StressCovidV1, PascalFrancis, Corpus, bibRecord, 000007

Knockdown of tropomyosin-related kinase B receptor expression in the nucleus accumbens shell prevents intermittent social defeat stress-induced cross-sensitization to amphetamine in rats

Identifieur interne : 000007 ( PascalFrancis/Corpus ); précédent : 000006; suivant : 000008

Knockdown of tropomyosin-related kinase B receptor expression in the nucleus accumbens shell prevents intermittent social defeat stress-induced cross-sensitization to amphetamine in rats

Auteurs : JUNSHI WANG ; Robert W. Bina ; Jeffrey C. Wingard ; Ernest F. Terwilliger ; Ronald P. Jr Hammer ; Ella M. Nikulina

Source :

European journal of neuroscience : (Print) [ 0953-816X ] ; 2014.

RBID : Pascal:14-0138262

Descripteurs français

Pascal (Inist)
- Tropomyosin kinase, Récepteur biologique, Noyau accumbens, Stress, Amfétamine, Facteur BDNF, Aire tegmentaire ventrale, Rat, Animal.

English descriptors

KwdEn :
- Amfetamine, Animal, Biological receptor, Brain derived neurotrophic factor, Nucleus accumbens, Rat, Stress, Tropomyosin kinase, Ventral tegmental area.

Abstract

The nucleus accumbens (NAc) is a critical brain region for the rewarding effects of drugs of abuse. Brain-derived neurotrophic factor (BDNF) can facilitate stress- and drug-induced neuroadaptation in the mesocorticolimbic system. BDNF-containing projections to the NAc originate from the ventral tegmental area (VTA) and the prefrontal cortex, and BDNF release activates tropomyosin-related kinase B (TrkB). In this study, we examined the necessity for BDNF-TrkB signaling in the NAc shell during social defeat stress-induced cross-sensitization to amphetamine. Adeno-associated virus expressing short hairpin RNA directed against TrkB (AAV-shTrkB) was infused bilaterally into the NAc shell to knock down TrkB, whereas AAV-GFP (green fluorescent protein) was used as the control virus. Rats were exposed to intermittent social defeat stress or handling procedures; amphetamine challenge was given at 10 days after the last defeat and locomotor activity was measured. Stressed rats that received the control virus showed cross-sensitization to amphetamine compared with the handled rats. In contrast, NAc TrkB knockdown prevented social defeat stress-induced cross-sensitization. TrkB knockdown in the NAc was found to reduce the level of phospho-extracellular signal-regulated kinase 1 in this region. NAc TrkB knockdown also prevented stress-induced elevation of BDNF and the glutamate receptor type 1 (GluA1) subunit of AMPA receptor in the VTA, as well as AFosB expression in the NAc. These findings indicated that BDNF-TrkB signaling in the NAc shell was required for social defeat stress-induced cross-sensitization. NAc TrkB-BDNF signaling also appeared to be involved in the regulation of GluA1 in the VTA, as well as in the NAc AFosB accumulation that could trigger cross-sensitization after social defeat stress.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A03		`1`		`@0 Eur. j. neurosci. : (Print)`
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A11	`02`	`1`		`@1 BINA (Robert W.)`
