Fig. 4.

Rabies virus labels direct inputs to PV⁺ cells in the barrel cortex of PV-Cre mice. Helper virus (AAV9-pEF1α-FLEX-GTB) and rabies virus [(EnvA)SAD-ΔG-mCherry] were injected into the barrel cortex of PV-Cre mice or into WT control animals. mCherry signal is visualized using the Redhot lookup table in B. (A) Rabies virus can infect PV cells and their retrogradely connected partners in the primary somatosensory cortex. (B) In contrast, rabies infection is almost completely absent in the WT animal. (C and D) Retrogradely infected cells can be detected in secondary somatosensory cortex in the PV-Cre mouse (C), but never in the WT animal (D). (E) Retrograde label in the thalamus of PV-Cre mice. Both somata and dense axon termini are reliably detected in thalamic nuclei VPm and Po, which are known to project into barrel fields of the primary somatosensory cortex. Axon terminal labeling arises from corticothalamic projection cells that are retrogradely labeled in A. (F) As expected, there is no mCherry signal in the thalamus of WT animals. (Scale bars: 100 μm.)