The parafascicular thalamic complex and basal ganglia circuitry: further complexity to the basal ganglia model

Gonzalo, Nancy; Lanciego, José L.; Castle, M.; Vázquez, Armando González; Erro, Elena; Obeso, José A.

doi:10.1016/s1472-9288(02)00007-9

Cited by 6 publications

(7 citation statements)

References 52 publications

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“…The same holds true for PPN neurons innervating the STN (Orieux et al 2000). In order to better understand the role that these subcortical glutamatergic loops play in the pathophysiology of PD, the temporal cascade of events triggering these increased activities should be elucidated in detail (Gonzalo et al 2002). In the parkinsonian state, the current basal ganglia model predicts that STN hyperactivity is due to a decrease in inhibition arising from the GPe (Crossman 1987;Albin et al 1989;DeLong 1990).…”

Section: Discussionmentioning

confidence: 99%

Glutamatergic and cholinergic pedunculopontine neurons innervate the thalamic parafascicular nucleus in rats: changes following experimental parkinsonism

et al. 2011

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The tegmental pedunculopontine nucleus (PPN) is a basal ganglia-related structure that has recently gained renewed interest as a potential surgical target for the treatment of several aspects of Parkinson's disease. However, the underlying anatomical substrates sustaining the choice of the PPN nucleus as a surgical candidate remain poorly understood. Here, we characterized the chemical phenotypes of different subtypes of PPN efferent neurons innervating the rat parafascicular (PF) nucleus. Emphasis was placed on elucidating the impact of unilateral nigrostriatal denervation on the expression patterns of the mRNA coding the vesicular glutamate transporter type 2 (vGlut2 mRNA). We found a bilateral projection from the PPN nucleus to the PF nucleus arising from cholinergic and glutamatergic efferent neurons, with a small fraction of projection neurons co-expressing both cholinergic and glutamatergic markers. Furthermore, the unilateral nigrostriatal depletion induced a bilateral twofold increase in the expression levels of vGlut2 mRNA within the PPN nucleus. Our results support the view that heterogeneous chemical profiles account for PPN efferent neurons innervating thalamic targets. Moreover, a bilateral enhancement of glutamatergic transmission arising from the PPN nucleus occurs following unilateral dopaminergic denervation, therefore sustaining the well-known hyperactivity of the PF nucleus in parkinsonian-like conditions. In conclusion, our data suggest that the ascending projections from the PPN that reach basal ganglia-related targets could play an important role in the pathophysiology of Parkinson's disease.

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Section: Discussionmentioning

confidence: 99%

Glutamatergic and cholinergic pedunculopontine neurons innervate the thalamic parafascicular nucleus in rats: changes following experimental parkinsonism

et al. 2011

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“…Apart from the ventral anterior nucleus (VA) and VL, target sites of the basal ganglia output nuclei have been identified in the centromedian-parafascicular complex (CM-Pf) (Kim et al, 1976;Parent et al, 2001). Neurons in VA, VL, and CM-Pf send axons back mainly to the matrix compartment of the striatum (Carpenter, 1981;Gonzalo et al, 2002;McFarland and Haber, 2000;Parent, 1990;Ragsdale and Graybiel, 1988;Sadikot et al, 1992). Studies suggest that the influence of these projections is excitatory (Haber and Gdowski, 2004;Sadikot et al, 1992).…”