A11	`03`	`1`		`@1 WINGARD (Jeffrey C.)`
A11	`04`	`1`		`@1 TERWILLIGER (Ernest F.)`
A11	`05`	`1`		`@1 HAMMER (Ronald P. JR)`
A11	`06`	`1`		`@1 NIKULINA (Ella M.)`
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A14	`02`			`@1 Department of Basic Medical Sciences, University of Arizona, College of Medicine, 425 N 5th Street @2 Phoenix, AZ, 85004 @3 USA @Z 2 aut. @Z 5 aut. @Z 6 aut.`
A14	`03`			`@1 Beth Israel Deaconess Medical Center @2 Boston, MA @3 USA @Z 3 aut. @Z 4 aut.`
A14	`04`			`@1 Departments of Pharmacology and Psychiatry, University of Arizona, College of Medicine @2 Phoenix, AZ @3 USA @Z 5 aut.`
A20				`@1 1009-1017`
A21				`@1 2014`
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C01	`01`		`ENG`	@0 The nucleus accumbens (NAc) is a critical brain region for the rewarding effects of drugs of abuse. Brain-derived neurotrophic factor (BDNF) can facilitate stress- and drug-induced neuroadaptation in the mesocorticolimbic system. BDNF-containing projections to the NAc originate from the ventral tegmental area (VTA) and the prefrontal cortex, and BDNF release activates tropomyosin-related kinase B (TrkB). In this study, we examined the necessity for BDNF-TrkB signaling in the NAc shell during social defeat stress-induced cross-sensitization to amphetamine. Adeno-associated virus expressing short hairpin RNA directed against TrkB (AAV-shTrkB) was infused bilaterally into the NAc shell to knock down TrkB, whereas AAV-GFP (green fluorescent protein) was used as the control virus. Rats were exposed to intermittent social defeat stress or handling procedures; amphetamine challenge was given at 10 days after the last defeat and locomotor activity was measured. Stressed rats that received the control virus showed cross-sensitization to amphetamine compared with the handled rats. In contrast, NAc TrkB knockdown prevented social defeat stress-induced cross-sensitization. TrkB knockdown in the NAc was found to reduce the level of phospho-extracellular signal-regulated kinase 1 in this region. NAc TrkB knockdown also prevented stress-induced elevation of BDNF and the glutamate receptor type 1 (GluA1) subunit of AMPA receptor in the VTA, as well as AFosB expression in the NAc. These findings indicated that BDNF-TrkB signaling in the NAc shell was required for social defeat stress-induced cross-sensitization. NAc TrkB-BDNF signaling also appeared to be involved in the regulation of GluA1 in the VTA, as well as in the NAc AFosB accumulation that could trigger cross-sensitization after social defeat stress.
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C03	`04`	`X`	`SPA`	`@0 Estrés @5 04`
C03	`05`	`X`	`FRE`	`@0 Amfétamine @2 NK @2 FR @5 05`
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C03	`06`	`X`	`ENG`	`@0 Brain derived neurotrophic factor @5 06`
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C07	`04`	`X`	`ENG`	`@0 Basal ganglion @5 21`
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N21				`@1 174`
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Format Inist (serveur)

