Regular ArticleUpregulation of Striatal Preproenkephalin Gene Expression Occurs before the Appearance of Parkinsonian Signs in 1-Methyl-4-phenyl- 1,2,3,6-tetrahydropyridine Monkeys
References (40)
- et al.
Functional architecture of basal ganglia circuits: Neural substrates of parallel processing
Trends Neurosci.
(1990) - et al.
Compensatory effects of glutamatergic inputs to the substantia nigra pars compacta in experimental parkinsonism
Neuroscience
(1997) - et al.
A chronic MPTP model reproducing the slow evolution of Parkinson's disease: Evolution of motor symptoms in the monkey
Brain Res.
(1997) Primate models of movement disorders of basal ganglia origin
Trends Neurosci.
(1990)- et al.
Topographical organization of opioid peptide precursor gene expression following repeated apomorphine treatment in the 6-hydroxydopamine-lesioned rat
Exp. Neurol.
(1998) - et al.
Terminal excitability of the corticostriatal pathway. I. Regulation by dopamine receptor stimulation
Brain Res.
(1991) - et al.
Effect of repeated -DOPA, bromocriptine, or lisuride administration on preproenkephalin-A and preproenkephalin-B mRNA levels in the striatum of the 6-hydroxydopamine-lesioned rat
Exp. Neurol.
(1999) - et al.
Effects of -Dopa on preproenkephalin and preprotachykinin gene expression in the MPTP-treated monkey striatum
Neuroscience
(1995) - et al.
Re-evaluation of the functional anatomy of the basal ganglia in normal and parkinsonian states
Neuroscience
(1997) - et al.
On the role of enkephalin cotransmission in the GABAergic striatal efferents to the Globus Pallidus
Exp. Neurol.
(1994)
Neural mechanisms underlying parkinsonian symptoms based upon regional uptake of 2-deoxyglucose in monkeys exposed to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine
Neuroscience
Preproenkephalin and preprotatachykinin messenger RNA expression in normal basal ganglia and in Parkinson's disease
Neuroscience
Temporal dissociation between changes in striatal enkephalin and substance P messenger RNAs following striatal dopamine depletion
Neuroscience
Functional anatomy of the basal ganglia. I. The cortico-basal ganglia-thalamo-cortical loop
Brain Res. Rev.
Dopamine-releasing action of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridine (MPP+) in the neostriatum of the rat as demonstrated in vivo by the push-pull perfusion technique: Dependence on sodium but not calcium ions
Brain Res.
Parkinson's disease: Pathophysiology
Lancet
Striatal changes in preproenkephalin mRNA levels in parkinsonian monkeys
Neuroreport
Parkinsonian-like locomotor impairment in mice lacking dopamine D2 receptors
Nature
Involvement of the subthalamic nucleus in glutamatergic compensatory mechanisms
Eur. J. Neurosci.
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2016, Biological PsychiatryPathophysiology of L-dopa-induced motor and non-motor complications in Parkinson's disease
2015, Progress in NeurobiologyCitation Excerpt :Overall, these studies bring evidence for a hyperactivity of glutamatergic neurons in response to chronic L-dopa that may operate in a region-dependent manner. Accordingly, L-dopa is expected to change GABA release in the basal ganglia (Bezard et al., 2001d; Cenci, 2007b). In dyskinetic mice, L-dopa enhances GABA release in the SNr and GP (Bido et al., 2011).
Direct targeted quantitative molecular imaging of neurotransmitters in brain tissue sections
2014, NeuronCitation Excerpt :One animal was kept untreated as control. The other animal received daily MPTP (0.2 mg/kg, i.v.) according to previously published protocol (Bezard et al., 1997, 2001a, 2001b). Following stabilization of the MPTP-induced syndrome, animal behavior was assessed as previously published (Ahmed et al., 2010; Fasano et al., 2010; Fernagut et al., 2010; Muñoz et al., 2008; Porras et al., 2012).
- 1
To whom correspondence and reprint requests should be addressed at his present address: Basal Gang, Laboratoire de Neurophysiologie, CNRS UMR 5543, Université Victor Segalen, 146 rue Léo Saignat, 33076 Bordeaux Cedex, France. Fax: 33 556 901 421. E-mail: [email protected].