Rasgrf2 controls noradrenergic involvement in the acute and subchronic effects of alcohol in the brain View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2014-04-16

AUTHORS

Alanna C. Easton, Andrea Rotter, Anbarasu Lourdusamy, Sylvane Desrivières, Alberto Fernández-Medarde, Teresa Biermann, Cathy Fernandes, Eugenio Santos, Johannes Kornhuber, Gunter Schumann, Christian P. Müller

ABSTRACT

RationaleAlcohol addiction is a major psychiatric disease, and yet, the underlying molecular adaptations in the brain remain unclear. Recent evidence suggests a functional role for the ras-specific guanine-nucleotide releasing factor 2 (Rasgrf2) in alcoholism. Rasgrf2−/− mice consume less alcohol and show entirely absent dopamine responses to an alcohol challenge compared to wild types (WT).ObjectiveIn order to further investigate how Rasgrf2 modifies the acute and subchronic effects of alcohol in the brain, we investigated its effects on the noradrenergic and serotonergic systems.MethodsWe measured noradrenaline and serotonin activity in the brain by in vivo microdialysis and RNA expression by chip analysis and RT-PCR after acute and sub-chronic alcohol exposure in Rasgrf2−/− and WT mice.ResultsIn vivo microdialysis showed a significantly reduced noradrenergic response and an absent serotonergic response in the nucleus accumbens (NAcc) and caudate putamen (CPu) after an alcohol challenge in Rasgrf2−/− mice. A co-expression analysis showed that there is a high correlation between Rasgrf2 and α2 adrenoceptor RNA expression in the ventral striatum in naïve animals. Accordingly, we further assessed the role of Rasgrf2 in the response of the noradrenergic system to subchronic alcohol exposure. A decrease in β1 adrenoceptor gene expression was seen in Rasgrf2+/+, but not Rasgrf2−/− mice following alcohol exposure. Conversely, alcohol resulted in a decrease in both β2 and α2 adrenoceptor gene expression in knockout but not WT Rasgrf2 mice.ConclusionsThese findings suggest that adaptations in the noradrenergic system contribute to the Rasgrf2 enhanced risk of alcoholism. More... »

PAGES

4199-4209

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00213-014-3562-x

DOI

http://dx.doi.org/10.1007/s00213-014-3562-x

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1033756969

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24737505


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26 schema:description RationaleAlcohol addiction is a major psychiatric disease, and yet, the underlying molecular adaptations in the brain remain unclear. Recent evidence suggests a functional role for the ras-specific guanine-nucleotide releasing factor 2 (Rasgrf2) in alcoholism. Rasgrf2−/− mice consume less alcohol and show entirely absent dopamine responses to an alcohol challenge compared to wild types (WT).ObjectiveIn order to further investigate how Rasgrf2 modifies the acute and subchronic effects of alcohol in the brain, we investigated its effects on the noradrenergic and serotonergic systems.MethodsWe measured noradrenaline and serotonin activity in the brain by in vivo microdialysis and RNA expression by chip analysis and RT-PCR after acute and sub-chronic alcohol exposure in Rasgrf2−/− and WT mice.ResultsIn vivo microdialysis showed a significantly reduced noradrenergic response and an absent serotonergic response in the nucleus accumbens (NAcc) and caudate putamen (CPu) after an alcohol challenge in Rasgrf2−/− mice. A co-expression analysis showed that there is a high correlation between Rasgrf2 and α2 adrenoceptor RNA expression in the ventral striatum in naïve animals. Accordingly, we further assessed the role of Rasgrf2 in the response of the noradrenergic system to subchronic alcohol exposure. A decrease in β1 adrenoceptor gene expression was seen in Rasgrf2+/+, but not Rasgrf2−/− mice following alcohol exposure. Conversely, alcohol resulted in a decrease in both β2 and α2 adrenoceptor gene expression in knockout but not WT Rasgrf2 mice.ConclusionsThese findings suggest that adaptations in the noradrenergic system contribute to the Rasgrf2 enhanced risk of alcoholism.
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32 schema:keywords ConclusionsThese findings
33 MethodsWe
34 ObjectiveIn order
35 RNA expression
36 RT-PCR
37 RasGRF2
38 Recent evidence
39 WT mice
40 accumbens
41 activity
42 adaptation
43 addiction
44 adrenoceptor gene expression
45 alcohol
46 alcohol challenge
47 alcohol exposure
48 alcoholism
49 analysis
50 animals
51 brain
52 caudate putamen
53 challenges
54 chip analysis
55 co-expression analysis
56 correlation
57 decrease
58 disease
59 dopamine response
60 effect
61 evidence
62 exposure
63 expression
64 factor 2
65 findings
66 functional role
67 gene expression
68 high correlation
69 involvement
70 knockout
71 less alcohol
72 major psychiatric diseases
73 mice
74 microdialysis
75 modifies
76 molecular adaptations
77 naïve animals
78 noradrenaline
79 noradrenergic involvement
80 noradrenergic responses
81 noradrenergic system
82 nucleus accumbens
83 order
84 psychiatric diseases
85 putamen
86 response
87 risk
88 risk of alcoholism
89 role
90 serotonergic responses
91 serotonergic system
92 serotonin activity
93 striatum
94 subchronic effects
95 system
96 types
97 ventral striatum
98 vivo microdialysis
99 wild type
100 β2
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