Extended Data Fig. 5: Characterization of the connection between OFC and striatum. | Nature

Extended Data Fig. 5: Characterization of the connection between OFC and striatum.

From: Stochastic synaptic plasticity underlying compulsion in a model of addiction

Extended Data Fig. 5

a, Retrograde tracing from the striatum with cholera toxin subunit B coupled to a red dye (CTB-555). Scale bar, 50 μm. Experiment was repeated in n = 8 mice. b, OFC–striatum optogenetic stimulation and recordings of EPSCs, blocked by the AMPAR antagonist (NBQX) and IPSCs blocked by GABAA antagonist (picrotoxin). Rise time and time to peak for IPSCs and EPSCs indicate a feed-forward circuit between principal neurons of the OFC and striatum (two-sided paired t-test for IPSCs versus EPSCs: t25 = 9.55, *P < 0.0001 and t25 = 7.57, P < 0.0001 for rise time and time to peak, respectively, n = 26 cells from five mice). Scale bars, 20 ms, 100 pA. c, Schematic of retrograde tracing from specific cell types of the striatum using a rabies virus that was injected in transgenic Cre-mouse lines encoding the dopamine D1 or D2 receptor and parvalbumin. A first injection (red) leads to cell-type-specific expression of the EnvA receptor TVA and the RG protein. After two weeks an EnvA-pseudotyped and glycoprotein (ΔG)-deleted rabies virus (EnvA and RVΔG–GFP) is injected (green) and taken up by the cells that express TVA and thus turn yellow (starters). Trans-complemented with glycoprotein by infection of the AAV8-CA-flex-RG and RVΔG–GFP transsynaptically caused a spread to upstream neurons (inputs). The injection site in the striatum (left) and high-magnification images show starter cells. Retrogradely infected neurons in the OFC at low and higher magnification (right). See Supplementary Table 1 for complete statistics. a, c, Images reproduced from Paxinos and Franklin44, copyright © 2001.

Back to article page