The Thalamostriatal System and Cognition

Smith, Yoland; Villalba, Rosa M.; Galván, Adriana

doi:10.1007/978-3-319-42743-0_4

Cited by 2 publications

(3 citation statements)

References 129 publications

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“…The striatum also receives a massive glutamatergic innervation from the thalamus. Although the thalamostriatal system originates from most thalamic nuclei, the caudal intralaminar nuclear complex, made up of the centromedian (CM) and parafascicular (Pf) nuclei in primates, is the main source of thalamic afferents to the striatum (Smith et al 2004, 2009a, 2014, 2016; Galvan et al 2016). It is noteworthy that the CM/Pf complex undergoes profound neuronal degeneration in PD (Henderson et al 2000a, b; Halliday 2009) and in chronically MPTP-treated monkeys (Villalba et al 2014) (see discussion below).…”

Section: Anatomy Connections and Cell Types Of The Striatummentioning

confidence: 99%

Loss and remodeling of striatal dendritic spines in Parkinson’s disease: from homeostasis to maladaptive plasticity?

Villalba

Smith

2017

J Neural Transm

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In Parkinson's disease (PD) patients and animal models of PD, the progressive degeneration of the nigrostriatal dopamine (DA) projection leads to two major changes in the morphology of striatal projection neurons (SPNs), i.e., a profound loss of dendritic spines and the remodeling of axospinous glutamatergic synapses. Striatal spine loss is an early event tightly associated with the extent of striatal DA denervation, but not the severity of parkinsonian motor symptoms, suggesting that striatal spine pruning might be a form of homeostatic plasticity that compensates for the loss of striatal DA innervation and the resulting dysregulation of corticostriatal glutamatergic transmission. On the other hand, the remodeling of axospinous corticostriatal and thalamostriatal glutamatergic synapses might represent a form of late maladaptive plasticity that underlies changes in the strength and plastic properties of these afferents and the resulting increased firing and bursting activity of striatal SPNs in the parkinsonian state. There is also evidence that these abnormal synaptic connections might contribute to the pathophysiology of L-DOPA-induced dyskinesia. Despite the significant advances made in this field over the last thirty years, many controversial issues remain about the striatal SPN subtypes affected, the role of spine changes in the altered activity of SPNs in the parkinsonisn state, and the importance of striatal spine plasticity in the pathophysiology of L-DOPA-induced dyskinesia. In this review, we will examine the current state of knowledge of these issues, discuss the limitations of the animal models used to address some of these questions, and assess the relevance of data from animal models to the human-diseased condition.

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Section: Anatomy Connections and Cell Types Of The Striatummentioning

confidence: 99%

Loss and remodeling of striatal dendritic spines in Parkinson’s disease: from homeostasis to maladaptive plasticity?

Villalba

Smith

2017

J Neural Transm

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“…Every time one drives a different car, for example, they would have to infer the slight differences in how hard to press the accelerator or brakes, or whether they are driving manual or automatic and thus need to change gears, all whilst paying attention to the road. If this ability is lost, as it potentially is in Parkinson’s disease patients who experience not only a loss of dopaminergic inputs to striatum but also a loss of thalamic inputs to striatal CINs (Smith et al, 2014 , 2016 ), it could deeply impair the ability of individuals to flexibly switch between actions as each situation dictates. This is potentially the neurobiological mechanism that underlies “cognitive rigidity” that is typical of individuals with Parkinson’s disease dementia (Kehagia et al, 2010 ; Smith et al, 2016 ).…”

Section: Introductionmentioning

confidence: 99%

“…If this ability is lost, as it potentially is in Parkinson’s disease patients who experience not only a loss of dopaminergic inputs to striatum but also a loss of thalamic inputs to striatal CINs (Smith et al, 2014 , 2016 ), it could deeply impair the ability of individuals to flexibly switch between actions as each situation dictates. This is potentially the neurobiological mechanism that underlies “cognitive rigidity” that is typical of individuals with Parkinson’s disease dementia (Kehagia et al, 2010 ; Smith et al, 2016 ).…”

Section: Introductionmentioning

confidence: 99%

Parafascicular Thalamic and Orbitofrontal Cortical Inputs to Striatum Represent States for Goal-Directed Action Selection

Stayte

Dhungana

Vissel

et al. 2021

Front. Behav. Neurosci.

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Several lines of evidence accrued over the last 5–10 years have converged to suggest that the parafascicular nucleus of the thalamus and the lateral orbitofrontal cortex each represent or contribute to internal state/context representations that guide action selection in partially observable task situations. In rodents, inactivations of each structure have been found to selectively impair performance in paradigms testing goal-directed action selection, but only when that action selection relies on state representations. Electrophysiological evidence has suggested that each structure achieves this function via inputs onto cholinergic interneurons (CINs) in the dorsomedial striatum. Here, we briefly review these studies, then point to anatomical evidence regarding the afferents of each structure and what they suggest about the specific features that each contribute to internal state representations. Finally, we speculate as to whether this role might be achieved interdependently through direct PF→OFC projections, or through the convergence of independent direct orbitofrontal cortex (OFC) and parafascicular nucleus of the thalamus (PF) inputs onto striatal targets.

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The Thalamostriatal System and Cognition

Cited by 2 publications

References 129 publications

Loss and remodeling of striatal dendritic spines in Parkinson’s disease: from homeostasis to maladaptive plasticity?

Loss and remodeling of striatal dendritic spines in Parkinson’s disease: from homeostasis to maladaptive plasticity?

Parafascicular Thalamic and Orbitofrontal Cortical Inputs to Striatum Represent States for Goal-Directed Action Selection

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