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Thorlabs optogenetic patch cable
Optogenetic Patch Cable, supplied by Thorlabs, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/optogenetic+patch+cable/cables+patch/pm41611073-83-27-35
Average 86 stars, based on 1 article reviews

optogenetic patch cable - by Bioz Stars, 2026-09

86/100 stars

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Article Title: Initiation site of experimentally-evoked spreading depolarizations influence tissue outcomes in a murine stroke model.
Article Snippet: SD was initiated optogenetically via focal illumination through the intact skull with a fiber-coupled LED (470 nm, #M470F4, ThorLabs; 30 s at 3 mW) connected to an optogenetic patch cable (400 μm core; 0.39NA fiber, ThorLabs).

Article Title: Chronic optogenetic activation of hippocampal CA1 neurons triggers Alzheimer’s disease-like proteomic remodeling
Article Snippet: 2.5 mm (FC) Ferrule Patch Cables , ThorLabs , Cat# M81L01.

Article Title: A prefrontal cortex-lateral hypothalamus circuit controls stress-driven increased food intake
Article Snippet: On stimulation days, mice were connected to optogenetic patch cables (Thorlabs, 200 μm, 0.39 NA, FT200UMT), which ended in a ceramic ferrule (230 μm bore size, Thorlabs or Precision Fiber Products) and connected to the implant through a sleeve (Precision Fiber Products).

Article Title: Dorsal hippocampal CA3 to CA1 circuit maintains contextual cocaine memories in a rat model of drug relapse.
Article Snippet: Exposure to a cocaine-associated environment triggers drug craving and relapse by prompting the retrieval of drug-related long-term memories.. Upon retrieval, memory traces enter a labile state during which they can be modified until their reconsolidation into long-term memory stores.. Disrupting labile memory traces is a promising therapeutic approach for treating neuropsychiatric disorders characterized by maladaptive memories, including substance use disorder.

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Neuronal activity-dependent engulfment of excitatory synapses in the healthy cortex is abrogated in glioma. (A) Xenograft, synaptic labeling, and optogenetics paradigm in NOD scid gamma (NSG) mice which underwent cortical xenograft with DMG, diffuse intrinsic pontine glioma (patient-derived cell line “SU-DIPG-VI”), or saline injections (“Nontumor control”), followed by viral injections with hSyn-PSD95-mCherry-eGFP (“Excitatory”) AAV9 or hSyn-gephyrin-mCherry-eGFP (“Inhibitory”) AAV9 and optogenetic ferrule implantation in mouse premotor frontal cortex (M2). NSG mice used were either positive or negative for Thy1::ChR2 transgene. One acute session of optogenetic stimulation was performed within DMG-xenografted or saline-injected M2 cortical regions, according to previously-established methods, on Thy1::ChR2 +/− cohorts. Synaptic engulfment analysis was then performed. P, postnatal day; hSyn, human synapsin promoter. (B) Representative histological and corresponding 3D rendered images (C) of HNA+ glioma cells (SU-DIPG-VI, violet), Iba1+ microglia (white), mCherry+ gephyrin+ synapses (red), and GFP+ gephyrin+ synapses (green) in xenografted deep-layer premotor cortex of Thy1::ChR2 negative (“ChR2−“) mice. Scale bar, 10 um. (D) Volumetric engulfment analysis of microglial engulfment of mCherry+ PSD95+ synapses (“Excitatory”), represented as the % volume of mCherry+ synapse contained in Iba1+ microglia in saline injected (“Nontumor control”) mice without Thy1::ChR2 expression (“ChR2−”) or with Thy1::ChR2 expression (“ChR2+”). (E) Volumetric engulfment analysis of microglial engulfment of mCherry+ gephyrin+ synapses (“Inhibitory”), represented as the % volume of mCherry+ synapse contained in Iba1+ microglia in saline injected (“Nontumor control”) mice without Thy1::ChR2 expression (“ChR2−”) or with Thy1::ChR2 expression (“ChR2+”). (F) Volumetric engulfment analysis of microglial engulfment of mCherry+ PSD95+ synapses (“Excitatory”), represented as the % volume of mCherry+ synapse contained in Iba1+ microglia in glioma xenografted (“DMG xenograft”, SU-DIPG-VI) mice without Thy1::ChR2 expression (“ChR2−”) or with Thy1::ChR2 expression (“ChR2+”). (G) Volumetric engulfment analysis of microglial engulfment of mCherry+ gephyrin+ synapses (“Inhibitory”), represented as the % volume of mCherry+ synapse contained in Iba1+ microglia in glioma xenografted (“DMG xenograft”, SU-DIPG-VI) mice without Thy1::ChR2 expression (“ChR2−”) or with Thy1::ChR2 expression (“ChR2+”). Each individual point represents the average volumetric quantification from images analyzed in one mouse (B-C, F-G). Data are mean ± s.e.m. One-way ANOVA with Tukey’s post hoc analysis (B-C, F-G); **P < 0.01, ****P < 0.0001; NS, not significant.

