Event Title

Cellular Pallidostriatal Connectivity Within a Parkinson's Disease Model

Session Number

Q36

Advisor(s)

Savio Chan, Northwestern University
Harry Xenias, Northwestern University

Location

A-133

Start Date

28-4-2016 11:05 AM

End Date

28-4-2016 11:30 AM

Disciplines

Neuroscience and Neurobiology

Abstract

Parkinson's disease (PD) is a neurodegenerative disorder of the basal ganglia. Within these nuclei, the dorsal striatum(dSTR) is innervated by the external globus pallidus (GPe) via an inhibitory pathway. However, specific striatal targets and locations of GPe- SPN contacts have not yet been described. We used transgenic mice and a technique called whole cell patch clamp recording, which allows filling of recorded cells, dStr spiny projection neurons (SPNs), with fluorescent dyes. We then used confocal microscopy to image pallidostriatal contacts. This aided us in determining if the pallidostriatal projection in a PD model is altered. Finding the exact location of GPe-SPN contacts relative to the SPN soma provides indication about the nature of the GPe input. Contacts closer to SPN somas elicit stronger inhibition. Between two SPN cell types, we found GPe-SPN interaction varied. Contacts onto D2+ SPNs were more proximal than D1+ SPNs. Additionally, we found that in a PD model, GPe-SPN contacts onto D2+ SPNs occurred closer to the soma than in a healty model. However, GPe-SPN contacts onto D1+ SPNs occurred farther from the soma, contrary to our expectation. Understanding the pallidostriatal projection could provide insight into the pathogenesis of PD, and subsequently, its treatment.


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Apr 28th, 11:05 AM Apr 28th, 11:30 AM

Cellular Pallidostriatal Connectivity Within a Parkinson's Disease Model

A-133

Parkinson's disease (PD) is a neurodegenerative disorder of the basal ganglia. Within these nuclei, the dorsal striatum(dSTR) is innervated by the external globus pallidus (GPe) via an inhibitory pathway. However, specific striatal targets and locations of GPe- SPN contacts have not yet been described. We used transgenic mice and a technique called whole cell patch clamp recording, which allows filling of recorded cells, dStr spiny projection neurons (SPNs), with fluorescent dyes. We then used confocal microscopy to image pallidostriatal contacts. This aided us in determining if the pallidostriatal projection in a PD model is altered. Finding the exact location of GPe-SPN contacts relative to the SPN soma provides indication about the nature of the GPe input. Contacts closer to SPN somas elicit stronger inhibition. Between two SPN cell types, we found GPe-SPN interaction varied. Contacts onto D2+ SPNs were more proximal than D1+ SPNs. Additionally, we found that in a PD model, GPe-SPN contacts onto D2+ SPNs occurred closer to the soma than in a healty model. However, GPe-SPN contacts onto D1+ SPNs occurred farther from the soma, contrary to our expectation. Understanding the pallidostriatal projection could provide insight into the pathogenesis of PD, and subsequently, its treatment.