Organization of projections from the anterior pole of the nucleus reticularis thalami (NRT) to subdivisions of the motor thalamus: Light and electron microscopic studies in the Rhesus monkey

Ilinsky, Igor A.; Ambardekar, Amrut V.; Kultas‐Ilinsky, K.

doi:10.1002/(sici)1096-9861(19990705)409:3<369::aid-cne3>3.0.co;2-h

Cited by 47 publications

(17 citation statements)

References 77 publications

(83 reference statements)

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“…We focused on MD, VA, and AM, three thalamic nuclei that receive the majority of prefrontal cortical input (Dermon and Barbas, 1994;Kultas-Ilinsky et al, 1995;Tai et al, 1995;Ilinsky et al, 1999;Xiao and Barbas, 2004) (for review, see Steriade et al, 1997). After injection of retrograde tracers in each of these thalamic nuclei (Fig.…”

Section: Prefrontal Terminations Colocalized With Trn Connections Witmentioning

confidence: 99%

“…In rats, cats, rabbits, and primates, cortical and thalamic afferents in TRN are topographically organized (Crabtree and Killackey, 1989;Cicirata et al, 1990;Conley and Diamond, 1990;Cornwall et al, 1990;Crabtree, 1992aCrabtree, ,b, 1996Crabtree, , 1998Crabtree, , 1999Lozsadi, 1994Lozsadi, , 1995Ilinsky et al, 1999). Along the rostrocaudal axis, centroposterior loci in TRN are respectively linked with the somatosensory, visual, and auditory cortices and their associated thalamic nuclei.…”

Section: Topography Of Cortical Projections In Trn: the Prefrontal Sementioning

confidence: 99%

“…In agreement with previous studies (for review, see Guillery and Harting, 2003), there was considerable overlap in the terminal fields of distinct prefrontal areas. Moreover, the prefrontal TRN sector projects to MD, VA, and AM, three thalamic nuclei connected with prefrontal cortices (Pinault and Deschenes, 1998;Ilinsky et al, 1999;Xiao and Barbas, 2004).…”

Section: Topography Of Cortical Projections In Trn: the Prefrontal Sementioning

confidence: 99%

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Prefrontal Projections to the Thalamic Reticular Nucleus form a Unique Circuit for Attentional Mechanisms

2006

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The inhibitory thalamic reticular nucleus (TRN) intercepts and modulates all corticothalamic and thalamocortical communications. Previous studies showed that projections from sensory and motor cortices originate in layer VI and terminate as small boutons in central and caudal TRN. Here we show that prefrontal projections to TRN in rhesus monkeys have a different topographic organization and mode of termination. Prefrontal cortices projected mainly to the anterior TRN, at sites connected with the mediodorsal, ventral anterior, and anterior medial thalamic nuclei. However, projections from areas 46, 13, and 9 terminated widely in TRN and colocalized caudally with projections from temporal auditory, visual, and polymodal association cortices. Population analysis and serial EM reconstruction revealed two distinct classes of corticoreticular terminals synapsing with GABA/parvalbumin-positive dendritic shafts of TRN neurons. Most labeled boutons from prefrontal axons were small, but a second class of large boutons was also prominent. This is in contrast to the homogeneous small TRN terminations from sensory cortices noted previously and in the present study, which are thought to arise exclusively from layer VI. The two bouton types were often observed on the same axon, suggesting that both prefrontal layers V and VI could project to TRN. The dual mode of termination suggests a more complex role of prefrontal input in the functional regulation of TRN and gating of thalamic output back to the cortex. The targeting of sensory tiers of TRN by specific prefrontal areas may underlie attentional regulation for the selection of relevant sensory signals and suppression of distractors.

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Section: Prefrontal Terminations Colocalized With Trn Connections Witmentioning

confidence: 99%

Section: Topography Of Cortical Projections In Trn: the Prefrontal Sementioning

confidence: 99%

Section: Topography Of Cortical Projections In Trn: the Prefrontal Sementioning

confidence: 99%

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Prefrontal Projections to the Thalamic Reticular Nucleus form a Unique Circuit for Attentional Mechanisms

2006

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“…The thalamic nuclei that receive input from basal ganglia output nuclei also receive diverse inputs from cortex, brainstem, reticular thalamic nucleus and in some cases from the cerebellum (Angaut et al, 1985; Capozzo et al, 2003; Cornwall and Phillipson, 1988; Guillery and Harting, 2003; Ilinsky et al, 1999; Ilinsky and Kultas-Ilinsky, 2001; Nakano et al, 1985; Royce, 1983; Shinoda et al, 1993; Van der Werf et al, 2002). Inputs to individual thalamic nuclei are frequently characterized as either ‘drivers’ or ‘modulators’, depending on their functional role.…”

