Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- Part I Basic aspects of neurodegeneration
- 1 Endogenous free radicals and antioxidants in the brain
- 2 Biological oxidants and therapeutic antioxidants
- 3 Mitochondria, metabolic inhibitors and neurodegeneration
- 4 Excitoxicity and excitatory amino acid antagonists in chronic neurodegenerative diseases
- 5 Glutamate transporters
- 6 Calcium binding proteins in selective vulnerability of motor neurons
- 7 Apoptosis in neurodegenerative diseases
- 8 Neurotrophic factors
- 9 Protein misfolding and cellular defense mechanisms in neurodegenerative diseases
- 10 Neurodegenerative disease and the repair of oxidatively damaged DNA
- 11 Compounds acting on ion channels
- 12 The role of nitric oxide and PARP in neuronal cell death
- 13 Copper and zinc in Alzheimer's disease and amyotrophic lateral sclerosis
- 14 The role of inflammation in Alzheimer's disease neuropathology and clinical dementia. From epidemiology to treatment
- 15 Selected genetically engineered models relevant to human neurodegenerative disease
- 16 Toxic animal models
- 17 A genetic outline of the pathways to cell death in Alzheimer's disease, Parkinson's disease, frontal dementias and related disorders
- 18 Neurophysiology of Parkinson's disease, levodopa-induced dyskinesias, dystonia, Huntington's disease and myoclonus
- Part II Neuroimaging in neurodegeneration
- Part III Therapeutic approaches in neurodegeneration
- Normal aging
- Part IV Alzheimer's disease
- Part VI Other Dementias
- Part VII Parkinson's and related movement disorders
- Part VIII Cerebellar degenerations
- Part IX Motor neuron diseases
- Part X Other neurodegenerative diseases
- Index
- References
18 - Neurophysiology of Parkinson's disease, levodopa-induced dyskinesias, dystonia, Huntington's disease and myoclonus
from Part I - Basic aspects of neurodegeneration
Published online by Cambridge University Press: 04 August 2010
- Frontmatter
- Contents
- List of contributors
- Preface
- Part I Basic aspects of neurodegeneration
- 1 Endogenous free radicals and antioxidants in the brain
- 2 Biological oxidants and therapeutic antioxidants
- 3 Mitochondria, metabolic inhibitors and neurodegeneration
- 4 Excitoxicity and excitatory amino acid antagonists in chronic neurodegenerative diseases
- 5 Glutamate transporters
- 6 Calcium binding proteins in selective vulnerability of motor neurons
- 7 Apoptosis in neurodegenerative diseases
- 8 Neurotrophic factors
- 9 Protein misfolding and cellular defense mechanisms in neurodegenerative diseases
- 10 Neurodegenerative disease and the repair of oxidatively damaged DNA
- 11 Compounds acting on ion channels
- 12 The role of nitric oxide and PARP in neuronal cell death
- 13 Copper and zinc in Alzheimer's disease and amyotrophic lateral sclerosis
- 14 The role of inflammation in Alzheimer's disease neuropathology and clinical dementia. From epidemiology to treatment
- 15 Selected genetically engineered models relevant to human neurodegenerative disease
- 16 Toxic animal models
- 17 A genetic outline of the pathways to cell death in Alzheimer's disease, Parkinson's disease, frontal dementias and related disorders
- 18 Neurophysiology of Parkinson's disease, levodopa-induced dyskinesias, dystonia, Huntington's disease and myoclonus
- Part II Neuroimaging in neurodegeneration
- Part III Therapeutic approaches in neurodegeneration
- Normal aging
- Part IV Alzheimer's disease
- Part VI Other Dementias
- Part VII Parkinson's and related movement disorders
- Part VIII Cerebellar degenerations
- Part IX Motor neuron diseases
- Part X Other neurodegenerative diseases
- Index
- References
Summary
Introduction
Movement disorders are a disease group related to functional or structural abnormalities of the basal ganglia.
The term “basal ganglia” refers to the following structures: the striatum (caudate and putamen), globus pallidus (internal and external segments, GPi and GPe), subthalamic nucleus, and substantia nigra (SN) (SN pars compacta, SNpc, and SN pars reticulata, SNpr). The striatum receives connections from specific cortical areas and from the SNpc; the basal ganglia output nuclei, the GPi and SNpr, exert an inhibitory effect on the thalamus. Diminished phasic activity in the GPi/SNpr disinhibits the thalamus thus facilitating cortical motor areas, whereas increased phasic activity in the GPi/SNpr causes the opposite effect. The GPi–SNpr inhibition of the thalamus is modulated through two parallel pathways. According to the classical model of basal ganglia functioning (Albin et al., 1989; Alexander & Crutcher, 1990; Alexander et al., 1990; De Long, 1990; Parent & Hazarati, 1995; Wichmann & De Long, 1996) the first is an inhibitory “direct” pathway that originates in the striatum and projects directly onto the GPi/SNr; the second is an “indirect” inhibitory pathway that crosses the GPe and subthalamic nucleus to project indirectly onto the GPi/SNpr. Activation of the direct pathway tends to disinhibit the thalamus. Activation of the indirect pathway disinhibits the subthalamic nucleus thereby increasing GPi/SNpr excitation thus resulting in increased thalamic inhibition: the two parallel circuits have an opposing action on the GPi/SNr and hence on the thalamus.
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- Information
- Neurodegenerative DiseasesNeurobiology, Pathogenesis and Therapeutics, pp. 227 - 250Publisher: Cambridge University PressPrint publication year: 2005