Differential organization of cortical inputs to striatal projection neurons of the matrix compartment in rats

Deng, Yunping; Lanciego, José L.; Goff, Lydia Kerkerian‐Le; Coulon, Patrice; Salin, Pascal; Kachidian, Philippe; Lei, Wanlong; Mar, Nobel Del; Reiner, Anton

doi:10.3389/fnsys.2015.00051

Cited by 40 publications

(44 citation statements)

References 86 publications

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“…The corticostriatal input arises from 2 neuron types, an intratelencephalically projecting (IT) type residing predominantly in layer III and upper layer V, and a pyramidal tract (PT) type located primarily in lower layer V . We and other investigators have found in rats and monkeys that PT‐type corticostriatal neurons preferentially contact striatal neurons projecting to GPe with larger terminals, while IT‐type cortical neurons preferentially target striatal neurons projecting to GPi or SNr with smaller terminals (Figure ) . In our study in 12‐month‐old Q140 mice, the loss of corticostriatal terminals occurred selectively for smaller terminals, suggesting they might be IT‐type terminals and preferentially lost from direct pathway type striatal neurons .…”

Section: Striatal Neuron Input Abnormalities In Hdmentioning

confidence: 60%

“…Schematic illustration of the relative abundances of axospinous IT ‐type and PT ‐type inputs to dSPN s and iSPN s. Both dSPN s and iSPN s receive axospinous IT ‐type and PT ‐type inputs, with dSPN s receiving about twice as much IT ‐type and iSPN s receiving twice as much PT ‐type axospinous input. Note that, as depicted, PT ‐type axospinous terminals are uniformly larger than IT ‐type axospinous terminals, and IT ‐type axospinous terminals on iSPN s are slightly larger than IT ‐type axospinous terminals on dSPN s. This illustration is Figure from Deng et al…”

Section: Striatal Neuron Input Abnormalities In Hdmentioning

confidence: 64%

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Disrupted striatal neuron inputs and outputs in Huntington's disease

Reiner

Deng

2018

CNS Neurosci Ther

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Huntington's disease (HD) is a hereditary progressive neurodegenerative disorder caused by a CAG repeat expansion in the gene coding for the protein huntingtin, resulting in a pathogenic expansion of the polyglutamine tract in the N-terminus of this protein. The HD pathology resulting from the mutation is most prominent in the striatal part of the basal ganglia, and progressive differential dysfunction and loss of striatal projection neurons and interneurons account for the progression of motor deficits seen in this disease. The present review summarizes current understanding regarding the progression in striatal neuron dysfunction and loss, based on studies both in human HD victims and in genetic mouse models of HD. We review evidence on early loss of inputs to striatum from cortex and thalamus, which may be the basis of the mild premanifest bradykinesia in HD, as well as on the subsequent loss of indirect pathway striatal projection neurons and their outputs to the external pallidal segment, which appears to be the basis of the chorea seen in early symptomatic HD. Later loss of direct pathway striatal projection neurons and their output to the internal pallidal segment account for the severe akinesia seen late in HD. Loss of parvalbuminergic striatal interneurons may contribute to the late dystonia and rigidity.

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Section: Striatal Neuron Input Abnormalities In Hdmentioning

confidence: 60%

Section: Striatal Neuron Input Abnormalities In Hdmentioning

confidence: 64%

Disrupted striatal neuron inputs and outputs in Huntington's disease

Reiner

Deng

2018

CNS Neurosci Ther

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“…Huntingtin has been reported to associate with synaptic vesicles and facilitate neurotransmitter release in pre-synaptic excitatory synaptic terminals (DiFiglia et al, 1995; Rozas et al, 2011). If the huntingtin depletion preferentially diminished neurotransmitter release from cortical terminals ending on indirect pathway neurons, for example those of the pyramidal tract type corticostriatal neurons (Deng et al, 2015), hyperactivity would be the predicted outcome (Albin et al, 1989). …”

Section: Discussionmentioning

confidence: 99%

Effect of early embryonic deletion of huntingtin from pyramidal neurons on the development and long-term survival of neurons in cerebral cortex and striatum

