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kainic acid  (MedChemExpress)


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    Structured Review

    MedChemExpress kainic acid
    Kainic Acid, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 40 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/kainic+acid/Kainic+acid/pm42218973-69-23-27
    Average 95 stars, based on 40 article reviews
    kainic acid - by Bioz Stars, 2026-09
    95/100 stars

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    Related Articles

    Injection:

    Article Title: Sensitive red fluorescent indicators for real-time visualization of potassium ion dynamics in vivo
    Article Snippet: Imaging was performed using a commercial Olympus FVMPE-RS microscope with a 25× water immersion objective lens. .. To induce seizures, kainic acid (20 mg/kg; cat#487-79-6, MedChemExpress, USA) was diluted in PBS and injected intraperitoneally into the mice. ..

    Article Title: Microglial HMGB2 mediates neuroinflammation and brain damage in Cx3cr1-creERT2 epileptic mice through astrocyte-derived CCL2.
    Article Snippet: Background: The activation of microglia in the epileptic brain is a complex process.. As a mediator of the inflammatory response of microglia, the role of High Mobility Group Box 2 (HMGB2) in epilepsy is not well

    other:

    Article Title: CGRP alleviates epilepsy via JAK1-STAT1-P2RX7 signaling: a novel neuroprotective axis targeting neuronal damage.
    Article Snippet: Background: Calcitonin gene-related peptide (CGRP), a 37-amino-acid neuropeptide, is widely distributed in the central and peripheral nervous systems and participates in regulating various physiological and pathological processes such as vasodilation, inflammation, and pain.. Recent studies have shown that CGRP also exhibits neuroprotective effects, however, its role in epileptic neuronal damage remains unclear.. Methods: We conducted experiments on kainic acid (KA)-induced epileptic mice in vivo and glutamate induced neuronal cell death models in vitro, with treatments of CGRP and agonists or inhibitors of the corresponding receptors and pathway proteins.

    Saline:

    Article Title: Targeting ROCK2 to Restore Epileptic Synaptic Networks via Mitophagy Activation: Insights from Translational Imaging of SV2A In Vivo
    Article Snippet: Cells were plated at 5 × 104 cells cm − 2 on poly‐ l ‐lysine‐coated (1 μg cm − 2 , Sigma P4707) culture vessels. .. At DIV 10, neurons were treated with 50 μ m kainic acid (MedChemExpress, HY‐N2309) in Mg2+‐free N ‐(2‐hydroxyethyl)piperazine‐29‐(2‐ethane‐sulfonic acid)‐buffered saline for 30 min, followed by three washes and 24 h recovery in a conditioned medium. ..

    In Vitro:

    Article Title: Clec7a promotes hippocampal microglial activation in rats with status epilepticus via inducing the TLR4/MyD88/NF-κB signaling pathway.
    Article Snippet: Microglial polarization imbalance between pro-inflammatory M1 and anti-inflammatory M2 phenotypes is a key mechanism in epilepsy-related neuroinflammation.. This study explores the role of C-type lectin domain containing 7A (Clec7a) in M1 microglial polarization in epilepsy.. An AAV-shClec7a was injected intra-hippocampally into Sprague-Dawley rats prior to induction of status epilepticus (SE) using lithium-pilocarpine.

    Bioprocessing:

    Article Title: Microglial HMGB2 mediates neuroinflammation and brain damage in Cx3cr1-creERT2 epileptic mice through astrocyte-derived CCL2.
    Article Snippet: Background: The activation of microglia in the epileptic brain is a complex process.. As a mediator of the inflammatory response of microglia, the role of High Mobility Group Box 2 (HMGB2) in epilepsy is not well



