mglur1 antagonist aida  (Tocris)

Journal: International Journal of General Medicine

Article Title: Effects of inhaled anesthetic isoflurane on long-term potentiation of CA3 pyramidal cell afferents in vivo

doi: 10.2147/IJGM.S30570

Figure Lengend Snippet: Characteristic LTP responses are observed in the MF pathway under isoflurane anesthesia. A plot of normalized field excitatory postsynaptic potential (fEPSP) slope magnitude of mossy fiber-CA3 responses over time using current intensities eliciting 50% of the maximal response and the percent change in amplitude (mean ± SEM). Notes: Blue diamonds: MF LTP is induced in the presence of Ringer’s solution in isoflurane (+43% ± 20%, n = 4) anesthetized animals. Green squares: MF LTP is induced in the presence of 3-[(R)-2-carboxypiperazin-4-yl]-propo-2-enyl-1-phosphonic acid (CPP; 3 nmol ic) with isoflurane (+29% ± 6% LTP, n = 4). Black triangles: LTP induction is blocked in the presence of naloxone (10 nmol ic) with isoflurane (−7% ± 20%, n = 4). Red circles: LTP induction is blocked in the presence of the class 1 metabotropic glutamate receptor (mGluR) antagonist AIDA (37.5 nmol ic) in isoflurane (−5% ± 18%, n = 4) anesthetized animals. Abbreviations: MF, mossy fiber; LTP, long-term potentiation; HFS, high-frequency stimulation; CA3, cornu ammonis region 3; SEM, standard error of the mean; AIDA, RS-aminoindan-1, 5-dicarboxylic acid.

Article Snippet: After the collection of baseline CA3 afferent responses for ≥20 min at 0.05 Hz, animals received Ringer’s solution, naloxone (μ-opioid receptor antagonist, 10 nmol intracerebrally (ic); (RBI; Sigma-Aldrich, St Louis, MO), AIDA (mGluR1 receptor antagonist, 37.5 nmol ic; Sigma-Aldrich), or CPP (NMDA-R antagonist, 3 nmol ic; Sigma-Aldrich), depending on the pathway’s dependence on NMDA receptor activation or opioid receptor activation for LTP induction at 0.2 μL/min (1 μL total).

Techniques:

Journal: International Journal of General Medicine

Article Title: Effects of inhaled anesthetic isoflurane on long-term potentiation of CA3 pyramidal cell afferents in vivo

doi: 10.2147/IJGM.S30570

Figure Lengend Snippet: Characteristic LTP responses are observed in the LPP under isoflurane anesthesia. A plot of normalized field excitatory postsynaptic potential (fEPSP) slope magnitude of lateral perforant path-CA3 responses over time using current intensities eliciting 50% of the maximal response and the percent change in amplitude (mean ± SEM). Notes: Blue diamonds: LPP LTP is induced in the presence of Ringer’s solution in isoflurane (+22% ± 11%, n = 4) anesthetized animals. Green squares: LPP LTP is induced in the presence of 3-[(R)-2-carboxypiperazin-4-yl]-propo-2-enyl-1-phosphonic acid (CPP; 3 nmol ic) with isoflurane (+34% ± 17%, n = 4). Black triangles: LTP induction is blocked in the presence of naloxone (10 nmol ic) with isoflurane (+9% ± 23%, n = 4). Red circles: LTP induction is blocked in the presence of the class 1 mGluR antagonist AIDA (37.5 nmol ic) in isoflurane (−11% ± 15%, n = 4) anesthetized animals. Abbreviations: LPP, lateral perforant pathway; LTP, long-term potentiation; HFS, high frequency stimulation; CA3, cornu ammonis region 3; SEM, standard error of the mean; AIDA, RS-aminoindan-1, 5-dicarboxylic acid.

Article Snippet: After the collection of baseline CA3 afferent responses for ≥20 min at 0.05 Hz, animals received Ringer’s solution, naloxone (μ-opioid receptor antagonist, 10 nmol intracerebrally (ic); (RBI; Sigma-Aldrich, St Louis, MO), AIDA (mGluR1 receptor antagonist, 37.5 nmol ic; Sigma-Aldrich), or CPP (NMDA-R antagonist, 3 nmol ic; Sigma-Aldrich), depending on the pathway’s dependence on NMDA receptor activation or opioid receptor activation for LTP induction at 0.2 μL/min (1 μL total).

Techniques:

Journal: Scientific Reports

Article Title: Glutamate signals through mGluR2 to control Schwann cell differentiation and proliferation

doi: 10.1038/srep29856

Figure Lengend Snippet: ( A,B ) In vitro myelination was performed using a co-culture of DRG neurons and SC with indicated mGluR antagonists (AIDA for mGluR1, PCCG-4 for mGluR2/3, and MPEP for mGluR5). Resultant myelination profiles were visualized by MBP immunocytochemistry. Representative myelination profiles ( A ) and their quantification data ( B ) are shown. Scale bar = 100 μm. For quantification, myelination profiles were counted from five randomly selected fields under a microscope using a 10x objective lens. The number of profiles relative to no inhibitor control is shown (mean profile numbers of 5 independent experiments ± SD). Asterisks indicate significant difference from control (Student’s t test, *p < 0.05). Note that myelination was promoted by PCCG-4, an mGluR2/3 antagonist. ( C ) Representative photomicrographs and quantification of EdU-positive SC in the proliferation assay with indicated conditions. Cells were co-stained with DAPI. Scale bar = 250 μm. For quantification, the percentage of EdU-possitive cells to the total number of cells were calculated in each condition (n = 3, mean ± SD). Statistical analysis was performed by Student’s t-test. Asterisks indicate significant difference (*p < 0.05). ( D,E ) Representative photomicrographs and quantification of neurofilament M (NFM) and MBP immunoreactivity of the DRG neuron-SC co-culture. Scale bar = 50 μm. For quantification in ( E ) the numbers of myelination profiles visualized by MBP staining and the intensity of NFM immunoreactivity were analyzed from five randomly selected fields under a microscope using a 20x objective lens (mean ± SD, n = 3). Asterisks indicate significant difference from control (Student’s t test, *p < 0.05).

Article Snippet: Primary SC cultures were prepared as described previously . mGluR antagonists were applied to the cultures at following concentrations: mGluR1 antagonist (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA, 100 μM; Tocris biosci.), mGluR2/3 antagonists PCCG-4 (100 μM) and mGluR5 antagonist MPEP (10 μM).

Techniques: In Vitro, Co-Culture Assay, Immunocytochemistry, Microscopy, Control, Proliferation Assay, Staining