Gene expression regulation following behavioral sensitization to cocaine in transgenic mice lacking the glucocorticoid receptor in the brain

Autor: M. Le Moal, Mohamed Jaber, Véronique Deroche-Gamonet, R. Izawa, Christoph Kellendonk, I. Sillaber, Pier Vincenzo Piazza, François Tronche
Přispěvatelé: Institut de physiologie et biologie cellulaires (IPBC), Université de Poitiers-Centre National de la Recherche Scientifique (CNRS), Génétique moléculaire, neurophysiologie et comportement (GMNC), Centre National de la Recherche Scientifique (CNRS)
Rok vydání: 2006
Předmět:
Male
comportement
Dynorphin
Substance P
Synaptic Transmission
Mice
0302 clinical medicine
Mineralocorticoid receptor
Glucocorticoid receptor
Cocaine
Dopamine Uptake Inhibitors
Receptors
Kainic Acid

neuromediateurs
neurone
In Situ Hybridization
PASCAL
0303 health sciences
Kainic Acid
Behavior
Animal

General Neuroscience
Enkephalins
3. Good health
Dopamine receptor
NMDA receptor
dépendance
hormones
hormone substitutes
and hormone antagonists

expression des gènes
medicine.medical_specialty
Mice
Transgenic

[SDV.BC]Life Sciences [q-bio]/Cellular Biology
Biology
Dynorphins
Receptors
N-Methyl-D-Aspartate

03 medical and health sciences
Receptors
Glucocorticoid

Internal medicine
Dopamine receptor D2
medicine
Animals
ACTH receptor
RNA
Messenger

030304 developmental biology
Brain Chemistry
Sigma-1 receptor
Receptors
Dopamine D2

Receptors
Dopamine D1

gène
neurosciences
adaptation au stress
Endocrinology
Gene Expression Regulation
030217 neurology & neurosurgery
Zdroj: Neuroscience
Neuroscience, Elsevier-International Brain Research Organization, 2006, 137, pp.915-924
ISSN: 0306-4522
1873-7544
Popis: Several findings suggest that glucocorticoid hormones influence the propensity of an individual to develop cocaine abuse. These hormones activate two related transcription factors, the glucocorticoid receptor and the mineralocorticoid receptor. We have shown previously that mice carrying a mutation of the glucocorticoid receptor gene specifically in neural cells, glucocorticoid receptor knock-out in the brain, show a dramatic decrease in cocaine-induced self-administration and no behavioral sensitization to this drug, two experimental procedures considered relevant models of addiction. Here, we investigated in glucocorticoid receptor knock-out in the brain mice the consequences of this mutation at the level of the expression of neuropeptide, dopamine receptor and glutamate receptor subunit mRNAs. We quantified mRNA levels in the cortex, striatum and accumbens under basal conditions and following acute or repeated cocaine treatments. Our results show that, under basal conditions, neuropeptide (substance P, dynorphin) and dopamine receptor (D1, D2) mRNAs were decreased in glucocorticoid receptor knock-out in the brain mice in the dorsal striatum but not in the accumbens. However, cocaine-induced changes in the levels of these mRNAs were not modified in glucocorticoid receptor knock-out in the brain mice. In contrast, mutant mice showed altered response in mRNA levels of N-methyl-D-aspartate, GLUR5 and GLUR6 glutamate receptor subunits as well as of enkephalin following cocaine administration. These modifications may be associated to decrease of behavioral effects of cocaine observed in glucocorticoid receptor knock-out in the brain mice.
Databáze: OpenAIRE