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    ( A ) Chronic epilepsy was induced in Thy1-ChR2 mice via intrahippocampal <t>kainic</t> <t>acid</t> injection into the CA3. ( B ) Mice were implanted with EEG recording apparatus consisting of two cortical screws, one set of insulated braided wire targeting the hippocampus, a ground screw, and a reference screw. A fiber was positioned so that the tip illuminated the CA1. ( C ) 10 Hz of 473 nm light delivered into the CA1 activated Thy1 ChR2 neurons and induced seizures on demand in vivo.
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    Experimental hypothesis and workflow for investigating astrocytic P2X7R receptor signaling in <t>kainic</t> <t>acid–induced</t> epilepsy. Hypothesis: Epileptic seizures trigger ATP release and P2X7 receptor activation, leading to morphological atrophy and functional impairment of hippocampal astrocytes. Workflow: Adult C57BL/6 mice received into the hippocampus viral injections for astrocyte-specific labeling with mCherry. After 3 weeks, epilepsy was induced by intraperitoneal (i.p.) injection of kainic acid (KA). For morphological analyses, brains were collected 2 weeks after KA administration, followed by immunofluorescence staining, image acquisition, and 3D reconstruction of astrocytes. In parallel, for electrophysiological recordings, acute hippocampal slices were prepared at 1 h or 2 weeks after KA treatment and subjected to patch-clamp recordings to assess astrocytic functional properties.
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    Experimental hypothesis and workflow for investigating astrocytic P2X7R receptor signaling in <t>kainic</t> <t>acid–induced</t> epilepsy. Hypothesis: Epileptic seizures trigger ATP release and P2X7 receptor activation, leading to morphological atrophy and functional impairment of hippocampal astrocytes. Workflow: Adult C57BL/6 mice received into the hippocampus viral injections for astrocyte-specific labeling with mCherry. After 3 weeks, epilepsy was induced by intraperitoneal (i.p.) injection of kainic acid (KA). For morphological analyses, brains were collected 2 weeks after KA administration, followed by immunofluorescence staining, image acquisition, and 3D reconstruction of astrocytes. In parallel, for electrophysiological recordings, acute hippocampal slices were prepared at 1 h or 2 weeks after KA treatment and subjected to patch-clamp recordings to assess astrocytic functional properties.
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    Experimental hypothesis and workflow for investigating astrocytic P2X7R receptor signaling in <t>kainic</t> <t>acid–induced</t> epilepsy. Hypothesis: Epileptic seizures trigger ATP release and P2X7 receptor activation, leading to morphological atrophy and functional impairment of hippocampal astrocytes. Workflow: Adult C57BL/6 mice received into the hippocampus viral injections for astrocyte-specific labeling with mCherry. After 3 weeks, epilepsy was induced by intraperitoneal (i.p.) injection of kainic acid (KA). For morphological analyses, brains were collected 2 weeks after KA administration, followed by immunofluorescence staining, image acquisition, and 3D reconstruction of astrocytes. In parallel, for electrophysiological recordings, acute hippocampal slices were prepared at 1 h or 2 weeks after KA treatment and subjected to patch-clamp recordings to assess astrocytic functional properties.
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    Experimental hypothesis and workflow for investigating astrocytic P2X7R receptor signaling in <t>kainic</t> <t>acid–induced</t> epilepsy. Hypothesis: Epileptic seizures trigger ATP release and P2X7 receptor activation, leading to morphological atrophy and functional impairment of hippocampal astrocytes. Workflow: Adult C57BL/6 mice received into the hippocampus viral injections for astrocyte-specific labeling with mCherry. After 3 weeks, epilepsy was induced by intraperitoneal (i.p.) injection of kainic acid (KA). For morphological analyses, brains were collected 2 weeks after KA administration, followed by immunofluorescence staining, image acquisition, and 3D reconstruction of astrocytes. In parallel, for electrophysiological recordings, acute hippocampal slices were prepared at 1 h or 2 weeks after KA treatment and subjected to patch-clamp recordings to assess astrocytic functional properties.
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    Image Search Results


    ( A ) Chronic epilepsy was induced in Thy1-ChR2 mice via intrahippocampal kainic acid injection into the CA3. ( B ) Mice were implanted with EEG recording apparatus consisting of two cortical screws, one set of insulated braided wire targeting the hippocampus, a ground screw, and a reference screw. A fiber was positioned so that the tip illuminated the CA1. ( C ) 10 Hz of 473 nm light delivered into the CA1 activated Thy1 ChR2 neurons and induced seizures on demand in vivo.

    Journal: eLife

    Article Title: On-demand seizures facilitate rapid screening of therapeutics for epilepsy

    doi: 10.7554/eLife.101859

    Figure Lengend Snippet: ( A ) Chronic epilepsy was induced in Thy1-ChR2 mice via intrahippocampal kainic acid injection into the CA3. ( B ) Mice were implanted with EEG recording apparatus consisting of two cortical screws, one set of insulated braided wire targeting the hippocampus, a ground screw, and a reference screw. A fiber was positioned so that the tip illuminated the CA1. ( C ) 10 Hz of 473 nm light delivered into the CA1 activated Thy1 ChR2 neurons and induced seizures on demand in vivo.