NO :	PASCAL 14-0138262 INIST
ET :	Knockdown of tropomyosin-related kinase B receptor expression in the nucleus accumbens shell prevents intermittent social defeat stress-induced cross-sensitization to amphetamine in rats
AU :	JUNSHI WANG; BINA (Robert W.); WINGARD (Jeffrey C.); TERWILLIGER (Ernest F.); HAMMER (Ronald P. JR); NIKULINA (Ella M.)
AF :	Neuroscience Program, Arizona State University/Tempe, AZ/Etats-Unis (1 aut., 5 aut.); Department of Basic Medical Sciences, University of Arizona, College of Medicine, 425 N 5th Street/Phoenix, AZ, 85004/Etats-Unis (2 aut., 5 aut., 6 aut.); Beth Israel Deaconess Medical Center/Boston, MA/Etats-Unis (3 aut., 4 aut.); Departments of Pharmacology and Psychiatry, University of Arizona, College of Medicine/Phoenix, AZ/Etats-Unis (5 aut.)
DT :	Publication en série; Niveau analytique
SO :	European journal of neuroscience : (Print); ISSN 0953-816X; Royaume-Uni; Da. 2014; Vol. 39; No. 5-6; Pp. 1009-1017; Bibl. 1 p.3/4
LA :	Anglais
EA :	The nucleus accumbens (NAc) is a critical brain region for the rewarding effects of drugs of abuse. Brain-derived neurotrophic factor (BDNF) can facilitate stress- and drug-induced neuroadaptation in the mesocorticolimbic system. BDNF-containing projections to the NAc originate from the ventral tegmental area (VTA) and the prefrontal cortex, and BDNF release activates tropomyosin-related kinase B (TrkB). In this study, we examined the necessity for BDNF-TrkB signaling in the NAc shell during social defeat stress-induced cross-sensitization to amphetamine. Adeno-associated virus expressing short hairpin RNA directed against TrkB (AAV-shTrkB) was infused bilaterally into the NAc shell to knock down TrkB, whereas AAV-GFP (green fluorescent protein) was used as the control virus. Rats were exposed to intermittent social defeat stress or handling procedures; amphetamine challenge was given at 10 days after the last defeat and locomotor activity was measured. Stressed rats that received the control virus showed cross-sensitization to amphetamine compared with the handled rats. In contrast, NAc TrkB knockdown prevented social defeat stress-induced cross-sensitization. TrkB knockdown in the NAc was found to reduce the level of phospho-extracellular signal-regulated kinase 1 in this region. NAc TrkB knockdown also prevented stress-induced elevation of BDNF and the glutamate receptor type 1 (GluA1) subunit of AMPA receptor in the VTA, as well as AFosB expression in the NAc. These findings indicated that BDNF-TrkB signaling in the NAc shell was required for social defeat stress-induced cross-sensitization. NAc TrkB-BDNF signaling also appeared to be involved in the regulation of GluA1 in the VTA, as well as in the NAc AFosB accumulation that could trigger cross-sensitization after social defeat stress.
CC :	002B02B02; 002A25
FD :	Tropomyosin kinase; Récepteur biologique; Noyau accumbens; Stress; Amfétamine; Facteur BDNF; Aire tegmentaire ventrale; Rat; Animal
FG :	Transferases; Enzyme; Encéphale; Noyau gris central; Système nerveux central; Stimulant SNC; Psychotrope; Rodentia; Mammalia; Vertebrata
ED :	Tropomyosin kinase; Biological receptor; Nucleus accumbens; Stress; Amfetamine; Brain derived neurotrophic factor; Ventral tegmental area; Rat; Animal
EG :	Transferases; Enzyme; Encephalon; Basal ganglion; Central nervous system; CNS stimulant; Psychotropic; Rodentia; Mammalia; Vertebrata
SD :	Tropomyosin kinase; Receptor biológico; Núcleo acumbens; Estrés; Anfetamina; Factor BDNF; Area tegmental ventral; Rata; Animal
LO :	INIST-22186.354000507517010270
ID :	14-0138262