Journal: bioRxiv

Article Title: Dysregulated Microglial Synaptic Engulfment in Diffuse Midline Glioma

doi: 10.64898/2025.12.22.696064

Figure Lengend Snippet: Neuronal activity-dependent engulfment of excitatory synapses in the healthy cortex is abrogated in glioma. (A) Xenograft, synaptic labeling, and optogenetics paradigm in NOD scid gamma (NSG) mice which underwent cortical xenograft with DMG, diffuse intrinsic pontine glioma (patient-derived cell line “SU-DIPG-VI”), or saline injections (“Nontumor control”), followed by viral injections with hSyn-PSD95-mCherry-eGFP (“Excitatory”) AAV9 or hSyn-gephyrin-mCherry-eGFP (“Inhibitory”) AAV9 and optogenetic ferrule implantation in mouse premotor frontal cortex (M2). NSG mice used were either positive or negative for Thy1::ChR2 transgene. One acute session of optogenetic stimulation was performed within DMG-xenografted or saline-injected M2 cortical regions, according to previously-established methods, on Thy1::ChR2 +/− cohorts. Synaptic engulfment analysis was then performed. P, postnatal day; hSyn, human synapsin promoter. (B) Representative histological and corresponding 3D rendered images (C) of HNA+ glioma cells (SU-DIPG-VI, violet), Iba1+ microglia (white), mCherry+ gephyrin+ synapses (red), and GFP+ gephyrin+ synapses (green) in xenografted deep-layer premotor cortex of Thy1::ChR2 negative (“ChR2−“) mice. Scale bar, 10 um. (D) Volumetric engulfment analysis of microglial engulfment of mCherry+ PSD95+ synapses (“Excitatory”), represented as the % volume of mCherry+ synapse contained in Iba1+ microglia in saline injected (“Nontumor control”) mice without Thy1::ChR2 expression (“ChR2−”) or with Thy1::ChR2 expression (“ChR2+”). (E) Volumetric engulfment analysis of microglial engulfment of mCherry+ gephyrin+ synapses (“Inhibitory”), represented as the % volume of mCherry+ synapse contained in Iba1+ microglia in saline injected (“Nontumor control”) mice without Thy1::ChR2 expression (“ChR2−”) or with Thy1::ChR2 expression (“ChR2+”). (F) Volumetric engulfment analysis of microglial engulfment of mCherry+ PSD95+ synapses (“Excitatory”), represented as the % volume of mCherry+ synapse contained in Iba1+ microglia in glioma xenografted (“DMG xenograft”, SU-DIPG-VI) mice without Thy1::ChR2 expression (“ChR2−”) or with Thy1::ChR2 expression (“ChR2+”). (G) Volumetric engulfment analysis of microglial engulfment of mCherry+ gephyrin+ synapses (“Inhibitory”), represented as the % volume of mCherry+ synapse contained in Iba1+ microglia in glioma xenografted (“DMG xenograft”, SU-DIPG-VI) mice without Thy1::ChR2 expression (“ChR2−”) or with Thy1::ChR2 expression (“ChR2+”). Each individual point represents the average volumetric quantification from images analyzed in one mouse (B-C, F-G). Data are mean ± s.e.m. One-way ANOVA with Tukey’s post hoc analysis (B-C, F-G); **P < 0.01, ****P < 0.0001; NS, not significant.

