Abstract
The activity of basal ganglia input receiving motor thalamus (BGMT) makes a critical impact on motor cortical processing, but modification in BGMT processing with Parkinsonian conditions has not be investigated at the cellular level. Such changes may well be expected because of homeostatic regulation of neural excitability in the presence of altered synaptic drive with dopamine depletion. We addressed this question by comparing BGMT properties in brain slice recordings between control and unilaterally 6-hydroxydopamine hydrochloride (6-OHDA)-treated adult mice. At a minimum of one month after 6-OHDA treatment, BGMT neurons showed a highly significant increase in intrinsic excitability, which was primarily because of a decrease in M-type potassium current. BGMT neurons after 6-OHDA treatment also showed an increase in T-type calcium rebound spikes following hyperpolarizing current steps. Biophysical computer modeling of a thalamic neuron demonstrated that an increase in rebound spiking can also be accounted for by a decrease in the M-type potassium current. Modeling also showed that an increase in sag with hyperpolarizing steps found after 6-OHDA treatment could in part but not fully be accounted for by the decrease in M-type current. These findings support the hypothesis that homeostatic changes in BGMT neural properties following 6-OHDA treatment likely influence the signal processing taking place in the BG thalamocortical network in Parkinson’s disease.
Highlights
The basal ganglia (BG) form strong connections with motor and premotor cerebral cortical areas through output from the substantia nigra pars reticulata (SNr) and internal globus pallidus (GPi; Alexander et al, 1986; Alexander and Crutcher, 1990)
The goal of our study was to determine any changes in neural properties in the area of motor thalamus that receives BG input (BGMT) in mice unilaterally treated with 6-OHDA in the median forebrain bundle as a standard rodent model of robust dopamine neuron lesioning
Changes in cellular properties have been observed in multiple key structures related to Parkinsonian motor dysfunction beyond primary striatal dysfunction directly elicited by dopamine depletion
Summary
The basal ganglia (BG) form strong connections with motor and premotor cerebral cortical areas through output from the substantia nigra pars reticulata (SNr) and internal globus pallidus (GPi; Alexander et al, 1986; Alexander and Crutcher, 1990) These BG outputs terminate as GABAergic inhibitory connections in the motor thalamus, in rodents primarily in the ventromedial (VM). January/February 2021, 8(1) ENEURO.0436-20.2021 1–18 and ventroanterior (VAL) nuclei (VM/VAL; Beckstead et al, 1979; Kuramoto et al, 2009, 2011; Bosch-Bouju et al, 2013) We refer to this as the BG input receiving motor thalamus (BGMT).
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