Journal: bioRxiv

Article Title: Neural correlates of licking behavior modulated by target position in the striatal matrix compartment

doi: 10.64898/2026.04.18.719363

Figure Lengend Snippet: A. Schematic illustration of the behavioral apparatus. The head and body of the water-deprived mouse were fixed using a metal plate and tube. A spout, adjustable in three dimensions—anterior–posterior (AP), medial–lateral (ML), and dorsal–ventral (DV)—was placed near the mouth. An optical fiber was connected to an implanted robe in the ventrolateral striatum (VLS) for fiber photometry recordings of GCaMP6f signals. B. Diagram of the operant conditioning task. Each trial began with illumination of a light-emitting diode (LED) in a soundproof operant box. A drop of sucrose water was delivered immediately after the mouse licked the spout. After water delivery, the LED was turned off, followed by an inter-trial interval (ITI). C. Schematic illustration of GCaMP fluorescence recording from matrix neurons. GCaMP6f was selectively expressed in matrix neurons via injection of AAV5.CAG.Flex.GCaMP6f into the VLS of Calb1-IRES-Cre mice. An optical probe measured calcium-dependent fluorescence of GCaMP6f excited at 465 nm. D. Schematic illustration of GCaMP fluorescence recording from striosomal neurons. GCaMP6f was selectively expressed in striosomal neurons via injection of AAV5.CAG.Flex.GCaMP6f into the VLS of Pdyn-IRES-Cre mice. E. Histological image of Cre-dependent GCaMP6f-expressing neurons in the striatum of a Calb1-IRES-Cre mouse. Scale bar: 100 µm. F. Histological image of Cre-dependent GCaMP6f-expressing neurons in the striatum of a Pdyn-IRES-Cre mouse. Scale bar: 100 µm

Article Snippet: We used seven adult male Calb1-IRES-Cre mice (129S-Calb1tm2.1(cre)Hze/J, Jackson Laboratory Cat# 028532) and six adult male Pdyn-IRES-Cre mice (129S-Pdyn(tm1.1(Cre)/Mjkr)/LowlJ, Jackson Laboratory Cat# 027958), which express Cre recombinase selectively in striatal matrix and striosomal neurons, respectively ( ).

Techniques: Fluorescence, Injection, Expressing

Journal: bioRxiv

Article Title: Genetic Identification of Dopamine Neurons Required for Circadian Food Anticipatory Activity in Mice

doi: 10.64898/2026.03.27.714759

Figure Lengend Snippet: A) Confocal imaging of immunofluorescence antibody staining of Th (magenta) and DAT (green) in the midbrain of Calb1 Cre ;Th Flox cKO midbrain tissue. B) Quantification of TH staining in the SN of WT (grey) and Calb1 Cre ;Th Flox cKO (gold) midbrain tissue. C) Normalized body weight of WT and Calb1 Cre ;Th Flox cKO mice over the course of the study; weight was normalized by dividing the weekly weight by the Day 0 weight, which was taken prior to beginning CR. The weight fraction was similar between the two groups at every time point. D) Normalized food intake of WT and Calb1 Cre ;Th Flox cKO mice. Food intake was normalized by dividing average 24-hour AL intake by the animal’s body weight. E) Total daily high activity in seconds of WT (grey) and Calb1 Cre ;Th Flox cKO (gold) mice throughout the course of the study. F) High activity in seconds during the 3-hour premeal window throughout the course of the study. G) Normalized high activity during the 3-hour premeal window; data is normalized by dividing the seconds of high activity in the premeal window by the total daily high activity. H-K) Group-averaged double-plotted ethograms for WT and Calb1 Cre ;Th Flox cKO mice over a 40-day period for wheel running activity (H), pellet intake (I), rewarded left nose pokes (J), and unrewarded right nose pokes are shown. Area within brown borders indicates periods of food availability, and dark phase is indicated by gray background. L-M) Group average profiles for wheel running activity, rewarded left nose pokes, and unrewarded right nose pokes during 48 h food deprivation. Blue vertical lines indicate onset and offset of food availability during previously restricted feeding schedule. Light-dark cycle indicated as black and white at the bottom of each graph.

Article Snippet: Calb1 Cre -driver mice were obtained from The Jackson Laboratory (Bar Harbor, ME; stock #028532); this allele contains an internal ribosomal entry site (IRES).

Techniques: Imaging, Immunofluorescence, Staining, Activity Assay

Journal: iScience

Article Title: Dual mechanisms of supporting cell regeneration in the neonatal mouse cochlea

doi: 10.1016/j.isci.2026.115113

Figure Lengend Snippet: ScRNA-seq reveals damage-induced transcriptomes of the greater epithelial ridge and inner phalangeal cells (A) UMAP showing integration of Epcam + cochlear epithelial cells from P4-P7 control ( Ki67 CreERT2/+ ; R26R tdTomato/+ ) and damage ( Ki67 CreERT2/+ ; Lgr5 DTR/+ ; R26R tdTomato/+ ) cochlea, resulting in 18 individual clusters. (B) UMAPs showing gene expression profiles of medial and lateral GER markers. (C) UMAPs showing cell clusters integrated from control and damage cochlea at individual time points. Arrows indicate cell clusters predominantly or exclusively found in the damaged cochlea. (D) Percent distribution of cells from each time point and condition by cluster. To account for differences in the number of profiled cells in each dataset, percent contribution to each cluster was normalized to the dataset size. Blue asterisk denotes proliferating GER cells, red asterisks denote native and responding DC/IPC populations. Note that cluster 10 (native DC/IPCs) are mainly composed of cells from control cochlea, whereas cluster 8 (responding DC/IPC) is entirely composed of cells from damaged cochlea. (E) UMAPs showing a reduction of Lgr5 + cells in the damaged cochlea, as well as an increase in Ki67-tdTomato + cells in the damaged lateral GER and Fabp3 + responding DC/IPCs. Cluster 17 (proliferating cells) express Mki67 . (F) Overlaid expression of “cell cycle” and “pathways of neurodegeneration—multiple diseases” gene signatures, extracted from KEGG Pathways mmu04110 and mmu05022 using clusterProfiler. Cell cycle gene signature is highly enriched in cluster 17 and moderately enriched in cluster 8. See also . (G) Volcano plots showing differentially expressed genes between damage and control GER and IPhC clusters at all four time points (excluding proliferating cell cluster). (H) Immunostaining showing that Galectin1 and Calb1 mark medial GER (white brackets) in all three turns of the control cochlea (P6-7). After damage, domains expressing Galectin1 and Calb1 expand laterally into the central GER. Note that Calb1 also labels hair cells. (I) Crabp1 is expressed in medial GER in all three turns of P4 and P7 control cochlea. At P4 after damage, its expression robustly increased and expanded to the central and lateral GER, before returning to similar levels and spatial pattern as controls at P7. (J) Immunostaining shows that Jag1 expression initially decreases in the lateral GER relative to controls at P4, before upregulation at P7 to more intense levels than controls. (K) Quantification of Crabp1-expressing regions shows a significant increase after damage relative to controls at P7 ( n = 3). Unpaired t tests were used for (K). ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001. Brackets represent GER. IHC = inner hair cell (arrows), OHC = outer hair cell, GER = greater epithelial ridge. Scale bars represent 50 μm.

Article Snippet: Rabbit anti-calbindin (Calb1) , Cell Signaling Technologies , Cat#13176: RRID: AB_2687400.

Techniques: Control, Gene Expression, Expressing, Immunostaining