Article Snippet: Fiber Optic Rotary Joint Patch Cables (Optogenetics) , Thorlabs , RJPSL2.

Techniques: Activity Assay, Labeling, Optogenetics, Derivative Assay, Saline, Control, Injection, Expressing

Neuronal activity alters microglial populations, modulating circuit refinement-related pathways in glioma. (A) Repetitive superimposed traces of field potentials recorded from mice with CA1 hippocampal murine glioma MADR allografts (“DMG allograft”) or from control saline-injected mice (“Nontumor control”). (B) Input-output (I-O) curve was performed in the CA1 region of hippocampal slices. Field excitatory postsynaptic potentials (fEPSPs) were recorded from mice with CA1 hippocampal murine glioma MADR allografts (“DMG allograft”) or from control saline-injected mice (“Nontumor control”). Changes in amplitude were measured relative to baseline following a series of current injections ranging from 0 to 140 μA in steps of 10 μA. (C-D) Frequency and amplitude of spontaneous excitatory postsynaptic currents (sEPSCs) were measured in mice with CA1 hippocampal murine glioma MADR allografts (“DMG allograft”) or from control saline-injected mice (“Nontumor control”). (E) Allograft and optogenetics paradigm in CD-1::C57BL/6J (CD1::BL6) mice which underwent cortical allograft with previously-established MADR (“Mosaic analysis by dual recombinase-mediated cassette exchange”) murine glioma (H3.3K27M+ murine-derived cell line), or saline injections (“Nontumor control”), followed by optogenetic ferrule implantation in mouse premotor frontal cortex (M2). CD1::BL6 mice used were either positive or negative for Thy1::ChR2 transgene. One acute session of optogenetic stimulation was performed within MADR-allografted or saline-injected M2 cortical regions, according to previously-established methods, on Thy1::ChR2 +/− cohorts. Single nuclei sequencing analysis was then performed. P, postnatal day. (F) Microglial subpopulation abundance (labeled by color) was calculated as the % of total microglia (“Proportion of Total Microglia”, y-axis) in either nontumor nonstimulated control mice or glioma allografted nonstimulated mice (x-axis). (G) Scatterplot demonstrating gene expression changes in microglia from stimulated, glioma-allografted mice, as compared to stimulated, nontumor controls. The x-axis demonstrates log2 (fold change of stimulated glioma- vs nontumor-associated microglia) and the y axis demonstrates Log10P of the gene expression level. Points shown in red represent genes showing statistically significant changes. (H) Complement-enriched microglial subpopulation abundance was calculated as the % of total microglia (“Proportion of Total Microglia”, y-axis) across all experimental cohorts (x-axis). (I) Complement-associated gene score (y-axis) quantifies the relative expression levels of a complement-associated gene set in microglia across all experimental conditions (x-axis). (J) Homeostasis-associated gene score (y-axis) quantifies the relative expression levels of a homeostasis-associated gene set in microglia across all experimental conditions (x-axis). Data are presented as mean ± s.e.m. Unpaired t test with Welch’s correction (D-E); **P < 0.01; NS, not significant.

Journal: bioRxiv

Article Title: Dysregulated Microglial Synaptic Engulfment in Diffuse Midline Glioma