    Article Snippet: Chemical compound , Kainic Acid , Hello Bio , HB0355 , .

    Techniques: Injection, In Vivo

    Experimental hypothesis and workflow for investigating astrocytic P2X7R receptor signaling in kainic acid–induced epilepsy. Hypothesis: Epileptic seizures trigger ATP release and P2X7 receptor activation, leading to morphological atrophy and functional impairment of hippocampal astrocytes. Workflow: Adult C57BL/6 mice received into the hippocampus viral injections for astrocyte-specific labeling with mCherry. After 3 weeks, epilepsy was induced by intraperitoneal (i.p.) injection of kainic acid (KA). For morphological analyses, brains were collected 2 weeks after KA administration, followed by immunofluorescence staining, image acquisition, and 3D reconstruction of astrocytes. In parallel, for electrophysiological recordings, acute hippocampal slices were prepared at 1 h or 2 weeks after KA treatment and subjected to patch-clamp recordings to assess astrocytic functional properties.

    Journal: bioRxiv

    Article Title: P2X7 receptor-mediated astrocytic atrophy in the hippocampus of mice after status epilepticus

    doi: 10.64898/2026.04.16.718853

    Figure Lengend Snippet: Experimental hypothesis and workflow for investigating astrocytic P2X7R receptor signaling in kainic acid–induced epilepsy. Hypothesis: Epileptic seizures trigger ATP release and P2X7 receptor activation, leading to morphological atrophy and functional impairment of hippocampal astrocytes. Workflow: Adult C57BL/6 mice received into the hippocampus viral injections for astrocyte-specific labeling with mCherry. After 3 weeks, epilepsy was induced by intraperitoneal (i.p.) injection of kainic acid (KA). For morphological analyses, brains were collected 2 weeks after KA administration, followed by immunofluorescence staining, image acquisition, and 3D reconstruction of astrocytes. In parallel, for electrophysiological recordings, acute hippocampal slices were prepared at 1 h or 2 weeks after KA treatment and subjected to patch-clamp recordings to assess astrocytic functional properties.

    Article Snippet: The drugs used were the following: JNJ-47965567, gabazine hydrobromide (Tocris Biosciences, Bristol, UK); kainic acid hydrate (MedChem Express, Monmouth Junction, NJ, USA); diazepam (Shanghai Xudong Haipu Pharmaceutical Co., Shanghai, China).

    Techniques: Activation Assay, Functional Assay, Labeling, Injection, Immunofluorescence, Staining, Patch Clamp

    JNJ-47965567 and diazepam-treatment preserve astrocytic morphology after kainic acid-induced atrophy in the hippocampal stratum oriens . All abbreviations in this and the - were as defined in . (A) Representative 3D surface reconstructions of hippocampal mCherry-labeled astrocytes (red) from mice treated with NS or kainic acid KA. Scale bar, 5 μm. (B, C) Morphometric quantification of astrocytes showing (B) astrocytic volume (**P<0.01) and (C) primary branch length (***P<0.001). (D) Schematic representation of Sholl analysis used to assess astrocytic complexity. (E) Maximal number of intersections (***P<0.001). (B-E) The unpaired two-tailed t test was used for statistical evaluation. (F) Intersection profile relative to the distance from the soma. (G) Representative 3D surface reconstructions of hippocampal mCherry-labeled astrocytes (red) from KA-, JNJ+KA-, and DZP+KA-treated mice. Scale bar, 5 μm. (H, I) Morphometric quantification of astrocytes showing (H) astrocytic volume (*P<0.05; **P<0.01) and (I) primary branch length (*P<0.05, **P<0.01). (J) Schematic representation of Sholl analysis. (K) Maximal number of intersections (*P<0.05, ***P<0.001) (H-I, K) One-way ANOVA followed by the Tukey’s test was used for statistical evaluaton. (L) Intersection profile relative to the distance from the soma. All data are presented as mean±S.E.M. Dots represent individual astrocytic values (n=15).

