Journal:

Article Title: Subplasmalemmal endoplasmic reticulum controls K Ca channel activity upon stimulation with a moderate histamine concentration in a human umbilical vein endothelial cell line

doi: 10.1113/jphysiol.2002.017053

Figure Lengend Snippet: A, current-voltage relationship obtained from inside-out patches in high symmetrical K+ (130 mm; linear regression fitting, r2 = 0.99), or in low intracellular K+ (5.6 mm; polynomial 2nd order fitting, r2 = 0.99). Each point is the mean of 6–10 single experiments. B, open state probability (Po) of the BKCa channel expressed as a function of holding membrane potential in the presence of various Ca2+ concentrations: 2 mm, 30 μm, 1 μm and 500 nm. Recordings were performed in high symmetrical KCl concentration. Each point shows the mean ± s.e.m. of 3–7 experiments. Curves were fitted according a Boltzmann equation for sigmoid curves (2 mm, 30 and 1 μm) or an exponential fit (500 nm) using Prism 3.0 (r2 = 0.86–0.88; GraphPad 3.0). C, correlation between Po and the Ca2+ concentration in the bath in an inside-out patch at holding potentials of +40 and −40 mV. Points represent means ± s.e.m.(n = 4–8). Curves were fitted according to the equation for sigmoid concentration-response curves using Prism 3.0 (GraphPad 3.0; r2 = 0.98 and 0.94 for aVh (Hp) of −40 and +40 mV, respectively).

Article Snippet: Curves were fitted according to the equation for sigmoid concentration-response curves using Prism 3.0 (GraphPad 3.0; r 2 = 0.98 and 0.94 for a V h (Hp) of −40 and +40 mV, respectively).

Techniques: Concentration Assay

Journal: The Journal of Neuroscience

Article Title: Synaptic Plasticity in the Amygdala in a Model of Arthritic Pain: Differential Roles of Metabotropic Glutamate Receptors 1 and 5

doi: 10.1523/JNEUROSCI.23-01-00052.2003

Figure Lengend Snippet: Differential changes of mGluR1- and mGluR5-mediated effects in the arthritis pain model. A, In a CeA neuron recorded in a brain slice from a normal rat, MPEP (1 μm; mGluR5 antagonist) inhibited synaptic transmission, whereas CPCCOEt (10 μm; mGluR1 antagonist) had no effect.B, In a CeA neuron from an arthritic rat (6 hr after induction), both CPCCOEt and MPEP inhibited synaptic transmission, suggesting a change in the endogenous activation of mGluR1 in the arthritis pain model. Each trace is the average of 8–10 monosynaptic EPSCs recorded at –60 mV. Drugs were applied by superfusion of the slice in ACSF for at least 10 min. Data shown were recorded at 10–12 min. C, CPCCOEt inhibited synaptic transmission in neurons from arthritic rats (EC50, 94 nm;n = 9) but not in neurons from normal rats (n = 11), suggesting a change in the activation state of mGluR1 in the arthritis pain model.D, Analysis of the raw data (EPSC peak amplitude in picoamperes) shows that blocking of mGluR1 by CPCCOEt significantly reduced the increased EPSC amplitude in CeA neurons from arthritic rats to control levels measured in neurons from nonarthritic rats.E, The inhibitory effects of MPEP on synaptic transmission in CeA neurons were not significantly different in normal rats (EC50, 28.3 nm;n = 10) and in arthritis (EC50, 27.7 nm;n = 9; p> 0.05; two-way ANOVA). F, Analysis of the raw data (picoamperes) shows that MPEP reduced a larger portion of the increased EPSC in arthritis than in control neurons; however, the MPEP-insensitive component of the EPSC also increased in arthritis. ***p < 0.001; unpaired ttest.

Article Snippet: Analysis of the concentration–response relationships showed that CPCCOEt (mGluR1 antagonist) (Fig. C ) inhibited synaptic transmission at the PB→CeA synapse in the arthritis pain model (EC 50 , 94 n m ; n = 9 neurons) (Fig. C , filled circles ), whereas CPCCOEt had no significant effect on synaptic transmission under normal conditions; i.e., the slope of the concentration-response curve was not significantly different from zero ( p > 0.05; F (1,3) = 6.482; n = 11; linear regression analysis, Prism 3.0, GraphPad software) (Fig. C , open circles ).

Techniques: Slice Preparation, Transmission Assay, Activation Assay, Blocking Assay, Control