doi: 10.64898/2025.12.22.696064

Figure Lengend Snippet: Neuronal activity alters microglial populations, modulating circuit refinement-related pathways in glioma. (A) Repetitive superimposed traces of field potentials recorded from mice with CA1 hippocampal murine glioma MADR allografts (“DMG allograft”) or from control saline-injected mice (“Nontumor control”). (B) Input-output (I-O) curve was performed in the CA1 region of hippocampal slices. Field excitatory postsynaptic potentials (fEPSPs) were recorded from mice with CA1 hippocampal murine glioma MADR allografts (“DMG allograft”) or from control saline-injected mice (“Nontumor control”). Changes in amplitude were measured relative to baseline following a series of current injections ranging from 0 to 140 μA in steps of 10 μA. (C-D) Frequency and amplitude of spontaneous excitatory postsynaptic currents (sEPSCs) were measured in mice with CA1 hippocampal murine glioma MADR allografts (“DMG allograft”) or from control saline-injected mice (“Nontumor control”). (E) Allograft and optogenetics paradigm in CD-1::C57BL/6J (CD1::BL6) mice which underwent cortical allograft with previously-established MADR (“Mosaic analysis by dual recombinase-mediated cassette exchange”) murine glioma (H3.3K27M+ murine-derived cell line), or saline injections (“Nontumor control”), followed by optogenetic ferrule implantation in mouse premotor frontal cortex (M2). CD1::BL6 mice used were either positive or negative for Thy1::ChR2 transgene. One acute session of optogenetic stimulation was performed within MADR-allografted or saline-injected M2 cortical regions, according to previously-established methods, on Thy1::ChR2 +/− cohorts. Single nuclei sequencing analysis was then performed. P, postnatal day. (F) Microglial subpopulation abundance (labeled by color) was calculated as the % of total microglia (“Proportion of Total Microglia”, y-axis) in either nontumor nonstimulated control mice or glioma allografted nonstimulated mice (x-axis). (G) Scatterplot demonstrating gene expression changes in microglia from stimulated, glioma-allografted mice, as compared to stimulated, nontumor controls. The x-axis demonstrates log2 (fold change of stimulated glioma- vs nontumor-associated microglia) and the y axis demonstrates Log10P of the gene expression level. Points shown in red represent genes showing statistically significant changes. (H) Complement-enriched microglial subpopulation abundance was calculated as the % of total microglia (“Proportion of Total Microglia”, y-axis) across all experimental cohorts (x-axis). (I) Complement-associated gene score (y-axis) quantifies the relative expression levels of a complement-associated gene set in microglia across all experimental conditions (x-axis). (J) Homeostasis-associated gene score (y-axis) quantifies the relative expression levels of a homeostasis-associated gene set in microglia across all experimental conditions (x-axis). Data are presented as mean ± s.e.m. Unpaired t test with Welch’s correction (D-E); **P < 0.01; NS, not significant.

Article Snippet: Fiber Optic Rotary Joint Patch Cables (Optogenetics) , Thorlabs , RJPSL2.

Techniques: Activity Assay, Control, Saline, Injection, Optogenetics, Derivative Assay, Sequencing, Labeling, Gene Expression, Expressing

