The role of the thalamus in motor control

Sommer, Marc A.

doi:10.1016/j.conb.2003.10.014

Cited by 184 publications

(139 citation statements)

References 66 publications

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“…1). Given that the thalamus (Groenewegen et al, 1999;Herrero et al, 2002;Sommer, 2003) and ventral striatum/Nac (Groenewegen et al, 1999;Herrero et al, 2002) function as relay centers for information and for paralimbic and motor processing in the brain, the net effect of smoking may be to enhance neurotransmission along cortico-basal ganglia-thalamic loops originating in prefrontal and paralimbic cortices. Neurotransmission through these circuits may be stimulated directly by the interconnected (Sherman, 2001;Sillito and Jones, 2002) nAChR-rich thalamus and visual systems, and/or indirectly through effects on MAO inhibition and DA release in the ventral striatum/NAc (as well as through nicotine stimulation of excitatory glutamatergic input to the dopamine system (Mansvelder et al, 2002)).…”

Section: Discussion: Functional Neuroanatomy Of Tobacco Use and Depenmentioning

confidence: 99%

Functional brain imaging of tobacco use and dependence

Brody

2006

Journal of Psychiatric Research

176

136

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While most cigarette smokers endorse a desire to quit smoking, only about 14% to 49% will achieve abstinence after 6 months or more of treatment. A greater understanding of the effects of smoking on brain function may (in conjunction with other lines of research) result in improved pharmacological (and behavioral) interventions. Many research groups have examined the effects of acute and chronic nicotine/cigarette exposure on brain activity using functional imaging; the purpose of this paper is to synthesize findings from such studies and present a coherent model of brain function in smokers. Responses to acute administration of nicotine/smoking include: a reduction in global brain activity; activation of the prefrontal cortex, thalamus, and visual system; activation of the thalamus and visual cortex during visual cognitive tasks; and increased dopamine (DA) concentration in the ventral striatum/nucleus accumbens. Responses to chronic nicotine/cigarette exposure include decreased monoamine oxidase (MAO) A and B activity in the basal ganglia and a reduction in α 4 β 2 nicotinic acetylcholine receptor (nAChR) availability in the thalamus and putamen. Taken together, these findings indicate that smoking enhances neurotransmission through cortico-basal ganglia-thalamic circuits either by direct stimulation of nAChRs, indirect stimulation via DA release or MAO inhibition, or a combination of these factors. Activation of this circuitry may be responsible for the effects of smoking seen in tobacco dependent subjects, such as improvements in attentional performance, mood, anxiety, and irritability.

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Section: Discussion: Functional Neuroanatomy Of Tobacco Use and Depenmentioning

confidence: 99%

Functional brain imaging of tobacco use and dependence

Brody

2006

Journal of Psychiatric Research

176

136

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“…Correspondingly, we assessed the fidelity of the TCNs in relaying cortical inputs (63), which has been proposed in refs. 34 and 35 as a measure of the restoration of the normal thalamic function.…”

Section: Resultsmentioning

confidence: 99%

“…These mechanisms are selectively elicited by HFS, facilitate the percolation of regularized discharge patterns from the striatum to the GPi, and have a primary role in (B), because the percolated striato-pallidal input combines with the local effects of STN DBS to restore the thalamic relay function (63).…”

mentioning

confidence: 99%

Therapeutic mechanisms of high-frequency stimulation in Parkinson’s disease and neural restoration via loop-based reinforcement

