RT Journal Article
SR Electronic
T1 Basal ganglia and cortical control of thalamic rebound spikes
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 386920
DO 10.1101/386920
A1 Mohammadreza Mohagheghi Nejad
A1 Stefan Rotter
A1 Robert Schmidt
YR 2021
UL http://biorxiv.org/content/early/2021/04/25/386920.abstract
AB Movement-related decreases in firing rate have been observed in basal ganglia output neurons. They may transmit motor signals to the thalamus, but the effect of these firing rate decreases on downstream neurons in the motor thalamus is not known. One possibility is that they lead to thalamic post-inhibitory rebound spikes. However, it has also been argued that the physiological conditions permitting rebound spiking are pathological, and primarily present in Parkinson’s disease. As in Parkinson’s disease neural activity becomes pathologically correlated, we investigated the impact of correlations in basal ganglia output on the transmission of motor signals using a Hodgkin-Huxley model of thalamocortical neurons. We found that such correlations disrupt the transmission of motor signals via rebound spikes by decreasing the signal-to-noise ratio and increasing the trial-to-trial variability. We further examined the role of sensory responses in basal ganglia output neurons and the effect of cortical excitation of motor thalamus in modulating rebound spiking. Interestingly, both could either promote or suppress the generation of rebound spikes depending on their timing relative to the motor signal. Finally, we determined parameter regimes, such as levels of excitation, under which rebound spiking is feasible in the model, and confirmed that the conditions for rebound spiking are primarily given in pathological regimes. However, we also identified specific conditions in the model that would allow rebound spiking to occur in healthy animals in a small subset of thalamic neurons. Overall, our model provides novel insights into differences between normal and pathological transmission of motor signals.Competing Interest StatementThe authors have declared no competing interest.AbbreviationsBINBinomially distributedCXCortexDBSDeep Brain StimulationDLMDorsolateral nucleus of the anterior thalamusEXPExponentially distributedGABAgamma-Aminobutyric acidGPeGlobus Pallidus externaGPiGlobus Pallidus internaSNrSubstantia Nigra pars reticulataSTNSubthalamic NucleusTCThalamocortical neuronTQTransmission Quality