Glioma-infiltrated brain-derived and activity-regulated secreted factors affect microglial synaptic engulfment and activation state in vitro. (A) Paradigm demonstrating ex vivo slice generation of conditioned media to acutely incubate with human microglial (“iMGL”) and glutamatergic/ GABAergic neuron tricultures and subsequently quantify microglial synaptic engulfment. Ex vivo slices were either saline-injected (“Nontumor”) or glioma xenografted (SU-DIPG-VI, “DMG”), with active optogenetic stimulation (Thy1::ChR2+, active conditioned media, “ACM”) or nonstimulated blue light control (Thy1::ChR2-, conditioned media, “CM”). (B) Representative 3D rendered images from human microglial/glutamatergic/GABAergic neuron tri-cultures exposed to ex vivo slice generated conditioned media. Microglia (white), neurons (blue), PSD95+ excitatory synapses (red), and gephyrin+ inhibitory synapses (green) illustrate microglial synaptic engulfment in tri-culture. Tri-cultures were either treated with conditioned media generated from nonstimulated glioma-bearing slices (“DMG CM”) or from stimulated glioma-bearing slices (“DMG ACM”). Scale bar, 15 um. (C) Volumetric engulfment analysis of microglial engulfment of PSD95+ synapses in tri-culture (“Excitatory”), represented as the % volume of PSD95+ synapse contained in Iba1+ microglia in tri-cultures exposed to ex vivo conditioned media from nonstimulated nontumor slices (“Nontumor CM”) or from stimulated nontumor slices (“Nontumor ACM”). (D) Volumetric engulfment analysis of microglial engulfment of gephyrin+ synapses in tri-culture (“Inhibitory”), represented as the % volume of gephyrin+ synapse contained in Iba1+ microglia in tri-cultures exposed to ex vivo conditioned media from nonstimulated nontumor slices (“Nontumor CM”) or from stimulated nontumor slices (“Nontumor ACM”). (E) Volumetric engulfment analysis of microglial engulfment of PSD95+ synapses in tri-culture (“Excitatory”), represented as the % volume of PSD95+ synapse contained in Iba1+ microglia in tri-cultures exposed to ex vivo conditioned media from nonstimulated glioma-bearing slices (“DMG CM”) or from stimulated glioma-bearing slices (“DMG ACM”). (F) Volumetric engulfment analysis of microglial engulfment of gephyrin+ synapses in tri-culture (“Inhibitory”), represented as the % volume of gephyrin+ synapse contained in Iba1+ microglia in tri-cultures exposed to ex vivo conditioned media from nonstimulated glioma-bearing slices (“DMG CM”) or from stimulated glioma-bearing slices (“DMG ACM”). (G) Ex vivo slice generated conditioned media underwent LC/MS analysis, calculating the ratio of protein abundance (“Protein Abundance Ratio”, y-axis) normalized on total peptide amount, and comparing conditioned media from stimulated glioma-bearing slices (“DMG ACM”) to conditioned media from nonstimulated glioma-bearing slices (“DMG CM”). Individual proteins with abundance ratios >1 are labeled and described. Each individual point represents the average volumetric quantification from images analyzed in one tri-culture (C-F). Data are mean ± s.e.m. One-way ANOVA with Tukey’s post hoc analysis (E); *P<0.05, NS, not significant.

Journal: bioRxiv

Article Title: Dysregulated Microglial Synaptic Engulfment in Diffuse Midline Glioma

doi: 10.64898/2025.12.22.696064

Figure Lengend Snippet: Glioma-infiltrated brain-derived and activity-regulated secreted factors affect microglial synaptic engulfment and activation state in vitro. (A) Paradigm demonstrating ex vivo slice generation of conditioned media to acutely incubate with human microglial (“iMGL”) and glutamatergic/ GABAergic neuron tricultures and subsequently quantify microglial synaptic engulfment. Ex vivo slices were either saline-injected (“Nontumor”) or glioma xenografted (SU-DIPG-VI, “DMG”), with active optogenetic stimulation (Thy1::ChR2+, active conditioned media, “ACM”) or nonstimulated blue light control (Thy1::ChR2-, conditioned media, “CM”). (B) Representative 3D rendered images from human microglial/glutamatergic/GABAergic neuron tri-cultures exposed to ex vivo slice generated conditioned media. Microglia (white), neurons (blue), PSD95+ excitatory synapses (red), and gephyrin+ inhibitory synapses (green) illustrate microglial synaptic engulfment in tri-culture. Tri-cultures were either treated with conditioned media generated from nonstimulated glioma-bearing slices (“DMG CM”) or from stimulated glioma-bearing slices (“DMG ACM”). Scale bar, 15 um. (C) Volumetric engulfment analysis of microglial engulfment of PSD95+ synapses in tri-culture (“Excitatory”), represented as the % volume of PSD95+ synapse contained in Iba1+ microglia in tri-cultures exposed to ex vivo conditioned media from nonstimulated nontumor slices (“Nontumor CM”) or from stimulated nontumor slices (“Nontumor ACM”). (D) Volumetric engulfment analysis of microglial engulfment of gephyrin+ synapses in tri-culture (“Inhibitory”), represented as the % volume of gephyrin+ synapse contained in Iba1+ microglia in tri-cultures exposed to ex vivo conditioned media from nonstimulated nontumor slices (“Nontumor CM”) or from stimulated nontumor slices (“Nontumor ACM”). (E) Volumetric engulfment analysis of microglial engulfment of PSD95+ synapses in tri-culture (“Excitatory”), represented as the % volume of PSD95+ synapse contained in Iba1+ microglia in tri-cultures exposed to ex vivo conditioned media from nonstimulated glioma-bearing slices (“DMG CM”) or from stimulated glioma-bearing slices (“DMG ACM”). (F) Volumetric engulfment analysis of microglial engulfment of gephyrin+ synapses in tri-culture (“Inhibitory”), represented as the % volume of gephyrin+ synapse contained in Iba1+ microglia in tri-cultures exposed to ex vivo conditioned media from nonstimulated glioma-bearing slices (“DMG CM”) or from stimulated glioma-bearing slices (“DMG ACM”). (G) Ex vivo slice generated conditioned media underwent LC/MS analysis, calculating the ratio of protein abundance (“Protein Abundance Ratio”, y-axis) normalized on total peptide amount, and comparing conditioned media from stimulated glioma-bearing slices (“DMG ACM”) to conditioned media from nonstimulated glioma-bearing slices (“DMG CM”). Individual proteins with abundance ratios >1 are labeled and described. Each individual point represents the average volumetric quantification from images analyzed in one tri-culture (C-F). Data are mean ± s.e.m. One-way ANOVA with Tukey’s post hoc analysis (E); *P<0.05, NS, not significant.

