Striatal Projection of dSPNs to GPe Pathway in Relation to Parkinson’s disease
Advisor(s)
Dr. Qiaoling Cui , Northwestern University
Dr. Savio Chan, Northwestern University
Location
Room A155
Start Date
26-4-2019 10:45 AM
End Date
26-4-2019 11:00 AM
Abstract
The external globus pallidus, located in the basal ganglia, is associated with a variety of functions including the control of voluntary motor movements. To fully understand the input control of the GPe, we focused upon the projection from the dSPN neuron class to the Npas1 neuron class within the GPe of Parkinson’s Disease models and control models of mice. Using cell-specific transgenic mice, measures of the current amplitudes of dSPN-Npas1 projection were recorded and investigated. To unveil the underlying mechanism, the difference in the number of dSPN-GPe synaptic contacts between a mouse model of PD and control mice will be explored. To explore if synaptic contacts are increased accordingly, synaptic contacts of dSPN-GPe pathway were visualized using immunohistochemistry and counted using FIJI software. Synaptic contact will be visualized and identified through two ways: 1) the immediate spatial relationship between GFP+ terminals from dSPNs and postsynaptic marker gephyrin; 2) the overlap between GFP+ terminals from dSPNs and presynaptic marker Vesicular GABA transporter (VGAT). Overall, the investigation of the dSPN-Npas1 pathway within the basal ganglia helps to lead to a better understanding of the wiring principle of the basal ganglia in the Parkinson’s disease, allowing for further research and cures for this movement disorder.
Striatal Projection of dSPNs to GPe Pathway in Relation to Parkinson’s disease
Room A155
The external globus pallidus, located in the basal ganglia, is associated with a variety of functions including the control of voluntary motor movements. To fully understand the input control of the GPe, we focused upon the projection from the dSPN neuron class to the Npas1 neuron class within the GPe of Parkinson’s Disease models and control models of mice. Using cell-specific transgenic mice, measures of the current amplitudes of dSPN-Npas1 projection were recorded and investigated. To unveil the underlying mechanism, the difference in the number of dSPN-GPe synaptic contacts between a mouse model of PD and control mice will be explored. To explore if synaptic contacts are increased accordingly, synaptic contacts of dSPN-GPe pathway were visualized using immunohistochemistry and counted using FIJI software. Synaptic contact will be visualized and identified through two ways: 1) the immediate spatial relationship between GFP+ terminals from dSPNs and postsynaptic marker gephyrin; 2) the overlap between GFP+ terminals from dSPNs and presynaptic marker Vesicular GABA transporter (VGAT). Overall, the investigation of the dSPN-Npas1 pathway within the basal ganglia helps to lead to a better understanding of the wiring principle of the basal ganglia in the Parkinson’s disease, allowing for further research and cures for this movement disorder.