Section: Directmentioning

confidence: 99%

Mean-field modeling of the basal ganglia-thalamocortical system. I

Albada¹,

Robinson²

2009

Journal of Theoretical Biology

151

161

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Parkinsonism leads to various electrophysiological changes in the basal ganglia-thalamocortical system (BGTCS), often including elevated discharge rates of the subthalamic nucleus (STN) and the output nuclei, and reduced activity of the globus pallidus external segment (GPe). These rate changes have been explained qualitatively in terms of the direct/indirect pathway model, involving projections of distinct striatal populations to the output nuclei and GPe. Although these populations partly overlap, evidence suggests dopamine depletion differentially affects cortico-striato-pallidal connection strengths to the two pallidal segments. Dopamine loss may also decrease the striatal signal-to-noise ratio, reducing both corticostriatal coupling and striatal firing thresholds. Additionally, nigrostriatal degeneration may cause secondary changes including weakened lateral inhibition in the GPe, and mesocortical dopamine loss may decrease intracortical excitation and especially inhibition. Here a meanfield model of the BGTCS is presented with structure and parameter estimates closely based on physiology and anatomy. Changes in model rates due to the possible effects of dopamine loss listed above are compared with experiment. Our results suggest that a stronger indirect pathway, possibly combined with a weakened direct pathway, is compatible with empirical evidence. However, altered corticostriatal connection strengths are probably not solely responsible for substantially increased STN activity often found. A lower STN firing threshold, weaker intracortical inhibition, and stronger striato-GPe inhibition help explain the relatively large increase in STN rate. Reduced GPe-GPe inhibition and a lower GPe firing threshold can account for the comparatively small decrease in GPe rate frequently observed. Changes in cortex, GPe, and STN help normalize the cortical rate, also in accord with experiments. The model integrates the basal ganglia into a unified framework along with an existing thalamocortical model that already accounts for a wide range of electrophysiological phenomena. A companion paper discusses the dynamics and oscillations of this combined system.

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“…Significant thalamostriatal projections arise from the relay nuclei CM-Pf, VA, and VL (Carpenter, 1981;Gonzalo et al, 2002;Parent, 1990;Sadikot et al, 1990Sadikot et al, , 1992. Empirical results indicate that the associated neurotransmitter is glutamate (Haber and Gdowski, 2004;Sadikot et al, 1992).…”

Section: Functional Connectivitymentioning

confidence: 99%

Mean-field modeling of the basal ganglia-thalamocortical system. II

Albada

Gray

Drysdale

et al. 2009

Journal of Theoretical Biology

104

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Neuronal correlates of Parkinson's disease (PD) include a shift to lower frequencies in the electroencephalogram (EEG) and enhanced synchronized oscillations at 3-7 and 7-30 Hz in the basal ganglia, thalamus, and cortex. This study describes the dynamics of a recent physiologically-based mean-field model of the basal ganglia-thalamocortical system, and shows how it accounts for many key electrophysiological correlates of PD. Its detailed functional connectivity comprises partially segregated direct and indirect pathways through two populations of striatal neurons, a hyperdirect pathway involving a corticosubthalamic projection, thalamostriatal feedback, and local inhibition in striatum and external pallidum (GPe). In a companion paper, realistic steady-state firing rates were obtained for the healthy state, and after dopamine loss modeled by weaker direct and stronger indirect pathways, reduced intrapallidal inhibition, lower firing thresholds of the GPe and subthalamic nucleus (STN), a stronger projection from striatum to GPe, and weaker cortical interactions. Here it is shown that oscillations around 5 and 20 Hz can arise with a strong indirect pathway, which also causes increased synchronization throughout the basal ganglia. Furthermore, increased theta power with progressive nigrostriatal degeneration is correlated with reduced alpha power and peak frequency, in agreement with empirical results. Unlike the hyperdirect pathway, the indirect pathway sustains oscillations with phase relationships that coincide with those found experimentally. Alterations in the responses of basal ganglia to transient stimuli accord with experimental observations. Reduced cortical gains due to both nigrostriatal and mesocortical dopamine loss lead to slower changes in cortical activity and may be related to bradykinesia. Finally, increased EEG power found in some studies may be partly explained by a lower effective GPe firing threshold, reduced GPe-GPe inhibition, and/or weaker intracortical connections in parkinsonian patients. Strict separation of the direct and indirect pathways is not necessary to obtain these results.

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The parafascicular thalamic complex and basal ganglia circuitry: further complexity to the basal ganglia model

Cited by 6 publications

References 52 publications

Glutamatergic and cholinergic pedunculopontine neurons innervate the thalamic parafascicular nucleus in rats: changes following experimental parkinsonism

Glutamatergic and cholinergic pedunculopontine neurons innervate the thalamic parafascicular nucleus in rats: changes following experimental parkinsonism

Mean-field modeling of the basal ganglia-thalamocortical system. I

Mean-field modeling of the basal ganglia-thalamocortical system. II

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