    Journal: bioRxiv

    Article Title: P2X7 receptor-mediated astrocytic atrophy in the hippocampus of mice after status epilepticus

    doi: 10.64898/2026.04.16.718853

    Figure Lengend Snippet: JNJ-47965567 and diazepam-treatment preserve astrocytic morphology after kainic acid-induced atrophy in the hippocampal stratum oriens . All abbreviations in this and the - were as defined in . (A) Representative 3D surface reconstructions of hippocampal mCherry-labeled astrocytes (red) from mice treated with NS or kainic acid KA. Scale bar, 5 μm. (B, C) Morphometric quantification of astrocytes showing (B) astrocytic volume (**P<0.01) and (C) primary branch length (***P<0.001). (D) Schematic representation of Sholl analysis used to assess astrocytic complexity. (E) Maximal number of intersections (***P<0.001). (B-E) The unpaired two-tailed t test was used for statistical evaluation. (F) Intersection profile relative to the distance from the soma. (G) Representative 3D surface reconstructions of hippocampal mCherry-labeled astrocytes (red) from KA-, JNJ+KA-, and DZP+KA-treated mice. Scale bar, 5 μm. (H, I) Morphometric quantification of astrocytes showing (H) astrocytic volume (*P<0.05; **P<0.01) and (I) primary branch length (*P<0.05, **P<0.01). (J) Schematic representation of Sholl analysis. (K) Maximal number of intersections (*P<0.05, ***P<0.001) (H-I, K) One-way ANOVA followed by the Tukey’s test was used for statistical evaluaton. (L) Intersection profile relative to the distance from the soma. All data are presented as mean±S.E.M. Dots represent individual astrocytic values (n=15).

    Article Snippet: The drugs used were the following: JNJ-47965567, gabazine hydrobromide (Tocris Biosciences, Bristol, UK); kainic acid hydrate (MedChem Express, Monmouth Junction, NJ, USA); diazepam (Shanghai Xudong Haipu Pharmaceutical Co., Shanghai, China).

    Techniques: Labeling, Two Tailed Test

    JNJ-47965567 and diazepam-treatment prevent the reduced expression of ezrin at astrocytic peripheral processes following kainic acid administration in the hippocampal stratum oriens . (A) Representative 3D surface reconstructions of hippocampal mCherry-labeled astrocytes (red) immunolabeled for ezrin (green) from mice treated with NS or KA. Scale bar, 5 μm. (B, C) Quantitative analysis of ezrin colocalization with astrocytes showing (B) ezrin puncta area localized to the astrocytic soma (P>0.05) and (C) ezrin puncta area localized to the astrocytic peripheral branches (***P<0.001). (D) Representative confocal images showing ezrin (green) and mCherry-labeled astrocytes (red); DAPI-stained nuclei (blue) in NS and KA groups. Scale bar, 10 μm. (E) Ezrin fluorescence intensity within the mCherry-defined astrocytic area (***P<0.001) (B, C, E) The Mann-Whitney test was used for statistical evaluation. (F) Representative 3D surface reconstructions of hippocampal mCherry-labeled astrocytes (red) immunolabeled for ezrin (green) from KA-, JNJ+KA-, and DZP+KA-treated mice. Scale bar, 5 μm. (G, H) Quantitative analysis of ezrin colocalization with astrocytes showing (G) ezrin puncta area at the soma (P>0.05) and (H) ezrin puncta area at the branches (**P<0.01, ***P<0.001). (I) Representative confocal images showing ezrin (green) and mCherry-labeled astrocytes (red); DAPI-stained nuclei (blue) in the KA, JNJ+KA, and DZP+KA groups. Scale bar, 10 μm. (J) Ezrin fluorescence intensity within the astrocytic area (**P<0.01) (G, H, J) The Kruskal-Wallis ANOVA followed by the Dunn’s test was used for statistical evaluation. All data are presented as mean±S.E.M. Dots represent individual astrocytic values (n=15).

    Journal: bioRxiv

    Article Title: P2X7 receptor-mediated astrocytic atrophy in the hippocampus of mice after status epilepticus