Dragatsis

Dietrich

Ren

et al. 2018

Neurobiology of Disease

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We evaluated the impact of early embryonic deletion of huntingtin (htt) from pyramidal neurons on cortical development, cortical neuron survival and motor behavior, using a cre-loxP strategy to inactivate the mouse htt gene (Hdh) in emx1-expressing cell lineages. Western blot confirmed substantial htt reduction in cerebral cortex of these Emx-httKO mice, with residual cortical htt in all likelihood restricted to cortical interneurons of the subpallial lineage and/or vascular endothelial cells. Despite the loss of htt early in development, cortical lamination was normal, as revealed by layer-specific markers. Cortical volume and neuron abundance were, however, significantly less than normal, and cortical neurons showed reduced brain-derived neurotrophic factor (BDNF) expression and reduced activation of BDNF signaling pathways. Nonetheless, cortical volume and neuron abundance did not show progressive age-related decline in Emx-httKO mice out to 24 months. Although striatal neurochemistry was normal, reductions in striatal volume and neuron abundance were seen in Emx-httKO mice, which were again not progressive. Weight maintenance was normal in Emx-httKO mice, but a slight rotarod deficit and persistent hyperactivity were observed throughout the lifespan. Our results show that embryonic deletion of htt from developing pallium does not substantially alter migration of cortical neurons to their correct laminar destinations, but does yield reduced cortical and striatal size and neuron numbers. The Emx-httKO mice were persistently hyperactive, possibly due to defects in corticostriatal development. Importantly, deletion of htt from cortical pyramidal neurons did not yield age-related progressive cortical or striatal pathology.

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“…Thus, the preferential innervation from IT and PT neurons to SPNs remains controversial (Deng et al, 2015). Thus, it is conceivable that PT neurons also play an important role in the development of LID.…”

Section: Introductionmentioning

confidence: 99%

Spine Enlargement of Pyramidal Tract-Type Neurons in the Motor Cortex of a Rat Model of Levodopa-Induced Dyskinesia

et al. 2017

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Growing evidence suggests that abnormal synaptic plasticity of cortical neurons underlies levodopa-induced dyskinesia (LID) in Parkinson's disease (PD). Spine morphology reflects synaptic plasticity resulting from glutamatergic transmission. We previously reported that enlargement of the dendritic spines of intratelencephalic-type (IT) neurons in the primary motor cortex (M1) is linked to the development of LID. However, the relevance of another M1 neuron type, pyramidal-tract (PT) neurons, to LID remains unknown. We examined the morphological changes of the dendritic spines of M1 PT neurons in a rat model of LID. We quantified the density and size of these spines in 6-hydroxydopamine-lesioned rats (a model of PD), 6-hydroxydopamine-lesioned rats chronically treated with levodopa (a model of LID), and control rats chronically treated with levodopa. Dopaminergic denervation alone had no effect on spine density and head area. However, the LID model showed significant increases in the density and spine head area and the development of dyskinetic movements. In contrast, levodopa treatment of normal rats increased spine density alone. Although, chronic levodopa treatment increases PT neuron spine density, with or without dopaminergic denervation, enlargement of PT neuron spines appears to be a specific feature of LID. This finding suggests that PT neurons become hyperexcited in the LID model, in parallel with the enlargement of spines. Thus, spine enlargement, and the resultant hyperexcitability of PT pyramidal neurons, in the M1 cortex might contribute to abnormal cortical neuronal plasticity in LID.

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Differential organization of cortical inputs to striatal projection neurons of the matrix compartment in rats

Cited by 40 publications

References 86 publications

Disrupted striatal neuron inputs and outputs in Huntington's disease

Disrupted striatal neuron inputs and outputs in Huntington's disease

Effect of early embryonic deletion of huntingtin from pyramidal neurons on the development and long-term survival of neurons in cerebral cortex and striatum

Spine Enlargement of Pyramidal Tract-Type Neurons in the Motor Cortex of a Rat Model of Levodopa-Induced Dyskinesia

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