1,721,116 research outputs found
L-3,4-dihydroxyphenylalanine-inducedsprouting of serotonin axon terminals: A useful biomarker for dyskinesias?
No full textDIRECT AND INDIRECT PATHWAYS IN LEVODOPA-INDUCED DYSKINESIA: A MORE COMPLEX MATTER THAN A NETWORK IMBALANCE.
No full textNew experimental and clinical links between the hippocampus and the dopaminergic system in Parkinson's disease.
No full textParkinson's disease is a common progressive neurodegenerative disease, of which the main neuropathological hallmark is dopaminergic neuronal loss. Increased attention has been directed towards non-motor symptoms in Parkinson's disease, such as cognitive impairment and behavioural disorders. Clinical and experimental findings support the view that the hippocampus, a temporal lobe structure involved in physiological learning and memory, is also implicated in the cognitive dysfunction seen in some patients with Parkinson's disease. Moreover, emerging data suggest interactions between the dopaminergic systems and the hippocampus in synaptic plasticity, adaptive memory, and motivated behaviour. This structure is also implicated in the pathophysiology of other non-motor symptoms, such as impulse control disorders, anosmia, and fatigue. Evidence from clinical observations and experimental studies suggest a complex hippocampal cross-talk among the dopaminergic and other transmitter systems. Furthermore, neurotrophic factors might interact with the hippocampal dopaminergic system having possible implications on the non-motor symptoms seen in patients with Parkinson's disease
Neuroinflammation and synaptic plasticity: theoretical basis for a novel, immune-centred, therapeutic approach to neurological disorders.
No full textrevie
Therapeutic doses of L-dopa reverse hypersensitivity of corticostriatal D2-dopamine receptors and glutamatergic overactivity in experimental parkinsonism
No full textLevodopa (l-dopa) therapy is still considered the gold-standard in the treatment of Parkinson's disease. However, the synaptic and cellular mechanisms involved in the amelioration of motor symptoms during this treatment are still unclear. To address this issue, we analysed the physiological and pharmacological properties of striatal glutamatergic and GABAergic synaptic transmission in an experimental model of Parkinson's disease. Single-cell recordings were performed in sham-operated rats, in 6-hydroxydopamine-lesioned animals and in rats receiving chronic l-dopa treatment following dopamine (DA) denervation. We utilized a dose of l-dopa (10 mg/kg, twice daily for 21 days) able to reverse motor deficits in about half of parkinsonian animals. In the striatum of parkinsonian animals showing therapeutic benefits following l-dopa treatment, we observed a reversal of glutamatergic overactivity and of the hypersensitivity of presynaptic D2 DA receptors controlling glutamate release from corticostriatal terminals. Conversely, no change was detected in the sensitivity of presynaptic D2 DA receptors modulating striatal GABA transmission in both parkinsonian and l-dopa-treated rats. We suggest that the reversal of striatal glutamatergic overactivity and the normalization of hypersensitive D2 DA receptors modulating excitatory transmission might underlie some of the therapeutic actions of l-dopa in Parkinson's disease
Mapping P2X and P2Y receptor proteins in striatum and substantia nigra: An immunohistological study.
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Dopaminergic control of synaptic plasticity in the dorsal striatum
No full textCortical glutamatergic and nigral dopaminergic afferents impinge on projection spiny neurons of the striatum, providing the most significant inputs to this structure. Isolated activation of glutamate or dopamine (DA) receptors produces short-term effects on striatal neurons, whereas the combined stimulation of both glutamate and DA receptors is able to induce long-lasting modifications of synaptic excitability. Repetitive stimulation of corticostriatal fibres causes a massive release of both glutamate and DA in the striatum and, depending on the glutamate receptor subtype preferentially activated, produces either long-term depression (LTD) or long-term potentiation (LTP) of excitatory synaptic transmission. D1-like and D2-like DA receptors interact synergistically to allow LTD formation, while they operate in opposition during the induction phase of LTP. Corticostriatal synaptic plasticity is severely impaired after chronic DA denervation and requires the stimulation of DARPP-32, a small protein expressed in dopaminoceptive spiny neurons which acts as a potent inhibitor of protein phosphatase-1. In addition, the formation of LTD and LTP requires the activation of PKG and PKA, respectively, in striatal projection neurons. These kinases appear to be stimulated by the activation of D1-like receptors in distinct neuronal populations
Functional interactions within striatal microcircuit in animal models of Huntington's disease
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