ParkinsonCanadaV1, PascalFrancis, Corpus, bibRecord, 000920

Maturation but not survival of dopaminergic nigrostriatal neurons is affected in developing and aging BDNF-deficient mice

Identifieur interne : 000920 ( PascalFrancis/Corpus ); précédent : 000919; suivant : 000921

Maturation but not survival of dopaminergic nigrostriatal neurons is affected in developing and aging BDNF-deficient mice

Auteurs : Sarah A. Baker ; Lianne E. Stanford ; Richard E. Brown ; Theo Hagg

Source :

Brain research [ 0006-8993 ] ; 2005.

RBID : Pascal:05-0200638

Descripteurs français

Pascal (Inist)
- Neurone dopaminergique, Voie nigrostriatale, Développement, Sénescence, Facteur BDNF, Locus niger, Mutation, Tyrosine 3-monooxygenase, Parkinson maladie, Animal, Souris.

English descriptors

KwdEn :
- Animal, Brain derived neurotrophic factor, Development, Dopaminergic neuron, Locus niger, Mouse, Mutation, Nigrostriatal pathway, Parkinson disease, Senescence, Tyrosine 3-monooxygenase.

Abstract

Brain-derived neurotrophic factor (BDNF) promotes survival of injured dopaminergic nigrostriatal neurons of the adult rodent substantia nigra pars compacta, as well their development in vitro. BDNF deficiency may play a role in Parkinson's disease, as the surviving dopaminergic nigrostriatal neurons have reduced levels of BDNF, and a BDNF gene polymorphism is present in a subpopulation of patients. Here, we investigated whether a lack of BDNF in early postnatal BDNF-/- mice or a chronic 50% reduction in BDNF levels in aging BDNF+/- mice would affect the survival of the dopaminergic nigrostriatal neurons. In general terms, BDNF-/- and BDNF+/- mice had morphologically and quantitatively normal nigrostriatal neurons at any time between postnatal day 14 (P14) and 18 months, when compared to their wild-type littermates. BDNF-/- mice (P14 and P21 only) had fewer dopaminergic dendrites in the substantia nigra, suggesting that BDNF plays a role in phenotypic maturation, but not in neuronal birth or survival. BDNF-/- mice also had aberrant tyrosine hydroxylase (TH) positive cell bodies in the pars reticulata. During adulthood and aging, BDNF+/- mice performed equally well as their wild-type littermates in tests of motor coordination, and both showed aging-related decreases in the size of the dopaminergic neurons as well as in motor coordination. These results suggest that chronic deficits in BDNF alone do not affect survival or function of dopaminergic nigrostriatal neurons during aging or potentially even in Parkinson's disease.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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Format Inist (serveur)