Santaniello¹,

McCarthy

Montgomery³

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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High-frequency deep brain stimulation (HFS) is clinically recognized to treat parkinsonian movement disorders, but its mechanisms remain elusive. Current hypotheses suggest that the therapeutic merit of HFS stems from increasing the regularity of the firing patterns in the basal ganglia (BG). Although this is consistent with experiments in humans and animal models of Parkinsonism, it is unclear how the pattern regularization would originate from HFS. To address this question, we built a computational model of the cortico-BG-thalamo-cortical loop in normal and parkinsonian conditions. We simulated the effects of subthalamic deep brain stimulation both proximally to the stimulation site and distally through orthodromic and antidromic mechanisms for several stimulation frequencies and, correspondingly, we studied the evolution of the firing patterns in the loop. The model closely reproduced experimental evidence for each structure in the loop and showed that neither the proximal effects nor the distal effects individually account for the observed pattern changes, whereas the combined impact of these effects increases with the stimulation frequency and becomes significant for HFS. Perturbations evoked proximally and distally propagate along the loop, rendezvous in the striatum, and, for HFS, positively overlap (reinforcement), thus causing larger poststimulus activation and more regular patterns in striatum. Reinforcement is maximal for the clinically relevant 130-Hz stimulation and restores a more normal activity in the nuclei downstream. These results suggest that reinforcement may be pivotal to achieve pattern regularization and restore the neural activity in the nuclei downstream and may stem from frequency-selective resonant properties of the loop.igh-frequency (i.e., above 100 Hz) deep brain stimulation (HFS) of the basal ganglia (BG) and thalamus is clinically recognized to treat movement disorders in Parkinson's disease (PD) (1-4), but its therapeutic mechanisms remain unclear (5, 6).Early hypotheses about HFS were derived from the rate-based model of the BG function (7,8) and postulated the disruption of the output of the BG-thalamic system via either the inactivation of neurons in the stimulated site (target) (9-15), which would provide an effect similar to a surgical lesion, or the abnormal excitation of axons projecting out of the target (16-19), which would disrupt the neuronal activity in the structures downstream, including any pathophysiological activity (20).More recently, an ever-growing number of experiments in PD humans and animal models of Parkinsonism has indicated that HFS affects the firing patterns of the neurons rather than the mean firing rate both in the target and the structures downstream (18,19,(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31) and it replaces repetitive low-frequency (i.e., ≤50 Hz) bursting patterns with regularized (i.e., more tonic) patterns at higher frequencies (25,26). It has been proposed that increased pattern regularity of neurons in the target may be therapeutic (...

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“…There are other signals arriving at higher order thalamic nuclei, however, that could be driver inputs but not corollaries. For example, inputs to MD other than those from the superior colliculus come from the cerebellum and the basal ganglia, and these may contribute to the control of movement rather than producing a corollary signal of that movement; thus far there is not enough evidence to decide (Sommer, 2003).…”

Section: Conclusion: Motor Drivers and Sensory Driversmentioning

confidence: 99%

Drivers from the deep: the contribution of collicular input to thalamocortical processing

Wurtz

Sommer

Cavanaugh

2005

Progress in Brain Research

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A traditional view of the thalamus is that it is a relay station which receives sensory input and conveys this information to cortex. This sensory input determines most of the properties of first order thalamic neurons, and so is said to drive, rather than modulate, these neurons. This holds as a rule for first order thalamic nuclei, but in contrast, higher order thalamic nuclei receive much of their driver input back from cerebral cortex. In addition, higher order thalamic neurons receive inputs from subcortical movement-related centers. In the terminology popularized from studies of the sensory system, can we consider these ascending motor inputs to thalamus from subcortical structures to be modulators, subtly influencing the activity of their target neurons, or drivers, dictating the activity of their target neurons? This chapter summarizes relevant evidence from neuronal recording, inactivation, and stimulation of pathways projecting from the superior colliculus through thalamus to cerebral cortex. The study concludes that many inputs to the higher order nuclei of the thalamus from subcortical oculomotor areas -from the superior colliculus and probably other midbrain and pontine regions -should be regarded as motor drivers analogous to the sensory drivers at the first order thalamic nuclei. These motor drivers at the thalamus are viewed as being at the top of a series of feedback loops that provide information on impending actions, just as sensory drivers provide information about the external environment.

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The role of the thalamus in motor control

Cited by 184 publications

References 66 publications

Functional brain imaging of tobacco use and dependence

Functional brain imaging of tobacco use and dependence

Therapeutic mechanisms of high-frequency stimulation in Parkinson’s disease and neural restoration via loop-based reinforcement

Drivers from the deep: the contribution of collicular input to thalamocortical processing

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