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Mohamed Jaber

Researcher at University of Bordeaux

Publications -  31
Citations -  9089

Mohamed Jaber is an academic researcher from University of Bordeaux. The author has contributed to research in topics: Dopamine & Dopaminergic. The author has an hindex of 18, co-authored 23 publications receiving 8659 citations. Previous affiliations of Mohamed Jaber include Howard Hughes Medical Institute & Duke University.

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Journal ArticleDOI

Cocaine and amphetamine elicit differential effects in rats with a unilateral injection of dopamine transporter antisense oligodeoxynucleotides

TL;DR: In vivo evidence is brought in vivo evidence for a different mode of action of amphetamine and cocaine on the dopamine transporter and direct support to the view that amphetamine acts as a dopamine releaser, whereas cocaine acts by blocking dopamine transport.
Journal ArticleDOI

Reserpine treatment stimulates enkephalin and D2 dopamine receptor gene expression in the rat striatum.

TL;DR: It is demonstrated that reserpine acts at the gene or the mRNA level to induce dopamine supersensitivity in striatal dopaminoceptive neurons and that catecholamine depletion has postsynaptic but not presynaptic consequences in the rat nigrostriatal complex.
Journal ArticleDOI

Prenatal D1, D1b and D3 dopamine receptor gene expression in the rat forebrain: detection by reverse polymerase chain reaction.

TL;DR: Three dopamine receptor mRNAs were detected by reverse polymerase chain reaction in the rat forebrain during ontogeny, each one with its specific time of appearance.
Journal ArticleDOI

Cerebellar and Striatal Implications in Autism Spectrum Disorders: From Clinical Observations to Animal Models

TL;DR: It is reported that motor and gait behaviors can constitute an early and quantitative window to the disease, as they often correlate with the severity of social impairments and loss of cerebellar Purkinje cells.
Book ChapterDOI

Inactivation of the dopamine transporter reveals essential roles of dopamine in the control of locomotion, psychostimulant response, and pituitary function.

TL;DR: The findings suggest that, in the absence of a functional DAT, (-/-) DAT mice have undergone major adaptive changes in their biochemical and neurochemical mediators of dopaminergic transmission in an attempt to dampen the presumed increased DA signal.