Selective elimination of glutamatergic synapses on striatopallidal neurons in Parkinson disease models.

Day M, Wang Z, Ding J, An X, Ingham CA, Shering AF, Wokosin D, Ilijic E, Sun Z, Sampson AR, Mugnaini E, Deutch AY, Sesack SR, Arbuthnott GW, Surmeier DJ
Nat Neurosci. 2006 9 (2): 251-9

PMID: 16415865 · DOI:10.1038/nn1632

Parkinson disease is a common neurodegenerative disorder that leads to difficulty in effectively translating thought into action. Although it is known that dopaminergic neurons that innervate the striatum die in Parkinson disease, it is not clear how this loss leads to symptoms. Recent work has implicated striatopallidal medium spiny neurons (MSNs) in this process, but how and precisely why these neurons change is not clear. Using multiphoton imaging, we show that dopamine depletion leads to a rapid and profound loss of spines and glutamatergic synapses on striatopallidal MSNs but not on neighboring striatonigral MSNs. This loss of connectivity is triggered by a new mechanism-dysregulation of intraspine Cav1.3 L-type Ca(2+) channels. The disconnection of striatopallidal neurons from motor command structures is likely to be a key step in the emergence of pathological activity that is responsible for symptoms in Parkinson disease.

MeSH Terms (15)

Animals Calcium Channels, L-Type Corpus Striatum Dendritic Spines Disease Models, Animal Glutamine Mice Mice, Inbred C57BL Microscopy, Immunoelectron Neural Pathways Organ Culture Techniques Parkinson Disease Patch-Clamp Techniques Reverse Transcriptase Polymerase Chain Reaction Synapses

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