Fondazione Santa Lucia Clinical and Research Center - IRCCS
Published August 8, 2021 | Version v1
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Raw data for: "CalDAG-GEFI mediates striatal cholinergic modulation of dendritic excitability, synaptic plasticity and psychomotor behaviors"

Creators

  • 1. aMcGovern Institute for Brain Research and Dept. of Brain and Cognitive Sciences, MIT, Cambridge, MA 02139, USA
  • 2. Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA
  • 3. Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan
  • 4. Laboratory of Neuropsychiatry, Psychiatric Centre Copenhagen and University, DK-2100, Copenhagen, Denmark
  • 5. Departments of Psychiatry, Pharmacology, Neurology, Columbia University, New York State Psychiatric Institute, New York, NY 10032, USA
  • 6. Neurological Clinic, Department of Medicine, Hospital Santa Maria della misericordia, University of Perugia, 06100 Perugia, Italy
  • 7. Laboratory of Neurophysiology and Plasticity, IRCCS Fondazione Santa Lucia, 00143 Rome, Italy
  • 8. San Raffaele University, 00166 Rome, Italy
  • 9. IRCCS San Raffaele Pisana, Rome 00166, Italy
  • 10. Department of Pharmacology and Center for Substance Abuse Research, Temple University School of Medicine, Philadelphia, PA 19140, USA
  • 11. Wallenberg Center for Molecular Medicine, Department of Clinical and Experimental Medicine, Linköping University, 581 83 Linköping, Sweden
  • 12. Koch Institute for Integrative Cancer Research, MIT, Cambridge, MA 02139, USA
  • 13. Basic Neuroscience Division, McLean Hospital/Harvard Medical School, Belmont, MA 02478, USA
  • 14. Neurological Clinic, Fondazione Policlinico Universitario Agostino Gemelli IRCCS; Department of Neuroscience, Faculty of Medicine, Università Cattolica del "Sacro Cuore", 00168 Rome, Italy
  • 15. Evelyn F. McKnight Brain Institute, University of Arizona, Tucson, AZ 85724, USA

Description

Figure 2. CDGI mediates the M1R modulation of dendritic excitability but not the M1R

modulation of somatic excitability.

(A and B) Sagittal sections through the brains of CDGI knockout mice in which the direct

pathway was visualized (red) in D1-tdTomato mice (A) and the indirect pathway was visualized

(green) in D2-GFP mice.

(C) Sample somatic voltage changes evoked by 120pA current injections in iSPNs from WT

(black) and CDGI-KO (red) before and after bath application of oxo-M (10 µM).

(C-D) Current-response curves of iSPNs from WT (B, n=5 cells) and CDGI-KO mice (C, n=7

cells). Somatic excitability of iSPNs was similarly enhanced by oxo-M in WT and CDGI-KO.

(E) Sample somatic recordings in response to 140pA current injections in dSPNs from WT

(black) and CDGI KO (red) before and after bath application of oxo-M (10 µM).

(F-H) Current-response curves of dSPNs from WT (E) and CDGI-KO (F) mice (n=4-6).

(I) Trains of five EPSPs were evoked by stimulation of glutamatergic afferent fibers at 40 Hz.

Oxo-M (10 µM) increased EPSP summation in iSPNs of WT, but not in CDGI-KO or when

M1Rs were blocked by M1R antagonist VU0255035 in WT (5 M).

(J) Box plot showing the effect of oxoM on synaptic summation. The EPSP5/EPSP1 ratio was

increased by oxoM in iSPNs of WT (p = 0.002, Wilcoxon test; n = 10), but not in iSPNs of 27

CDGI-KO mice (p = 0.25, n = 9) or in iSPNs of WT mice in the presence of VU0255035 (p =

0.69, n = 6).

(K) Box plot showing the effect of oxoM on the kinetics of synaptic response. The decay time

constant of EPSP5 was significantly increased by oxoM in iSPNs of WT (p = 0.002); but not

when CDGI was genetically deleted (p = 0.65) or when M1R was pharmacologically blocked (p

= 0.84).

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Additional details

Related works

Is supplement to
Journal article: 10.1016/j.nbd.2021.105473 (DOI)