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Striatal plasticity and extrapyramidal motor dysfunction.

Abstract：

:Knowledge of molecular events contributing to motor dysfunction in Parkinson's disease has advanced rapidly during the past decade. Studies in animal models as well as in patients afflicted by this disorder suggest that the nonphysiologic stimulation of striatal dopamine receptors, first as a result of dopaminergic denervation and later as a consequence of the intermittent high-intensity stimulation produced by standard therapeutic regimens, leads to plastic changes in striatal medium spiny neurons. The clinical appearance of parkinsonism and subsequently of motor response complications is associated with the aberrant activation of signaling cascades within medium spiny neurons that modify the phosphorylation state of their ionotropic glutamatergic receptors. Resultant NMDA and AMPA receptor sensitization augments cortical excitatory input to these spiny efferent neurons, thus altering striatal output in ways that compromise motor function. These findings have already yielded new insight into mechanisms subserving motor memory and synaptic integration as well as accelerated development of novel approaches to the improved treatment of motor disability.

journal_name

Parkinsonism Relat Disord

journal_title

Parkinsonism & related disorders

authors

Chase TN

doi

10.1016/j.parkreldis.2004.02.012

subject

Has Abstract

pub_date

2004-07-01 00:00:00

pages

305-13

issue

5

eissn

1353-8020

issn

1873-5126

pii

S1353802004000434

journal_volume

10

pub_type

杂志文章,评审

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