NO :	PASCAL 05-0200638 INIST
ET :	Maturation but not survival of dopaminergic nigrostriatal neurons is affected in developing and aging BDNF-deficient mice
AU :	BAKER (Sarah A.); STANFORD (Lianne E.); BROWN (Richard E.); HAGG (Theo)
AF :	Kentucky Spinal Cord Injury Research Center, University of Louisville/Louisville, KY 40292/Etats-Unis (1 aut., 4 aut.); Department of Anatomical Sciences and Neurobiology, University of Louisville/Louisville, KY 40292/Etats-Unis (1 aut.); Department of Psychology, Dalhousie University/Halifax, Nova Scotia/Canada (2 aut., 3 aut.); Department of Neurological Surgery, University of Louisville/Louisville, KY 40292/Etats-Unis (4 aut.); Department of Pharmacology and Toxicology, University of Louisville/Louisville, KY 40292/Etats-Unis (4 aut.)
DT :	Publication en série; Niveau analytique
SO :	Brain research; ISSN 0006-8993; Coden BRREAP; Pays-Bas; Da. 2005; Vol. 1039; No. 1-2; Pp. 177-188; Bibl. 78 ref.
LA :	Anglais
EA :	Brain-derived neurotrophic factor (BDNF) promotes survival of injured dopaminergic nigrostriatal neurons of the adult rodent substantia nigra pars compacta, as well their development in vitro. BDNF deficiency may play a role in Parkinson's disease, as the surviving dopaminergic nigrostriatal neurons have reduced levels of BDNF, and a BDNF gene polymorphism is present in a subpopulation of patients. Here, we investigated whether a lack of BDNF in early postnatal BDNF-/- mice or a chronic 50% reduction in BDNF levels in aging BDNF+/- mice would affect the survival of the dopaminergic nigrostriatal neurons. In general terms, BDNF-/- and BDNF+/- mice had morphologically and quantitatively normal nigrostriatal neurons at any time between postnatal day 14 (P14) and 18 months, when compared to their wild-type littermates. BDNF-/- mice (P14 and P21 only) had fewer dopaminergic dendrites in the substantia nigra, suggesting that BDNF plays a role in phenotypic maturation, but not in neuronal birth or survival. BDNF-/- mice also had aberrant tyrosine hydroxylase (TH) positive cell bodies in the pars reticulata. During adulthood and aging, BDNF+/- mice performed equally well as their wild-type littermates in tests of motor coordination, and both showed aging-related decreases in the size of the dopaminergic neurons as well as in motor coordination. These results suggest that chronic deficits in BDNF alone do not affect survival or function of dopaminergic nigrostriatal neurons during aging or potentially even in Parkinson's disease.
CC :	002B17G; 002B17A01
FD :	Neurone dopaminergique; Voie nigrostriatale; Développement; Sénescence; Facteur BDNF; Locus niger; Mutation; Tyrosine 3-monooxygenase; Parkinson maladie; Animal; Souris
FG :	Oxidoreductases; Enzyme; Encéphale pathologie; Système nerveux central; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Système nerveux pathologie; Rodentia; Mammalia; Vertebrata
ED :	Dopaminergic neuron; Nigrostriatal pathway; Development; Senescence; Brain derived neurotrophic factor; Locus niger; Mutation; Tyrosine 3-monooxygenase; Parkinson disease; Animal; Mouse
EG :	Oxidoreductases; Enzyme; Cerebral disorder; Central nervous system; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Nervous system diseases; Rodentia; Mammalia; Vertebrata
SD :	Neurona dopaminérgica; Vía nigroestriatal; Desarrollo; Senescencia; Factor BDNF; Locus níger; Mutación; Tyrosine 3-monooxygenase; Parkinson enfermedad; Animal; Ratón
LO :	INIST-12895.354000125607780210
ID :	05-0200638

