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ca1 tissue punches  (Fine Science Tools)
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Fine Science Tools ca1 tissue punches
Figure4. a,Timespentwiththenovelobject48hafterintracerebroventricular(ICV),intra- hippocampal(IH),orintraperitonealdrugadministration(barsforthefamiliarobjectareomit- tedforsimplicity).Micetreatedwithintracerebroventricular5MBSA-E2plusintrahippocam- pal 5 g of ICI 182,780, 0.2 mg/kg E2 (intraperitoneal), intracerebroventricular 5 M BSA-E2 plusintrahippocampalvehicle,andintracerebroventricularvehicleplusintrahippocampal5M BSA-E2 spent significantly more time with the novel object than chance (dashed line at 15 s) after 48 h, demonstrating memory for the familiar object. All other groups failed to exhibit a significant preference for the novel object relative to chance. In brief, these data show that 0.2 mg/kgE2andBSA-E2administeredintoeitherthedorsalthirdventricleordorsalhippocampus enhance object recognition, and that ICI 182,780 can block the effects of E2, but not of BSA-E2, onobjectrecognition.ThedataalsoshowthatICI182,780doesnotactasanagonistinthistask, and that dorsal hippocampal inactivation with muscimol reduces the beneficial effects of BSA-E2 on object memory. Each bar represents the mean (SEM) time spent with each object (*p 0.05 relative to chance). b, Phospho-p42 ERK levels in dorsal <t>CA1</t> were measured 5 min after infusion in all groups but those receiving 0.2 mg/kg E2, in which mice were killed 60 min after E2 injection (5 min after ICI 182,780 infusion in the E2 plus ICI 182,780 group). Phospho- p42 ERK levels in dorsal CA1 were significantly increased relative to intracerebroventricular vehicle plus intrahippocampal vehicle controls in groups receiving 0.2 mg/kg E2, intracerebro- ventricular BSA-E2 plus intrahippocampal vehicle, and intracerebroventricular vehicle plus in- trahippocampal BSA-E2 (*p 0.05 relative to vehicle controls). Thus, administration of E2 or BSA-E2 alone significantly increased phospho-p42 ERK levels in dorsal CA1. Phospho-p42 ERK levels in other groups did not differ significantly from controls. Of note, levels in the intracere- broventricularBSA-E2plusintrahippocampalICI182,780groupwerenotsignificantlydifferent fromvehiclecontrolsorfromthegroupreceivingintracerebroventricularBSA-E2plusintrahip- pocampal vehicle ( p 0.05 relative to both groups), suggesting a partial blockade of the effects of BSA-E2 by ICI 182,780. Each bar represents mean (SEM) percentage change from intracerebroventricular vehicle plus intrahippocampal vehicle controls. Inset, Representative Westernblotsshowingphosphorylatedp42ERKproteinlevels(notethattheorderofthebands matches the order of the bars in the figure; group names are abbreviated for simplicity).
Ca1 Tissue Punches, supplied by Fine Science Tools, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Figure4. a,Timespentwiththenovelobject48hafterintracerebroventricular(ICV),intra- hippocampal(IH),orintraperitonealdrugadministration(barsforthefamiliarobjectareomit- tedforsimplicity).Micetreatedwithintracerebroventricular5MBSA-E2plusintrahippocam- pal 5 g of ICI 182,780, 0.2 mg/kg E2 (intraperitoneal), intracerebroventricular 5 M BSA-E2 plusintrahippocampalvehicle,andintracerebroventricularvehicleplusintrahippocampal5M BSA-E2 spent significantly more time with the novel object than chance (dashed line at 15 s) after 48 h, demonstrating memory for the familiar object. All other groups failed to exhibit a significant preference for the novel object relative to chance. In brief, these data show that 0.2 mg/kgE2andBSA-E2administeredintoeitherthedorsalthirdventricleordorsalhippocampus enhance object recognition, and that ICI 182,780 can block the effects of E2, but not of BSA-E2, onobjectrecognition.ThedataalsoshowthatICI182,780doesnotactasanagonistinthistask, and that dorsal hippocampal inactivation with muscimol reduces the beneficial effects of BSA-E2 on object memory. Each bar represents the mean (SEM) time spent with each object (*p 0.05 relative to chance). b, Phospho-p42 ERK levels in dorsal CA1 were measured 5 min after infusion in all groups but those receiving 0.2 mg/kg E2, in which mice were killed 60 min after E2 injection (5 min after ICI 182,780 infusion in the E2 plus ICI 182,780 group). Phospho- p42 ERK levels in dorsal CA1 were significantly increased relative to intracerebroventricular vehicle plus intrahippocampal vehicle controls in groups receiving 0.2 mg/kg E2, intracerebro- ventricular BSA-E2 plus intrahippocampal vehicle, and intracerebroventricular vehicle plus in- trahippocampal BSA-E2 (*p 0.05 relative to vehicle controls). Thus, administration of E2 or BSA-E2 alone significantly increased phospho-p42 ERK levels in dorsal CA1. Phospho-p42 ERK levels in other groups did not differ significantly from controls. Of note, levels in the intracere- broventricularBSA-E2plusintrahippocampalICI182,780groupwerenotsignificantlydifferent fromvehiclecontrolsorfromthegroupreceivingintracerebroventricularBSA-E2plusintrahip- pocampal vehicle ( p 0.05 relative to both groups), suggesting a partial blockade of the effects of BSA-E2 by ICI 182,780. Each bar represents mean (SEM) percentage change from intracerebroventricular vehicle plus intrahippocampal vehicle controls. Inset, Representative Westernblotsshowingphosphorylatedp42ERKproteinlevels(notethattheorderofthebands matches the order of the bars in the figure; group names are abbreviated for simplicity).

