Differences in synaptic integration between direct and indirect striatal projection neurons: Role of Ca V 3 channels
Por:
Garcia-Vilchis, Brisa, Suarez, Paola, Serrano-Reyes, Miguel, Arias-Garcia, Mario, Tapia, Dagoberto, Duhne, Mariana, Bargas, Jose, Galarraga, Elvira
Publicada:
1 abr 2019
Ahead of Print:
1 ene 2018
Categoría:
Cellular and molecular neuroscience
Resumen:
Different corticostriatal suprathreshold responses in direct and indirect striatal projection neurons (SPNs) of rodents have been reported. Responses consist in prolonged synaptic potentials of polysynaptic and intrinsic origin, in which voltage-gated Ca 2 ? currents play a role. Recording simultaneous Ca 2 ? imaging and voltage responses at the soma, while activating the corticostriatal pathway, we show that encoding of synaptic responses into trains of action potentials (APs) is different in SPNs: firing of APs in D1-SPNs increase gradually, in parallel with Ca 2 ? entry, as a function of stimulus intensity. In contrast, D2-SPNs attain a maximum number of evoked spikes at low stimulus intensities, Ca 2 ? entry is limited, and both remain the same in spite of increasing stimulus strength. Stimulus needs to reach certain intensity, to have propagated Ca 2 ? potentials to the soma plus a sudden step in Ca 2 ? entry, without changing the number of fired APs, phenomena never seen in D1-SPNs. Constant firing in spite of changing stimulus, suggested the involvement of underlying inactivating potentials. We found that Ca?3 currents contribute to Ca 2+ entry in both classes of SPNs, but have a more notable effect in D2-SPNs, where a low-threshold spike was disclosed. Blockade of Ca V 3 channels retarded the steep rise in firing in D2-SPNs. Inhibition block increased the number of spikes fired by D2-SPNs, without changing firing in D1-SPNs. These differences in synaptic integration enable a biophysical dissimilarity: dendritic inhibition appears to be more relevant for D2-SPNs. This may imply distinctions in the set of interneurons affecting each SPN class. © 2018 Wiley Periodicals, Inc.
Filiaciones:
Garcia-Vilchis, Brisa:
División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
Univ Nacl Autonoma Mexico, Inst Fisiol Celular, Div Neurociencias, Mexico City, DF, Mexico
Suarez, Paola:
División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
Univ Nacl Autonoma Mexico, Inst Fisiol Celular, Div Neurociencias, Mexico City, DF, Mexico
Serrano-Reyes, Miguel:
División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
Univ Nacl Autonoma Mexico, Inst Fisiol Celular, Div Neurociencias, Mexico City, DF, Mexico
Arias-Garcia, Mario:
División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
Univ Nacl Autonoma Mexico, Inst Fisiol Celular, Div Neurociencias, Mexico City, DF, Mexico
Tapia, Dagoberto:
División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
Univ Nacl Autonoma Mexico, Inst Fisiol Celular, Div Neurociencias, Mexico City, DF, Mexico
Duhne, Mariana:
División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
Univ Nacl Autonoma Mexico, Inst Fisiol Celular, Div Neurociencias, Mexico City, DF, Mexico
Bargas, Jose:
División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
Univ Nacl Autonoma Mexico, Inst Fisiol Celular, Div Neurociencias, Mexico City, DF, Mexico
Galarraga, Elvira:
División de Neurociencias, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Mexico City, Mexico
Univ Nacl Autonoma Mexico, Inst Fisiol Celular, Div Neurociencias, Mexico City, DF, Mexico
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