Biology subjects

Mirzaei, A.

Publications and source records attributed to Mirzaei, A..

3 recordsLinked to original sources

bioRxiv2020

Effect of Stimulation of Subthalamic Nucleus on Beta Oscillations and Thalamus Tremor Activity in a Computational Model of Parkinson's Disease

Parkinsons disease (PD) is associated with abnormal {beta} band oscillations (13-30 Hz) in the cortico-basal ganglia circuits. Abnormally increased striato-pallidal inhibition and strengthening the synaptic coupling between subthalamic nucleus (STN) and globus pallidus externa (GPe), due to the loss of dopamine, are considered as the potential sources of {beta} oscillations in the basal ganglia. Deep brain stimulation (DBS) of the basal ganglia subregions is known as a way to reduce the pathological {beta} oscillations and motor deficits related to PD. Despite the success of the DBS, its underlying mechanism is poorly understood and, there is controversy about the inhibitory or excitatory role of the DBS in the literature. Here, we utilized a computational network model of basal ganglia which consists of STN, GPe, globus pallidus interna (GPi), and thalamic neuronal population. This model can reproduce healthy and pathological {beta} oscillations similar to what has been observed in experimental studies. Using this model, we investigated the effect of DBS to understand whether its effect is excitatory or inhibitory. Our results show that the excitatory DBS (EDBS) is able to quench the pathological synchrony and {beta} oscillations, while, applying inhibitory DBS (IDBS) failed to quench the PD signs. In light of simulation results, we conclude that the effect of the DBS on its target is excitatory.

neuroscience↗

bioRxiv2017

Modulation of high frequency by low-frequency Oscillations in the basal ganglia

Modulation of beta band fioscillatory activity (15-30 Hz) by delta band oscillatory activity (1-3 Hz) in the cortico-basal ganglia loop is important for normal basal ganglia functions. However, the neural mechanisms underlying this modulation are poorly understood. To understand the mechanisms underlying such frequency modulations in the basal ganglia, we use large scale subthalamo-pallidal network model stimulated via a delta-frequency input signal. We show that inhibition of external Globus Pallidus (GPe) and excitation of the Subthalamic nucleus (STN) using the delta-band stimulation leads to the same delta-beta interactions in the network model as the experimental results observed in healthy basal ganglia. In addition, we show that pathological beta oscillations in the network model decorrelates the delta-beta link in the network model. In general, using our simulation results, we propose that striato-pallidal inhibition and cortico-subthalamic excitation are the potential sources of the delta-beta link observed in the intact basal ganglia.

neuroscience↗

bioRxiv2017

Sensorimotor Processing In The Basal Ganglia Leads To Transient Beta Oscillations During Behavior

Brief epochs of beta oscillations have been implicated in sensorimotor control in the basal ganglia of task-performing healthy animals. However, which neural processes underlie their generation and how they are affected by sensorimotor processing remains unclear. To determine the mechanisms underlying transient beta oscillations in the local field potential (LFP), we combined computational modeling of the subthalamo-pallidal network for the generation of beta oscillations with realistic stimulation patterns derived from single unit data. The single unit data were recorded from different basal ganglia subregions in rats performing a cued choice task. In the recordings we found distinct firing patterns in the striatum, globus pallidus and subthalamic nucleus related to sensory and motor events during the behavioral task. Using these firing patterns to generate realistic inputs to our network model lead to transient beta oscillations with the same time course as the rat LFP data. In addition, our model can account for further non-intuitive aspects of beta modulation, including beta phase resets following sensory cues and correlations with reaction time. Overall, our model can explain how the combination of temporally regulated sensory responses of the subthalamic nucleus, ramping activity of the subthalamic nucleus, and movement-related activity of the globus pallidus, leads to transient beta oscillations during behavior.\n\nSignificance StatementTransient beta oscillations emerge in the normal functioning cortico-basal ganglia loop during behavior. In this work we employ a unique approach connecting a computational model closely with experimental data. In this way we achieve a simulation environment for our model that mimics natural input patterns in awake behaving animals. Using this approach we demonstrate that a computational model for beta oscillations in Parkinsons disease can also account for complex patterns of transient beta oscillations in healthy animals. Therefore, we propose that transient beta oscillations in healthy animals share the same mechanism with pathological beta oscillations in Parkinsons disease. This important result connects functional and pathological roles of beta oscillations in the basal ganglia.

neuroscience↗