    doi: 10.64898/2026.04.16.718853

    Figure Lengend Snippet: JNJ-47965567 and diazepam-treatment prevent the reduced expression of ezrin at astrocytic peripheral processes following kainic acid administration in the hippocampal stratum oriens . (A) Representative 3D surface reconstructions of hippocampal mCherry-labeled astrocytes (red) immunolabeled for ezrin (green) from mice treated with NS or KA. Scale bar, 5 μm. (B, C) Quantitative analysis of ezrin colocalization with astrocytes showing (B) ezrin puncta area localized to the astrocytic soma (P>0.05) and (C) ezrin puncta area localized to the astrocytic peripheral branches (***P<0.001). (D) Representative confocal images showing ezrin (green) and mCherry-labeled astrocytes (red); DAPI-stained nuclei (blue) in NS and KA groups. Scale bar, 10 μm. (E) Ezrin fluorescence intensity within the mCherry-defined astrocytic area (***P<0.001) (B, C, E) The Mann-Whitney test was used for statistical evaluation. (F) Representative 3D surface reconstructions of hippocampal mCherry-labeled astrocytes (red) immunolabeled for ezrin (green) from KA-, JNJ+KA-, and DZP+KA-treated mice. Scale bar, 5 μm. (G, H) Quantitative analysis of ezrin colocalization with astrocytes showing (G) ezrin puncta area at the soma (P>0.05) and (H) ezrin puncta area at the branches (**P<0.01, ***P<0.001). (I) Representative confocal images showing ezrin (green) and mCherry-labeled astrocytes (red); DAPI-stained nuclei (blue) in the KA, JNJ+KA, and DZP+KA groups. Scale bar, 10 μm. (J) Ezrin fluorescence intensity within the astrocytic area (**P<0.01) (G, H, J) The Kruskal-Wallis ANOVA followed by the Dunn’s test was used for statistical evaluation. All data are presented as mean±S.E.M. Dots represent individual astrocytic values (n=15).

    Article Snippet: The drugs used were the following: JNJ-47965567, gabazine hydrobromide (Tocris Biosciences, Bristol, UK); kainic acid hydrate (MedChem Express, Monmouth Junction, NJ, USA); diazepam (Shanghai Xudong Haipu Pharmaceutical Co., Shanghai, China).

    Techniques: Expressing, Labeling, Immunolabeling, Staining, Fluorescence, MANN-WHITNEY

    JNJ-47965567-treatment attenuates kainic acid-induced reactive astrogliosis in the hippocampal stratum radiatum , whereas there is no effect in the stratum oriens . (A) Representative immunofluorescence images of GFAP- (red) and DAPI-staining (blue) in the hippocampus from mice treated NS, KA, JNJ, or JNJ+KA. Dashed yellow lines delineate the stratum oriens (SO) and stratum radiatum (SR). Scale bar, 200 μm. (B, C) Quantitative analysis of GFAP-positive astrocytic density showing (B) in the SO (P>0.05) and (C) in the SR (**P<0.01, ***P<0.001; in both cases one-way ANOVA followed by the Tukey’s test). (D) Representative immunofluorescence images of S100β- (green) and DAPI-staining (blue) in the hippocampus from mice under the indicated treatment conditions. Dashed yellow lines indicate SO and SR. Scale bar, 200 μm. (E, F) Quantitative analysis of S100β-positive astrocytic density (E) in the SO (P>0.05) and (F) in the SR (P>0.05; in both cases one-way ANOVA followed by the Tukey’s test). All data are presented as mean±S.E.M. Dots represent individual values in 6 mice.

    Journal: bioRxiv

    Article Title: P2X7 receptor-mediated astrocytic atrophy in the hippocampus of mice after status epilepticus

    doi: 10.64898/2026.04.16.718853

    Figure Lengend Snippet: JNJ-47965567-treatment attenuates kainic acid-induced reactive astrogliosis in the hippocampal stratum radiatum , whereas there is no effect in the stratum oriens . (A) Representative immunofluorescence images of GFAP- (red) and DAPI-staining (blue) in the hippocampus from mice treated NS, KA, JNJ, or JNJ+KA. Dashed yellow lines delineate the stratum oriens (SO) and stratum radiatum (SR). Scale bar, 200 μm. (B, C) Quantitative analysis of GFAP-positive astrocytic density showing (B) in the SO (P>0.05) and (C) in the SR (**P<0.01, ***P<0.001; in both cases one-way ANOVA followed by the Tukey’s test). (D) Representative immunofluorescence images of S100β- (green) and DAPI-staining (blue) in the hippocampus from mice under the indicated treatment conditions. Dashed yellow lines indicate SO and SR. Scale bar, 200 μm. (E, F) Quantitative analysis of S100β-positive astrocytic density (E) in the SO (P>0.05) and (F) in the SR (P>0.05; in both cases one-way ANOVA followed by the Tukey’s test). All data are presented as mean±S.E.M. Dots represent individual values in 6 mice.

    Article Snippet: The drugs used were the following: JNJ-47965567, gabazine hydrobromide (Tocris Biosciences, Bristol, UK); kainic acid hydrate (MedChem Express, Monmouth Junction, NJ, USA); diazepam (Shanghai Xudong Haipu Pharmaceutical Co., Shanghai, China).