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Pascal:14-0138262

Le document en format XML

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<front><div type="abstract" xml:lang="en">The nucleus accumbens (NAc) is a critical brain region for the rewarding effects of drugs of abuse. Brain-derived neurotrophic factor (BDNF) can facilitate stress- and drug-induced neuroadaptation in the mesocorticolimbic system. BDNF-containing projections to the NAc originate from the ventral tegmental area (VTA) and the prefrontal cortex, and BDNF release activates tropomyosin-related kinase B (TrkB). In this study, we examined the necessity for BDNF-TrkB signaling in the NAc shell during social defeat stress-induced cross-sensitization to amphetamine. Adeno-associated virus expressing short hairpin RNA directed against TrkB (AAV-shTrkB) was infused bilaterally into the NAc shell to knock down TrkB, whereas AAV-GFP (green fluorescent protein) was used as the control virus. Rats were exposed to intermittent social defeat stress or handling procedures; amphetamine challenge was given at 10 days after the last defeat and locomotor activity was measured. Stressed rats that received the control virus showed cross-sensitization to amphetamine compared with the handled rats. In contrast, NAc TrkB knockdown prevented social defeat stress-induced cross-sensitization. TrkB knockdown in the NAc was found to reduce the level of phospho-extracellular signal-regulated kinase 1 in this region. NAc TrkB knockdown also prevented stress-induced elevation of BDNF and the glutamate receptor type 1 (GluA1) subunit of AMPA receptor in the VTA, as well as AFosB expression in the NAc. These findings indicated that BDNF-TrkB signaling in the NAc shell was required for social defeat stress-induced cross-sensitization. NAc TrkB-BDNF signaling also appeared to be involved in the regulation of GluA1 in the VTA, as well as in the NAc AFosB accumulation that could trigger cross-sensitization after social defeat stress.</div>
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<fA08 i1="01" i2="1" l="ENG"><s1>Knockdown of tropomyosin-related kinase B receptor expression in the nucleus accumbens shell prevents intermittent social defeat stress-induced cross-sensitization to amphetamine in rats</s1>
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<fA11 i1="01" i2="1"><s1>JUNSHI WANG</s1>
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<fA11 i1="02" i2="1"><s1>BINA (Robert W.)</s1>
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<fA11 i1="03" i2="1"><s1>WINGARD (Jeffrey C.)</s1>
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<fA11 i1="06" i2="1"><s1>NIKULINA (Ella M.)</s1>
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<fA14 i1="02"><s1>Department of Basic Medical Sciences, University of Arizona, College of Medicine, 425 N 5th Street</s1>
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<sZ>2 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>6 aut.</sZ>
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<fA14 i1="03"><s1>Beth Israel Deaconess Medical Center</s1>
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<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Departments of Pharmacology and Psychiatry, University of Arizona, College of Medicine</s1>
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<sZ>5 aut.</sZ>
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<fC01 i1="01" l="ENG"><s0>The nucleus accumbens (NAc) is a critical brain region for the rewarding effects of drugs of abuse. Brain-derived neurotrophic factor (BDNF) can facilitate stress- and drug-induced neuroadaptation in the mesocorticolimbic system. BDNF-containing projections to the NAc originate from the ventral tegmental area (VTA) and the prefrontal cortex, and BDNF release activates tropomyosin-related kinase B (TrkB). In this study, we examined the necessity for BDNF-TrkB signaling in the NAc shell during social defeat stress-induced cross-sensitization to amphetamine. Adeno-associated virus expressing short hairpin RNA directed against TrkB (AAV-shTrkB) was infused bilaterally into the NAc shell to knock down TrkB, whereas AAV-GFP (green fluorescent protein) was used as the control virus. Rats were exposed to intermittent social defeat stress or handling procedures; amphetamine challenge was given at 10 days after the last defeat and locomotor activity was measured. Stressed rats that received the control virus showed cross-sensitization to amphetamine compared with the handled rats. In contrast, NAc TrkB knockdown prevented social defeat stress-induced cross-sensitization. TrkB knockdown in the NAc was found to reduce the level of phospho-extracellular signal-regulated kinase 1 in this region. NAc TrkB knockdown also prevented stress-induced elevation of BDNF and the glutamate receptor type 1 (GluA1) subunit of AMPA receptor in the VTA, as well as AFosB expression in the NAc. These findings indicated that BDNF-TrkB signaling in the NAc shell was required for social defeat stress-induced cross-sensitization. NAc TrkB-BDNF signaling also appeared to be involved in the regulation of GluA1 in the VTA, as well as in the NAc AFosB accumulation that could trigger cross-sensitization after social defeat stress.</s0>
