Motor thalamus integration of cortical, cerebellar and basal ganglia information: implications for normal and parkinsonian conditions

Abstract

Motor thalamus (Mthal) is implicated in the control of movement because it is strategically located between motor areas of the cerebral cortex and motor-related subcortical structures, such as the cerebellum and basal ganglia (BG). The role of BG and cerebellum in motor control has been extensively studied but how Mthal processes inputs from these two networks is unclear. Specifically, there is considerable debate about the role of BG inputs on Mthal activity. This review summarizes anatomical and physiological knowledge of the Mthal and its afferents and reviews current theories of Mthal function by discussing the impact of cortical, BG and cerebellar inputs on Mthal activity. One view is that Mthal activity in BG and cerebellar-receiving territories is primarily “driven” by glutamatergic inputs from the cortex or cerebellum, respectively, whereas BG inputs are modulatory and do not strongly determine Mthal activity. This theory is steeped in the assumption that the Mthal processes information in the same way as sensory thalamus, through interactions of modulatory inputs with a single driver input. Another view, from BG models, is that BG exert primary control on the BG-receiving Mthal so it effectively relays information from BG to cortex. We propose a new “super-integrator” theory where each Mthal territory processes multiple driver or driver-like inputs (cortex and BG, cortex and cerebellum), which are the result of considerable integrative processing. Thus, BG and cerebellar Mthal territories assimilate motivational and proprioceptive motor information previously integrated in cortico-BG and cortico-cerebellar networks, respectively, to develop sophisticated motor signals that are transmitted in parallel pathways to cortical areas for optimal generation of motor programmes. Finally, we briefly review the pathophysiological changes that occur in the BG in parkinsonism and generate testable hypotheses about how these may affect processing of inputs in the Mthal.

Anatomical localization of Cav3.1 calcium channels and electrophysiological effects of T-type calcium channel blockade in the motor thalamus of MPTP-treated monkeys

“…Similar decreases in firing rates were found in several previous studies, including Parkinsonian patients (Chen et al 2010;Molnar et al 2005), MPTP-treated cats (Schneider and Rothblat 1996), and 6-hydroxydopamine (6-OHDA)-lesioned rats (Ni et al 2000). However, other studies found either no change in thalamic firing activity in MPTP-treated monkeys (Pessiglione et al 2005) or increases in firing in 6-OHDA-treated rats (Bosch-Bouju et al 2014). The discrepancies between these studies may be related to species and experimental differences across studies, such as the specific cell types selected for recording, the state of wakefulness of the animals, or the severity of Parkinsonism.…”

“…The borders between the cerebellar-and the basal ganglia-receiving territories are interdigitating; however, the cerebellar-and basal ganglia-receiving thalamic cells are distinct in primates [for review, see Bosch-Bouju et al (2013)]. The overlap should not be a concern for the present study, because almost all cells included in the presented analysis were at least 0.5 mm away from the border between the cerebellar and basal ganglia territories, as defined in Lanciego's atlas (Lanciego and Vazquez 2012).…”

CACNA1Hmissense mutations associated with amyotrophic lateral sclerosis alter Cav3.2 T-type calcium channel activity and reticular thalamic neuron firing

“…21,22 All of these aspects are particularly important to the functioning of the thalamocortical network, a brain structure implicated in motor-related activities. [23][24][25][26] In the present study, we analyzed the functional expression of the 2 ALS-associated missense mutations in Ca v 3.2 channels. We show that both mutations produce significant alterations on the channel activity, consistent with a loss of channel function.…”

Treatment of Chronic Pain: Diffusion Tensor Imaging Identification of the Ventroposterolateral Nucleus Confirmed with Successful Deep Brain Stimulation

“…Studies in non-human primates have shown that the thalamic ventrobasal complex (the caudal division of the VPL nucleus and the large-celled part of the ventroposteromedial nucleus) project to primary and secondary somatosensory areas (S1 and S2) [10]. The ventral lateral and ventral anterior nuclei project to primary motor cortex (M1) and premotor cortex [10].…”