| First Author | Ketzef M | Year | 2017 |
| Journal | Neuron | Volume | 94 |
| Issue | 4 | Pages | 855-865.e5 |
| PubMed ID | 28521136 | Mgi Jnum | J:249915 |
| Mgi Id | MGI:6100426 | Doi | 10.1016/j.neuron.2017.05.004 |
| Citation | Ketzef M, et al. (2017) Dopamine Depletion Impairs Bilateral Sensory Processing in the Striatum in a Pathway-Dependent Manner. Neuron 94(4):855-865.e5 |
| abstractText | Parkinson's disease (PD) is a movement disorder caused by the loss of dopaminergic innervation, particularly to the striatum. PD patients often exhibit sensory impairments, yet the underlying network mechanisms are unknown. Here we examined how dopamine (DA) depletion affects sensory processing in the mouse striatum. We used the optopatcher for online identification of direct and indirect pathway projection neurons (MSNs) during in vivo whole-cell recordings. In control mice, MSNs encoded the laterality of sensory inputs with larger and earlier responses to contralateral than ipsilateral whisker deflection. This laterality coding was lost in DA-depleted mice due to adaptive changes in the intrinsic and synaptic properties, mainly, of direct pathway MSNs. L-DOPA treatment restored laterality coding by increasing the separation between ipsilateral and contralateral responses. Our results show that DA depletion impairs bilateral tactile acuity in a pathway-dependent manner, thus providing unexpected insights into the network mechanisms underlying sensory deficits in PD. VIDEO ABSTRACT. |
