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Journal: Movement Disorders
Article Title: Morphological Changes in Direct Pathway Striatal Neurons in a Rat Model of Tardive Dyskinesia
doi: 10.1002/mds.70068
Figure Lengend Snippet: Electron microscopic and quantitative analysis of axon terminals synapsing on dendrites in the internal segment of the globus pallidus (GPi) and external segment of the globus pallidus (GPe), with additional immunoelectron microscopy identifying vesicular gamma‐aminobutyric acid (GABA) transporter (VGAT)‐labeled GABAergic terminals in the GPi. (A, B) Representative electron micrographs showing axon terminals forming synapses on GPi dendrites. (C) Box plot comparing axon terminal areas in the GPi between haloperidol‐treated and control rats (* P < 0.05, Student's t ‐test). (D, E) Electron micrographs of GPe terminals. (F) Box plots of terminal areas in the GPe show no significant group differences. (G, H) Immunoelectron micrographs of VGAT‐labeled terminals in the GPi. (I) VGAT‐labeled terminals were significantly larger in the haloperidol group (* P < 0.05). (J, K) Vesicular glutamate transporter 2 (VGLUT2)‐labeled terminals in the GPi. (L) No significant group differences in VGLUT2‐labeled terminal areas. Purple indicates dendrites (D) of GPi or GPe; green indicates axon terminals synapsing on the dendrites. Scale bar = 1 μm. The “×” in the boxplot and line represents the mean value and median, respectively.
Article Snippet: We used a rabbit anti‐vesicular glutamate transporter 2 (VGLUT2) antibody (ab216463; Abcam, Cambridge, UK; 1:500) as a marker for glutamatergic terminals and a rabbit
Techniques: Immuno-Electron Microscopy, Labeling, Control
Journal: bioRxiv
Article Title: Perineuronal Net and Inhibitory Synapse Remodeling on Striatal Fast-spiking Interneurons by Chronic Alcohol Exposure
doi: 10.1101/2025.07.08.663744
Figure Lengend Snippet: A ) Schematic of viral injection of virus expressing a cre-dependent Gephyrin-GFP intrabody into parvalbumin (PV)-cre mice. B ) Representative image of an FSI expressing gephyrin-GFP intrabody (green) colocalized to an immunofluorescent marker for vesicular GABA transporter (VGAT) puncta. VGAT positive puncta were masked onto the GFP signal and colocalized signals (white dots) were labeled with a dot function model to quantify GABAergic synapses (scale bar 10µm). (right) Representative fluorescent image of proximal neuronal branch from control and CIE treated mice depicting colocalized presynaptic VGAT (purple) puncta onto gephyrin (green)-positive postsynaptic elements (scale bar 1µm). CIE dramatically reduced the density of colocalized VGAT puncta onto somata ( C ), proximal dendrites ( D ), and distal dendrites ( E ) (N=8 mice per group, 4M 4F). F ) Schematic of whole-cell patch clamp recording from an FSI during photo-uncaging of RuBi-GABA. G ) Representative traces of photo-uncaged GABA currents from FSIs of control (left) and CIE (right) treated mice at increasing stimulus intensities (scale bar = 200pA, 100ms). H ) CIE did not impact photo-uncaged IPSCs compared to control treated mice (n=8 mice per group, 4M 4F). All data represented as mean + SEM. *P < .05, **p<.01. Portions of this figure were created with BioRender.com
Article Snippet: Presynaptic GABAergic terminals were fluorescently labeled with an
Techniques: Injection, Virus, Expressing, Marker, Labeling, Control, Patch Clamp
Journal: bioRxiv
Article Title: Perineuronal Net and Inhibitory Synapse Remodeling on Striatal Fast-spiking Interneurons by Chronic Alcohol Exposure
doi: 10.1101/2025.07.08.663744
Figure Lengend Snippet: A ) schematic of whole-cell patch recording from PNN enriched (PNN+) or PNN poor (PNN-) FSI identified by WFA stain after recordings. B ) PNN+ FSIs exhibited larger eIPSC amplitudes compared to undetected PNN-FSIs (N=11 PNN+ cells, 5M 6F; 6 PNN-cells, 3M 3F). Inset: representative traces from PNN+ (pink) and PNN+ (black) FSIs (scale bar 1nA, 100ms). C ) The presence of PNNs did not impact GABA release probability onto FSIs. D-F ) Spontaneous IPSC events (sIPCSs) recorded from FSIs (N=11 PNN+ cells, 5M 6F; 6 PNN-cells, 3M 3F). Inset: representative traces from PNN+(pink) and PNN-(black) FSIs (scale bar 100pA, 1s). D,E ) PNN+ FSIs exhibited a greater frequency of spontaneous IPSC events but ( F ) no change in IPSC amplitude compared to PNN-FSIs. G ) Schematic of unilateral microinjection of chondroitinase ABC (ChABC) into the dorsolateral striatum to enzymatically degrade PNNs. H ) Degrading PNNs with ChABC reduced eIPSC event amplitude onto FSIs but ( I ) did not impact GABA release probability (N=10 mice, 5M 5F; scale bar 1nA, 100ms). J,K ) Degrading PNNs with ChABC reduced the frequency of sIPSC events onto FSIs but ( L ) did not impact event amplitude (N=8 mice, 4M 4F; scale bar 100pA, 1s). M ) Schematic of viral injection of cre-dependent Gephyrin-GFP intrabody into PV-cre mice followed by ChABC. N) Degrading PNNs with ChABC did not reduce inhibitory synapses onto somata but ( O ) did reduce inhibitory synapse number on proximal dendrites (N= 13 mice, 6M 7F). P ) Schematic of whole-cell patch clamp recording during photo-uncaging of RuBi-GABA onto FSIs treated with ChABC. Q ) Representative traces of photo-uncaged GABA postsynaptic currents on control (left) and ChABC (right) treated FSIs at increasing stimulus intensity (scale bar = 200pA, 100ms). G ) There was no change in photo-uncaged IPSC event amplitude between control (black) and ChABC (pink) FSIs (N=8 mice per group, 4M 4F). All data represented as mean + SEM. *P < 0.05. ** P < 0.01. Portions of this figure were created with BioRender.com
Article Snippet: Presynaptic GABAergic terminals were fluorescently labeled with an
Techniques: Staining, Microinjection, Injection, Patch Clamp, Control