    Techniques: Immunofluorescence, Staining

    NMDA, Bz-ATP and muscimol-induced current responses in hippocampal stratum oriens astrocytes of mice. Each agonist was superfused twice for 10 s each with an inter-application interval of 3 min, at a holding potential of −80 mV. The concentrations of the agonists were 100 µM (NMDA, muscimol) and 1000 µM (Bz-ATP) in a low X 2+ bath medium (see Methods). The current response was calculated for each agonist as a mean of the two subsequent applications. Mice were 1 h or 2 weeks before preparation of hippocampal brain slices injected with normal saline (NS) or kainic acid (KA, 30 mg/kg, i.p.). (A) Representative recording 1 h after saline injection. (B) Representative recording 1 h after KA injection. (C) Comparison of the effects of NMDA, Bz-ATP, and muscimol, 1 h after saline or KA-application. P>0.05 all, n=6; Kruskal-Wallis ANOVA, followed by the Dunn’s test. (D) Representative recording 1 h after saline injection in the continuous presence of A438079 (10 µM). (E) Representative recording 1 h after KA injection in the continuous presence of A438079 (10 µM). (F) Comparison of the effects of NMDA, Bz-ATP, and muscimol, 1 h after saline or KA-application in the continuous presence of A438079 (10 µM). P>0.05 all, n=6; one-way ANOVA followed by the Tukey’s test. (G) Comparison of the effects of NMDA, Bz-ATP, and muscimol, 1 h after saline or KA-application. *P<0.05, as indicated; n=6; Kruskal-Wallis ANOVA, followed by the Dunn’s test. (H) Comparison of the effects of NMDA, Bz-ATP, and muscimol, 1 h after saline or KA-application in the continuous presence of A438079 (10 µM). P>0.05 all, n=6; one-way ANOVA followed by the Tukey’s test. For further details see the Materials and Methods Section. All data are presented as mean±S.E.M. Dots represent individual values in 6 mice.

    Journal: bioRxiv

    Article Title: P2X7 receptor-mediated astrocytic atrophy in the hippocampus of mice after status epilepticus

    doi: 10.64898/2026.04.16.718853

    Figure Lengend Snippet: NMDA, Bz-ATP and muscimol-induced current responses in hippocampal stratum oriens astrocytes of mice. Each agonist was superfused twice for 10 s each with an inter-application interval of 3 min, at a holding potential of −80 mV. The concentrations of the agonists were 100 µM (NMDA, muscimol) and 1000 µM (Bz-ATP) in a low X 2+ bath medium (see Methods). The current response was calculated for each agonist as a mean of the two subsequent applications. Mice were 1 h or 2 weeks before preparation of hippocampal brain slices injected with normal saline (NS) or kainic acid (KA, 30 mg/kg, i.p.). (A) Representative recording 1 h after saline injection. (B) Representative recording 1 h after KA injection. (C) Comparison of the effects of NMDA, Bz-ATP, and muscimol, 1 h after saline or KA-application. P>0.05 all, n=6; Kruskal-Wallis ANOVA, followed by the Dunn’s test. (D) Representative recording 1 h after saline injection in the continuous presence of A438079 (10 µM). (E) Representative recording 1 h after KA injection in the continuous presence of A438079 (10 µM). (F) Comparison of the effects of NMDA, Bz-ATP, and muscimol, 1 h after saline or KA-application in the continuous presence of A438079 (10 µM). P>0.05 all, n=6; one-way ANOVA followed by the Tukey’s test. (G) Comparison of the effects of NMDA, Bz-ATP, and muscimol, 1 h after saline or KA-application. *P<0.05, as indicated; n=6; Kruskal-Wallis ANOVA, followed by the Dunn’s test. (H) Comparison of the effects of NMDA, Bz-ATP, and muscimol, 1 h after saline or KA-application in the continuous presence of A438079 (10 µM). P>0.05 all, n=6; one-way ANOVA followed by the Tukey’s test. For further details see the Materials and Methods Section. All data are presented as mean±S.E.M. Dots represent individual values in 6 mice.

    Article Snippet: The drugs used were the following: JNJ-47965567, gabazine hydrobromide (Tocris Biosciences, Bristol, UK); kainic acid hydrate (MedChem Express, Monmouth Junction, NJ, USA); diazepam (Shanghai Xudong Haipu Pharmaceutical Co., Shanghai, China).

    Techniques: Injection, Saline, Comparison