Impaired water maze learning performance without altered dopaminergic function in mice heterozygous for the GDNF mutation.

UI - 21541160

PMID- 11683907

DA - 20011030

DCOM- 20011207

IS - 0953-816X

VI - 14

IP - 7

DP - 2001 Oct

TI - Impaired water maze learning performance without altered dopaminergic function in mice heterozygous for the GDNF mutation.

PG - 1153-63 AB - Exogenous glial cell line-derived neurotrophic factor (GDNF) exhibits potent survival-promoting effects on dopaminergic neurons of the nigrostriatal pathway that is implicated in Parkinson's disease and also protects neurons in forebrain ischemia of animal models. However, a role for endogenous GDNF in brain function has not been established. Although mice homozygous for a targeted deletion of the GDNF gene have been generated, these mice die within hours of birth because of deficits in kidney morphogenesis, and, thus, the effect of the absence of GDNF on brain function could not be studied. Herein, we sought to determine whether adult mice, heterozygous for a GDNF mutation on two different genetic backgrounds, demonstrate alterations in the nigrostriatal dopaminergic system or in cognitive function. While both neurochemical and behavioural measures suggested that reduction of GDNF gene expression in the mutant mice does not alter the nigrostriatal dopaminergic system, it led to a significant and selective impairment of performance in the spatial version of the Morris water maze. A standard panel of blood chemistry tests and basic pathological analyses did not reveal alterations in the mutants that could account for the observed performance deficit. These results suggest that endogenous GDNF may not be critical for the development and functioning of the nigrostriatal dopaminergic system but it plays an important role in cognitive abilities.

AD - Department of Neuroscience, Genentech Inc, 1 DNA Way, South San Francisco,

[emd]

FAU - Gerlai, R

AU - Gerlai R

FAU - McNamara, A

AU - McNamara A

FAU - Choi-Lundberg, D L

AU - Choi-Lundberg DL

FAU - Armanini, M

AU - Armanini M

FAU - Ross, J

AU - Ross J

FAU - Powell-Braxton, L

AU - Powell-Braxton L

FAU - Phillips, H S

AU - Phillips HS

LA - eng

PT - Journal Article

CY - France

TA - Eur J Neurosci

JID - 8918110

RN - 0 (Nerve Tissue Proteins)

RN - 0 (glial cell-line derived neurotrophic factor)

RN - 102-32-9 (3,4-Dihydroxyphenylacetic Acid)

RN - 51-61-6 (Dopamine)

SB - IM

MH - 3,4-Dihydroxyphenylacetic Acid/metabolism

MH - Animal

MH - Brain/*metabolism/physiopathology

MH - Dopamine/*metabolism

MH - Gene Expression/genetics

MH - *Heterozygote

MH - Learning Disorders/*genetics/metabolism/physiopathology

MH - Maze Learning/*physiology

MH - Mice

MH - Mice, Knockout

MH - Motor Activity/genetics

MH - Mutation/*physiology

MH - Neostriatum/metabolism/physiopathology

MH - Nerve Tissue Proteins/*deficiency/genetics

MH - Neural Pathways/metabolism/physiopathology

MH - Organ Weight/genetics

MH - Substantia Nigra/metabolism/physiopathology

EDAT- 2001/10/31 10:00

MHDA- 2002/01/05 10:01

AID - 1724 [pii]

PST - ppublish

SO - Eur J Neurosci 2001 Oct;14(7):1153-63.


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