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Pascal:05-0200638

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<front><div type="abstract" xml:lang="en">Brain-derived neurotrophic factor (BDNF) promotes survival of injured dopaminergic nigrostriatal neurons of the adult rodent substantia nigra pars compacta, as well their development in vitro. BDNF deficiency may play a role in Parkinson's disease, as the surviving dopaminergic nigrostriatal neurons have reduced levels of BDNF, and a BDNF gene polymorphism is present in a subpopulation of patients. Here, we investigated whether a lack of BDNF in early postnatal BDNF-/- mice or a chronic 50% reduction in BDNF levels in aging BDNF+/- mice would affect the survival of the dopaminergic nigrostriatal neurons. In general terms, BDNF-/- and BDNF+/- mice had morphologically and quantitatively normal nigrostriatal neurons at any time between postnatal day 14 (P14) and 18 months, when compared to their wild-type littermates. BDNF-/- mice (P14 and P21 only) had fewer dopaminergic dendrites in the substantia nigra, suggesting that BDNF plays a role in phenotypic maturation, but not in neuronal birth or survival. BDNF-/- mice also had aberrant tyrosine hydroxylase (TH) positive cell bodies in the pars reticulata. During adulthood and aging, BDNF+/- mice performed equally well as their wild-type littermates in tests of motor coordination, and both showed aging-related decreases in the size of the dopaminergic neurons as well as in motor coordination. These results suggest that chronic deficits in BDNF alone do not affect survival or function of dopaminergic nigrostriatal neurons during aging or potentially even in Parkinson's disease.</div>
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<sZ>3 aut.</sZ>
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<fA14 i1="04"><s1>Department of Neurological Surgery, University of Louisville</s1>
<s2>Louisville, KY 40292</s2>
<s3>USA</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Department of Pharmacology and Toxicology, University of Louisville</s1>
<s2>Louisville, KY 40292</s2>
<s3>USA</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA20><s1>177-188</s1>
</fA20>
<fA21><s1>2005</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>12895</s2>
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<fA44><s0>0000</s0>
<s1>© 2005 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>78 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>05-0200638</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
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<fA64 i1="01" i2="1"><s0>Brain research</s0>
</fA64>
<fA66 i1="01"><s0>NLD</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Brain-derived neurotrophic factor (BDNF) promotes survival of injured dopaminergic nigrostriatal neurons of the adult rodent substantia nigra pars compacta, as well their development in vitro. BDNF deficiency may play a role in Parkinson's disease, as the surviving dopaminergic nigrostriatal neurons have reduced levels of BDNF, and a BDNF gene polymorphism is present in a subpopulation of patients. Here, we investigated whether a lack of BDNF in early postnatal BDNF-/- mice or a chronic 50% reduction in BDNF levels in aging BDNF+/- mice would affect the survival of the dopaminergic nigrostriatal neurons. In general terms, BDNF-/- and BDNF+/- mice had morphologically and quantitatively normal nigrostriatal neurons at any time between postnatal day 14 (P14) and 18 months, when compared to their wild-type littermates. BDNF-/- mice (P14 and P21 only) had fewer dopaminergic dendrites in the substantia nigra, suggesting that BDNF plays a role in phenotypic maturation, but not in neuronal birth or survival. BDNF-/- mice also had aberrant tyrosine hydroxylase (TH) positive cell bodies in the pars reticulata. During adulthood and aging, BDNF+/- mice performed equally well as their wild-type littermates in tests of motor coordination, and both showed aging-related decreases in the size of the dopaminergic neurons as well as in motor coordination. These results suggest that chronic deficits in BDNF alone do not affect survival or function of dopaminergic nigrostriatal neurons during aging or potentially even in Parkinson's disease.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17G</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B17A01</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Neurone dopaminergique</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Dopaminergic neuron</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Neurona dopaminérgica</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Voie nigrostriatale</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Nigrostriatal pathway</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Vía nigroestriatal</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Développement</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Development</s0>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Desarrollo</s0>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Sénescence</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Senescence</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Senescencia</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Facteur BDNF</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Brain derived neurotrophic factor</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Factor BDNF</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Locus niger</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Locus niger</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Locus níger</s0>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Mutation</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Mutation</s0>
<s5>07</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Mutación</s0>
<s5>07</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Tyrosine 3-monooxygenase</s0>
<s2>FE</s2>
<s5>08</s5>
<s6>Tyrosine «3»-monooxygenase</s6>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Tyrosine 3-monooxygenase</s0>
<s2>FE</s2>
<s5>08</s5>
<s6>Tyrosine «3»-monooxygenase</s6>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Tyrosine 3-monooxygenase</s0>
<s2>FE</s2>
<s5>08</s5>
<s6>Tyrosine «3»-monooxygenase</s6>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Parkinson maladie</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s5>09</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE"><s0>Animal</s0>