Article Snippet: Fiber Optic Rotary Joint Patch Cables (Optogenetics) , Thorlabs , RJPSL2.

Techniques: Derivative Assay, Activity Assay, Activation Assay, In Vitro, Ex Vivo, Saline, Injection, Control, Generated, Liquid Chromatography with Mass Spectroscopy, Quantitative Proteomics, Labeling

(A) Experimental setup integrating optogenetics, cystometry (CMG), and electromyography (EMG) to record bladder pressure and EUS activity during Bar Penk photostimulation. (B) Schematic of unilateral FLEX-ChrimsonR injection into Bar with an optic fiber above. (C) Representative urodynamic tracings showing bladder pressure (red) and EUS-EMG activity (black) with 10s light pulses (orange shading), and a magnified 30s window capturing baseline, stimulation, and recovery phases. (D, E) EUS-EMG total power (D) and average bladder pressure (E) before, during, and after stimulation ( n = 30 events from 3 mice, equally weighted ; in (D) , **** p <0.0001, **** p = 0.0037; in (E) , p = 0.91, p > 0.99; Friedman test followed by Dunn’s multiple comparisons test ). Blue lines indicate medians. (F) Likelihood of EUS and bladder responses during photostimulation ( n = 3 mice, 74 events ). Abbreviations: Bar, Barrington’s nucleus; EUS, external urethral sphincter. See also .

Journal: bioRxiv

Article Title: “Enkephalinergic Neurons Gate Sex-Specific Control of Voluntary Micturition”

doi: 10.1101/2025.05.16.654570

Figure Lengend Snippet: (A) Experimental setup integrating optogenetics, cystometry (CMG), and electromyography (EMG) to record bladder pressure and EUS activity during Bar Penk photostimulation. (B) Schematic of unilateral FLEX-ChrimsonR injection into Bar with an optic fiber above. (C) Representative urodynamic tracings showing bladder pressure (red) and EUS-EMG activity (black) with 10s light pulses (orange shading), and a magnified 30s window capturing baseline, stimulation, and recovery phases. (D, E) EUS-EMG total power (D) and average bladder pressure (E) before, during, and after stimulation ( n = 30 events from 3 mice, equally weighted ; in (D) , **** p <0.0001, **** p = 0.0037; in (E) , p = 0.91, p > 0.99; Friedman test followed by Dunn’s multiple comparisons test ). Blue lines indicate medians. (F) Likelihood of EUS and bladder responses during photostimulation ( n = 3 mice, 74 events ). Abbreviations: Bar, Barrington’s nucleus; EUS, external urethral sphincter. See also .

Article Snippet: For photostimulation experiments, fiber-implanted mice were briefly anesthetized with 4% isoflurane before being connected to optogenetic patch cables (Plexon OPT/PC-FC-LCF-200/230-HP-1.0L KIT) via a ceramic mating sleeve (included in the same kit).

Techniques: Optogenetics, Activity Assay, Injection

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