Journal: Journal of Neuroscience

Article Title: Estradiol-Induced Enhancement of Object Memory Consolidation Involves Hippocampal Extracellular Signal-Regulated Kinase Activation and Membrane-Bound Estrogen Receptors

doi: 10.1523/jneurosci.1968-08.2008

Figure Lengend Snippet: Figure4. a,Timespentwiththenovelobject48hafterintracerebroventricular(ICV),intra- hippocampal(IH),orintraperitonealdrugadministration(barsforthefamiliarobjectareomit- tedforsimplicity).Micetreatedwithintracerebroventricular5MBSA-E2plusintrahippocam- pal 5 g of ICI 182,780, 0.2 mg/kg E2 (intraperitoneal), intracerebroventricular 5 M BSA-E2 plusintrahippocampalvehicle,andintracerebroventricularvehicleplusintrahippocampal5M BSA-E2 spent significantly more time with the novel object than chance (dashed line at 15 s) after 48 h, demonstrating memory for the familiar object. All other groups failed to exhibit a significant preference for the novel object relative to chance. In brief, these data show that 0.2 mg/kgE2andBSA-E2administeredintoeitherthedorsalthirdventricleordorsalhippocampus enhance object recognition, and that ICI 182,780 can block the effects of E2, but not of BSA-E2, onobjectrecognition.ThedataalsoshowthatICI182,780doesnotactasanagonistinthistask, and that dorsal hippocampal inactivation with muscimol reduces the beneficial effects of BSA-E2 on object memory. Each bar represents the mean (SEM) time spent with each object (*p 0.05 relative to chance). b, Phospho-p42 ERK levels in dorsal CA1 were measured 5 min after infusion in all groups but those receiving 0.2 mg/kg E2, in which mice were killed 60 min after E2 injection (5 min after ICI 182,780 infusion in the E2 plus ICI 182,780 group). Phospho- p42 ERK levels in dorsal CA1 were significantly increased relative to intracerebroventricular vehicle plus intrahippocampal vehicle controls in groups receiving 0.2 mg/kg E2, intracerebro- ventricular BSA-E2 plus intrahippocampal vehicle, and intracerebroventricular vehicle plus in- trahippocampal BSA-E2 (*p 0.05 relative to vehicle controls). Thus, administration of E2 or BSA-E2 alone significantly increased phospho-p42 ERK levels in dorsal CA1. Phospho-p42 ERK levels in other groups did not differ significantly from controls. Of note, levels in the intracere- broventricularBSA-E2plusintrahippocampalICI182,780groupwerenotsignificantlydifferent fromvehiclecontrolsorfromthegroupreceivingintracerebroventricularBSA-E2plusintrahip- pocampal vehicle ( p 0.05 relative to both groups), suggesting a partial blockade of the effects of BSA-E2 by ICI 182,780. Each bar represents mean (SEM) percentage change from intracerebroventricular vehicle plus intrahippocampal vehicle controls. Inset, Representative Westernblotsshowingphosphorylatedp42ERKproteinlevels(notethattheorderofthebands matches the order of the bars in the figure; group names are abbreviated for simplicity).

Article Snippet: CA1 tissue punches (1 mm; Fine Science Tools) were taken from 480- m-thick fresh frozen sections cut on a microtome.

Techniques: Blocking Assay, Injection