<s5>13</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG"><s0>Animal</s0>
<s5>13</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA"><s0>Animal</s0>
<s5>13</s5>
</fC03>
<fC03 i1="11" i2="X" l="FRE"><s0>Souris</s0>
<s5>54</s5>
</fC03>
<fC03 i1="11" i2="X" l="ENG"><s0>Mouse</s0>
<s5>54</s5>
</fC03>
<fC03 i1="11" i2="X" l="SPA"><s0>Ratón</s0>
<s5>54</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Oxidoreductases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Enzima</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>20</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>20</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>20</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Système nerveux central</s0>
<s5>21</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Central nervous system</s0>
<s5>21</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Sistema nervioso central</s0>
<s5>21</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Extrapyramidal syndrome</s0>
<s5>22</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>22</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>22</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>23</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Degenerative disease</s0>
<s5>23</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>23</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0>
<s5>24</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>24</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>24</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>25</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>25</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>25</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="09" i2="X" l="ENG"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="09" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="10" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="10" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="10" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="11" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="11" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="11" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fN21><s1>136</s1>
</fN21>
</pA>
</standard>
<server><NO>PASCAL 05-0200638 INIST</NO>
<ET>Maturation but not survival of dopaminergic nigrostriatal neurons is affected in developing and aging BDNF-deficient mice</ET>
<AU>BAKER (Sarah A.); STANFORD (Lianne E.); BROWN (Richard E.); HAGG (Theo)</AU>
<AF>Kentucky Spinal Cord Injury Research Center, University of Louisville/Louisville, KY 40292/Etats-Unis (1 aut., 4 aut.); Department of Anatomical Sciences and Neurobiology, University of Louisville/Louisville, KY 40292/Etats-Unis (1 aut.); Department of Psychology, Dalhousie University/Halifax, Nova Scotia/Canada (2 aut., 3 aut.); Department of Neurological Surgery, University of Louisville/Louisville, KY 40292/Etats-Unis (4 aut.); Department of Pharmacology and Toxicology, University of Louisville/Louisville, KY 40292/Etats-Unis (4 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Brain research; ISSN 0006-8993; Coden BRREAP; Pays-Bas; Da. 2005; Vol. 1039; No. 1-2; Pp. 177-188; Bibl. 78 ref.</SO>
<LA>Anglais</LA>
<EA>Brain-derived neurotrophic factor (BDNF) promotes survival of injured dopaminergic nigrostriatal neurons of the adult rodent substantia nigra pars compacta, as well their development in vitro. BDNF deficiency may play a role in Parkinson's disease, as the surviving dopaminergic nigrostriatal neurons have reduced levels of BDNF, and a BDNF gene polymorphism is present in a subpopulation of patients. Here, we investigated whether a lack of BDNF in early postnatal BDNF-/- mice or a chronic 50% reduction in BDNF levels in aging BDNF+/- mice would affect the survival of the dopaminergic nigrostriatal neurons. In general terms, BDNF-/- and BDNF+/- mice had morphologically and quantitatively normal nigrostriatal neurons at any time between postnatal day 14 (P14) and 18 months, when compared to their wild-type littermates. BDNF-/- mice (P14 and P21 only) had fewer dopaminergic dendrites in the substantia nigra, suggesting that BDNF plays a role in phenotypic maturation, but not in neuronal birth or survival. BDNF-/- mice also had aberrant tyrosine hydroxylase (TH) positive cell bodies in the pars reticulata. During adulthood and aging, BDNF+/- mice performed equally well as their wild-type littermates in tests of motor coordination, and both showed aging-related decreases in the size of the dopaminergic neurons as well as in motor coordination. These results suggest that chronic deficits in BDNF alone do not affect survival or function of dopaminergic nigrostriatal neurons during aging or potentially even in Parkinson's disease.</EA>
<CC>002B17G; 002B17A01</CC>
<FD>Neurone dopaminergique; Voie nigrostriatale; Développement; Sénescence; Facteur BDNF; Locus niger; Mutation; Tyrosine 3-monooxygenase; Parkinson maladie; Animal; Souris</FD>
<FG>Oxidoreductases; Enzyme; Encéphale pathologie; Système nerveux central; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie; Système nerveux pathologie; Rodentia; Mammalia; Vertebrata</FG>
<ED>Dopaminergic neuron; Nigrostriatal pathway; Development; Senescence; Brain derived neurotrophic factor; Locus niger; Mutation; Tyrosine 3-monooxygenase; Parkinson disease; Animal; Mouse</ED>
<EG>Oxidoreductases; Enzyme; Cerebral disorder; Central nervous system; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease; Nervous system diseases; Rodentia; Mammalia; Vertebrata</EG>
<SD>Neurona dopaminérgica; Vía nigroestriatal; Desarrollo; Senescencia; Factor BDNF; Locus níger; Mutación; Tyrosine 3-monooxygenase; Parkinson enfermedad; Animal; Ratón</SD>
<LO>INIST-12895.354000125607780210</LO>
<ID>05-0200638</ID>
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	La maladie de Parkinson au Canada (serveur d'exploration)
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La maladie de Parkinson au Canada (serveur d'exploration)

Maturation but not survival of dopaminergic nigrostriatal neurons is affected in developing and aging BDNF-deficient mice

Maturation but not survival of dopaminergic nigrostriatal neurons is affected in developing and aging BDNF-deficient mice

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