Synchronized activation of striatal direct and indirect pathways underlies the behavior in unilateral dopamine-depleted mice.
For more than three decades it has been known, that striatal neurons become hyperactive after the loss of dopamine input, but the involvement of dopamine (DA) D1- or D2-receptor-expressing neurons has only been demonstrated indirectly. By recording neuronal activity using fluorescent calcium indicators in D1 or D2 eGFP-expressing mice, we showed that following dopamine depletion, both types of striatal output neurons are involved in the large increase in neuronal activity generating a characteristic cell assembly of particular neurons that dominate the pattern. When we expressed channelrhodopsin in all the output neurons, light activation in freely moving animals, caused turning like that following dopamine loss. However, if the light stimulation was patterned in pulses the animals circled in the other direction. To explore the neuronal participation during this stimulation we infected normal mice with channelrhodopsin and calcium indicator in striatal output neurons. In slices made from these animals, continuous light stimulation for 15 s induced many cells to be active together and a particular dominant group of neurons, whereas light in patterned pulses activated fewer cells in more variable groups. These results suggest that the simultaneous activity of a large dominant group of striatal output neurons is intimately associated with parkinsonian symptoms.
['Jáidar|Omar|O|', 'Carrillo-Reid|Luis|L|', 'Nakano|Yoko|Y|', 'Lopez-Huerta|Violeta Gisselle|VG|', 'Hernandez-Cruz|Arturo|A|', 'Bargas|José|J|0000-0002-8205-8163', 'Garcia-Munoz|Marianela|M|', 'Arbuthnott|Gordon William|GW|0000-0002-3386-8362']
D000818:Animals D001479:Basal Ganglia D002118:Calcium D003342:Corpus Striatum D004298:Dopamine D008297:Male D051379:Mice D009474:Neurons D010302:Parkinson Disease, Secondary D017447:Receptors, Dopamine D1 D017448:Receptors, Dopamine D2
assemblies Parkinson's disease basal ganglia calcium imaging optogenetics