Section: Introductionmentioning

confidence: 99%

Parafascicular thalamic nucleus activity in a rat model of Parkinson's disease

Parr‐Brownlie

Poloskey

Bergstrom

et al. 2009

Experimental Neurology

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Parkinson's disease is associated with increased oscillatory firing patterns in basal ganglia output, which are thought to disrupt thalamocortical activity. However, it is unclear how specific thalamic nuclei are affected by these changes in basal ganglia activity. The thalamic parafascicular nucleus (PFN) receives input from basal ganglia output nuclei and directly projects to the subthalamic nucleus (STN), striatum and cortex; thus basal ganglia mediated changes on PFN activity may further impact basal ganglia and cortical functions. To investigate the impact of increased oscillatory activity in basal ganglia output on PFN activity after dopamine cell lesion, PFN single-unit and local field potential activities were recorded in neurologically intact (control) rats and in both non-lesioned and dopamine lesioned hemispheres of unilateral 6-hydroxydopamine lesioned rats anesthetized with urethane. Firing rates were unchanged 1-2 weeks after lesion; however, significantly fewer spontaneously active PFN neurons were evident. Firing pattern assessments after lesion showed a larger proportion of PFN spike trains had 0.3-2.5 Hz oscillatory activity and significantly fewer spike trains exhibited low threshold calcium spike (LTS) bursts. In paired recordings, more PFN-STN spike oscillations were significantly correlated, but as these oscillations were in-phase, results are inconsistent with feedforward control of PFN activity by inhibitory oscillatory basal ganglia output. Furthermore, the decreased incidence of LTS bursts is incompatible with inhibitory basal ganglia output inducing rebound bursting in PFN after dopamine lesion. Together, results show that robust oscillatory activity observed in basal ganglia output nuclei after dopamine cell lesion does not directly drive changes in PFN oscillatory activity.

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“…To our knowledge, this is the first direct evidence for perisynaptic expression of T-type calcium channels in the mammalian thalamus. Although the source(s) of terminals associated with these channels was not determined, their ultrastructural features suggest that those forming asymmetric synapses likely originate from the cerebral cortex, while those forming symmetric synapses may come from GABAergic reticular neurons or interneurons (Liu et al, 1995; Ilinsky et al, 1999; Jones, 2007). However, we cannot rule out that some of these inputs may also arise from monoaminergic or cholinergic ascending brainstem afferents.…”

Section: Discussionmentioning

confidence: 99%

Sub-synaptic localization of Cav3.1 T-type calcium channels in the thalamus of normal and parkinsonian monkeys

et al. 2016

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T-type calcium channels (Cav3) are key mediators of thalamic bursting activity, but also regulate single cells excitability, dendritic integration, synaptic strength and transmitter release. These functions are strongly influenced by the subcellular and subsynaptic localization of Cav3 channels along the somatodendritic domain of thalamic cells. In Parkinson’s disease, T-type calcium channels dysfunction in the basal ganglia-receiving thalamic nuclei likely contributes to pathological thalamic bursting activity. In this study, we analyzed the cellular, subcellular, and subsynaptic localization of the Cav3.1 channel in the ventral anterior (VA) and centromedian/parafascicular (CM/Pf) thalamic nuclei, the main thalamic targets of basal ganglia output, in normal and parkinsonian monkeys. All thalamic nuclei displayed strong Cav3.1 neuropil immunoreactivity, although the intensity of immunolabeling in CM/Pf was significantly lower than in VA. Ultrastructurally, 70–80% of the Cav3.1-immunoreactive structures were dendritic shafts. Using immunogold labeling, Cav3.1 was commonly found perisynaptic to asymmetric and symmetric axo-dendritic synapses, suggesting a role of Cav3.1 in regulating excitatory and inhibitory neurotransmission. Significant labeling was also found at non-synaptic sites along the plasma membrane of thalamic neurons. There was no difference in the overall pattern and intensity of immunostaining between normal and parkinsonian monkeys, suggesting that the increased rebound bursting in the parkinsonian state is not driven by changes in Cav3.1 expression. Thus, T-type calcium channels are located to subserve neuronal bursting, but also regulate glutamatergic and non-glutamatergic transmission along the whole somatodendritic domain of basal ganglia-receiving neurons of the primate thalamus.

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Organization of projections from the anterior pole of the nucleus reticularis thalami (NRT) to subdivisions of the motor thalamus: Light and electron microscopic studies in the Rhesus monkey

Cited by 47 publications

References 77 publications

Prefrontal Projections to the Thalamic Reticular Nucleus form a Unique Circuit for Attentional Mechanisms

Prefrontal Projections to the Thalamic Reticular Nucleus form a Unique Circuit for Attentional Mechanisms

Parafascicular thalamic nucleus activity in a rat model of Parkinson's disease

Sub-synaptic localization of Cav3.1 T-type calcium channels in the thalamus of normal and parkinsonian monkeys

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