constitutively active YAP

Equal protein concentrations were resolved using sodium dodecyl sulphate–polyacrylamide gel electrophoresis (SDS–PAGE) and transferred to an Immobilon‐P polyvinylidene difluoride membrane (Millipore). For GPRC5A Western blots, samples were not boiled.

Western blotting

The most striking neuropathological hallmark of HD is the atrophy of GABA medium spiny neurons (MSNs) in the striatum as seen by post mortem histological evaluation, but several cerebral regions also show signs of neurodegeneration as the disease progresse

The marked striatal atrophy observed in HD is a main argument in favour of cell replacement therapy

The mechanisms underlying neurodegeneration in HD are not totally elucidated

HD is due to mutations in the HTT gene encoding huntingtin, a ubiquitously expressed protein of 350 kDa (Huntington's Disease Collaborative Research Group 1993)

Huntingtin contains a polyglutamine tract encoded by uninterrupted CAG trinucleotide repeats in the first exon of HTT

Wild-type alleles contain up to 35 CAG repeats, whereas HD patients carry expansions of 36 or more repeats

Dopamine degradation

Dopamine biosynthesis

Monoamine oxidase

The present study aimed at describing in vivo the amplitude and time course of DA autoinhibition. In anesthetized mice, DA release was evoked by brief electrical stimulations at 100 Hz and at frequencies mimicking the discharge patterns of dopaminergic neurons.

Presynaptic inhibition is mainly attributable to the activation of G-protein-coupled receptors, which reduces the presynaptic entry of calcium, a flux necessary for transmitter release

Autoinhibition of DA release was measured by comparing evoked DA release in wild-type (WT) mice and in mice lacking dopaminergic D2 receptors, because autoreceptors are of the D2 type

Physiological and Functional Basis of Dopamine Receptors and Their Role in Neurogenesis: Possible Implication for Parkinson’s disease

cting on its receptors D1, D2, D3, D4, and D5.

receptors are G protein–coupled receptors involved in the regulation of motor activity and several neurological disorders such as schizophrenia, bipolar disorder, Parkinson’s disease (PD), Alzheimer’s disease, and attention-deficit/hyperactivity disorder.

a) Learning curves for sham-lesioned rats (black, vehicle), rats with dopaminergic terminals destroyed (red, 6-OHDA+D), and rats with noradrenergic terminals destroyed (blue, 6-OHDA+N). Cortical injections (vertical arrows) were performed following an initial training session to determine paw preference. After 3 days of recovery from surgery (horizontal arrow, necessary interval determined in d) rats were trained for 6 successive days. The success rate of skill acquisition was significantly impaired in animals with without dopaminergic terminals but not in animals without noradrenergic terminals (

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