is an active compound in tobacco and has a rewarding effect in the central nervous system (CNS), which may lead to dependence. Although nicotine dependence is elucidated by brain mechanisms, synaptic molecular substrates underlying the dependence remain unclear. We hypothesized that reward signaling is mediated by dopamine and glutamate receptors, in where calcium/calmodulin-dependent kinase II (CaMKII) and extracellular signal-regulated kinase (ERK) may mediate the synaptic signaling of dependence. Methods: To investigate the roles of both CaMKII and ERK on nicotine dependence were assessed by conditioned place preference (CPP) methods followed by dissection. One day after conditioning, preference scores were measured to evaluate nicotine dependence. Mice were sacrificed and their striatum were dissected out for immunoblotting analyses of CaMKII and ERK phosphorylation. Results: Nicotine-induced conditioned place preference as a symptom of nicotine dependence. CaMKII and ERK phosphorylation in striatum significantly increased along with the development of nicotine dependence. Conclusion: We should next apply pharmacological strategies to manipulate CaMKII and ERK signaling. In particular, disruption of reconsolidation by disrupting CaMKII and ERK signaling may propose an attractive therapeutic approach to inhibit nicotine dependence.


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