Striosome-matrix pathology and motor deficits in the YAC128 mouse model of Huntington's disease

Lawhorn, Collene; Smith, Diane; Brown, Lucy L.

doi:10.1016/j.nbd.2008.08.006

Cited by 24 publications

(27 citation statements)

References 60 publications

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“…Whether the appearance of “novel” TH neurons as a result of dopamine loss follows a distinct anatomical pattern would be very interesting to uncover, as striatal compartments were shown to display separable degrees of susceptibility to toxins and disease-related degeneration (Lawhorn et al, 2008; Sato et al, 2008; Granado et al, 2010). The present findings indicate that TH-eGFP neurons follow a non-random, distinct pattern of distribution across striosome–matrix compartments throughout the dorsal–ventral axis of the striatum.…”

Section: Resultsmentioning

confidence: 99%

Distribution of Tyrosine Hydroxylase-Expressing Interneurons with Respect to Anatomical Organization of the Neostriatum

Ünal¹,

Ibáñez-Sandoval²,

Shah³

et al. 2011

Front. Syst. Neurosci.

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We have recently shown in vitro that striatal tyrosine hydroxylase-expressing interneurons identified in transgenic mice by expression of enhanced green fluorescent protein (TH-eGFP) display electrophysiological profiles that are distinct from those of other striatal interneurons. Furthermore, striatal TH-eGFP interneurons show marked diversity in their electrophysiological properties and have been divided into four distinct subtypes. One question that arises from these observations is whether striatal TH-eGFP interneurons are distributed randomly, or obey some sort of organizational plan as has been shown to be the case with other striatal interneurons. An understanding of the striatal TH-eGFP interneuronal patterning is a vital step in understanding the role of these neurons in striatal functioning. Therefore, in the present set of studies the location of electrophysiologically identified striatal TH-eGFP interneurons was mapped. In addition, the distribution of TH-eGFP interneurons with respect to the striatal striosome–matrix compartmental organization was determined using μ-opioid receptor (MOR) immunofluorescence or intrinsic TH-eGFP fluorescence to delineate striosome and matrix compartments. Overall, the distribution of the different TH-eGFP interneuronal subtypes did not differ in dorsal versus ventral striatum. However, striatal TH-eGFP interneurons were found to be mostly in the matrix in the dorsal striatum whereas a significantly higher proportion of these neurons was located in MOR-enriched domains of the ventral striatum. Further, the majority of striatal TH-eGFP interneurons was found to be located within 100 μm of a striosome–matrix boundary. Taken together, the current results suggest that TH-eGFP interneurons obey different organizational principles in dorsal versus ventral striatum, and may play a role in communication between striatal striosome and matrix compartments.

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Section: Resultsmentioning

confidence: 99%

Distribution of Tyrosine Hydroxylase-Expressing Interneurons with Respect to Anatomical Organization of the Neostriatum

Ünal¹,

Ibáñez-Sandoval²,

Shah³

et al. 2011

Front. Syst. Neurosci.

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“…Since autopsied brains are usually acquired at the end stage of the disease, it may be useful to investigate the striatal neuropathology of animal models. In a study of a transgenic rodent model of HD, preferential loss of striosomal neurons was reported [224]. Moreover, a PET study of early premanifest HD gene carriers revealed that extra-striatal PDE10A expression decreased by 25% and 50% in the insular cortex and occipital fusiform gyrus, respectively [136].…”

Section: Striatal Pathologymentioning

confidence: 99%

Striatal Vulnerability in Huntington’s Disease: Neuroprotection Versus Neurotoxicity

Morigaki

Goto

2017

Brain Sciences

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Huntington’s disease (HD) is an autosomal dominant neurodegenerative disease caused by the expansion of a CAG trinucleotide repeat encoding an abnormally long polyglutamine tract (PolyQ) in the huntingtin (Htt) protein. In HD, striking neuropathological changes occur in the striatum, including loss of medium spiny neurons and parvalbumin-expressing interneurons accompanied by neurodegeneration of the striosome and matrix compartments, leading to progressive impairment of reasoning, walking and speaking abilities. The precise cause of striatal pathology in HD is still unknown; however, accumulating clinical and experimental evidence suggests multiple plausible pathophysiological mechanisms underlying striatal neurodegeneration in HD. Here, we review and discuss the characteristic neurodegenerative patterns observed in the striatum of HD patients and consider the role of various huntingtin-related and striatum-enriched proteins in neurotoxicity and neuroprotection.

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“…Furthermore, patch/matrix are differentially affected in neurological pathologies such as Parkinson’s disease (Koizumi et al, 2013), Huntington’s disease (Lawhorn et al, 2008), drug addiction (Hurd and Herkenham, 1993), and others (Crittenden and Graybiel, 2011). …”

Section: Introductionmentioning

confidence: 99%

Genetic-Based Dissection Unveils the Inputs and Outputs of Striatal Patch and Matrix Compartments

Smith

Klug

Ross

et al. 2016

Neuron

143

184

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SUMMARY The striatum contains neurochemically defined compartments termed patches and matrix. Previous studies suggest patches preferentially receive limbic inputs and project to dopamine neurons in substantia nigra (SNc), whereas matrix neurons receive sensorimotor inputs and do not innervate SNc. Using BAC-Cre transgenic mice with viral tracing techniques we mapped brain-wide differences in the input-output organization of the patch/matrix. Findings reveal a displaced population of striatal patch neurons termed “exo-patch”, which reside in matrix zones but have neurochemistry, connectivity, and electrophysiological characteristics resembling patch neurons. Contrary to previous studies, results show patch/exo-patch and matrix neurons receive both limbic and sensorimotor information. A novel inhibitory projection from bed nucleus of the stria terminalis to patch/exo-patch neurons was revealed. Projections to SNc were found to originate from patch/exo-patch and matrix neurons. These findings redefine patch/matrix beyond traditional neurochemical topography and reveal new principles about their input-output connectivity, providing a foundation for future functional studies.

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Striosome-matrix pathology and motor deficits in the YAC128 mouse model of Huntington's disease

Cited by 24 publications

References 60 publications

Distribution of Tyrosine Hydroxylase-Expressing Interneurons with Respect to Anatomical Organization of the Neostriatum

Distribution of Tyrosine Hydroxylase-Expressing Interneurons with Respect to Anatomical Organization of the Neostriatum

Striatal Vulnerability in Huntington’s Disease: Neuroprotection Versus Neurotoxicity

Genetic-Based Dissection Unveils the Inputs and Outputs of Striatal Patch and Matrix Compartments

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