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<s5>01</s5>
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<server><NO>PASCAL 14-0138262 INIST</NO>
<ET>Knockdown of tropomyosin-related kinase B receptor expression in the nucleus accumbens shell prevents intermittent social defeat stress-induced cross-sensitization to amphetamine in rats</ET>
<AU>JUNSHI WANG; BINA (Robert W.); WINGARD (Jeffrey C.); TERWILLIGER (Ernest F.); HAMMER (Ronald P. JR); NIKULINA (Ella M.)</AU>
<AF>Neuroscience Program, Arizona State University/Tempe, AZ/Etats-Unis (1 aut., 5 aut.); Department of Basic Medical Sciences, University of Arizona, College of Medicine, 425 N 5th Street/Phoenix, AZ, 85004/Etats-Unis (2 aut., 5 aut., 6 aut.); Beth Israel Deaconess Medical Center/Boston, MA/Etats-Unis (3 aut., 4 aut.); Departments of Pharmacology and Psychiatry, University of Arizona, College of Medicine/Phoenix, AZ/Etats-Unis (5 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>European journal of neuroscience : (Print); ISSN 0953-816X; Royaume-Uni; Da. 2014; Vol. 39; No. 5-6; Pp. 1009-1017; Bibl. 1 p.3/4</SO>
<LA>Anglais</LA>
<EA>The nucleus accumbens (NAc) is a critical brain region for the rewarding effects of drugs of abuse. Brain-derived neurotrophic factor (BDNF) can facilitate stress- and drug-induced neuroadaptation in the mesocorticolimbic system. BDNF-containing projections to the NAc originate from the ventral tegmental area (VTA) and the prefrontal cortex, and BDNF release activates tropomyosin-related kinase B (TrkB). In this study, we examined the necessity for BDNF-TrkB signaling in the NAc shell during social defeat stress-induced cross-sensitization to amphetamine. Adeno-associated virus expressing short hairpin RNA directed against TrkB (AAV-shTrkB) was infused bilaterally into the NAc shell to knock down TrkB, whereas AAV-GFP (green fluorescent protein) was used as the control virus. Rats were exposed to intermittent social defeat stress or handling procedures; amphetamine challenge was given at 10 days after the last defeat and locomotor activity was measured. Stressed rats that received the control virus showed cross-sensitization to amphetamine compared with the handled rats. In contrast, NAc TrkB knockdown prevented social defeat stress-induced cross-sensitization. TrkB knockdown in the NAc was found to reduce the level of phospho-extracellular signal-regulated kinase 1 in this region. NAc TrkB knockdown also prevented stress-induced elevation of BDNF and the glutamate receptor type 1 (GluA1) subunit of AMPA receptor in the VTA, as well as AFosB expression in the NAc. These findings indicated that BDNF-TrkB signaling in the NAc shell was required for social defeat stress-induced cross-sensitization. NAc TrkB-BDNF signaling also appeared to be involved in the regulation of GluA1 in the VTA, as well as in the NAc AFosB accumulation that could trigger cross-sensitization after social defeat stress.</EA>
<CC>002B02B02; 002A25</CC>
<FD>Tropomyosin kinase; Récepteur biologique; Noyau accumbens; Stress; Amfétamine; Facteur BDNF; Aire tegmentaire ventrale; Rat; Animal</FD>
<FG>Transferases; Enzyme; Encéphale; Noyau gris central; Système nerveux central; Stimulant SNC; Psychotrope; Rodentia; Mammalia; Vertebrata</FG>
<ED>Tropomyosin kinase; Biological receptor; Nucleus accumbens; Stress; Amfetamine; Brain derived neurotrophic factor; Ventral tegmental area; Rat; Animal</ED>
<EG>Transferases; Enzyme; Encephalon; Basal ganglion; Central nervous system; CNS stimulant; Psychotropic; Rodentia; Mammalia; Vertebrata</EG>
<SD>Tropomyosin kinase; Receptor biológico; Núcleo acumbens; Estrés; Anfetamina; Factor BDNF; Area tegmental ventral; Rata; Animal</SD>
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Knockdown of tropomyosin-related kinase B receptor expression in the nucleus accumbens shell prevents intermittent social defeat stress-induced cross-sensitization to amphetamine in rats

Knockdown of tropomyosin-related kinase B receptor expression in the nucleus accumbens shell prevents intermittent social defeat stress-induced cross-sensitization to amphetamine in rats

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