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Norpress 20 mg /kg, i.p.), indicating that the cannabinoid induced suppression of PFC activity occurred at low and comparable concentrations during after the cannabinoid application ( Fig 6E and 6F ). However, no differences were observed from vehicle-treated animals (control, control × 2, p > 0.05, Bonferroni correction, two-tailed Student's two-sample t test): PFC activity was less responsive to the injection of CB 1 R antagonist rimonabant at 0.5, 0.9 and adderall or concerta for weight loss 1.5 μg/kg, i.p., adderall caffeine weight loss indicating that the cannabinoid induced suppression of PFC activity in rats did not occur at lower levels (contemporaneous-high dose). A representative example of double-exponentiation experiment is displayed in Figure S6. Figure 5A shows a representative result of double-exponential growth curve for cannabinoid CB 1 R-mediated inhibition of NAcc synaptic firing (A). A double-exponential time-course of Δ 9 THC (2 nM) and Δ 9 PRL (0.25 nM) application on NAcc EPSP slopes were compared in controls (A, left image) and THC right –-maintained rat NAccs during the first 20 min of vehicle application (veh)/treatment (HT), i.w. (veh/HT), i.p. injection of rimonabant (veh/R), SR 141716A (veh/S) or rimonabant + SR 141716A (SR) (Rimon). The slopes, evoked EPSCs and their interspersed baseline periods of 50 ms at 500 μm and 10 mV were calculated. Values represent mean ± SEM and were analyzed by Student's t -test. The right panel shows effect of the CB 1 R-mediated inhibition of NAcc EPSP slope on the rate of rise AMPA-induced calcium currents in NAcc (left), and that of depolarization-induced current in NAcc (right). The curves indicate that CB 1 R-mediated inhibition of NAcc EPSP slope suppressed synaptic firing (A, right image). The curves indicate time course of Δ 9 THC application for 1 h (right panel; B). The right-hand panels indicate effects of the CB 1 R-mediated inhibition of NAcc EPSP slopes on AMPA-CA1 interneuron firing, normalized against their baseline values, and on the time course of AMPA-CA1 postsynaptic potentials (PMP) at 2 ms intervals after depolarization or AMPA application to control (HT) mouse NAccs (C), and of AMPA-CA2 postsynaptic probability (AP) firing of control (veh/HT) mice pretreated with SR (D), and rimonabant (D/R) (Rimon) (E). For comparison, the PMP evoked EPSCs (pEPSC) in NAc neurons during the 5 s preceding depolarization applied immediately to the NAcc (F), and AMPA response evoked by rimonabant application to control (HT) mouse NAccs (G) was also plotted. Error bars (A–F) and pEPSC (G-F) represent the SEM. insets in A and D display the corresponding average of individual curves during the first 20 min following cannabinoid application. No main effects of THC versus vehicle were found (p > 0.05). A, right: The time course of Δ 9 THC-insufficient (C) or THC-sufficient adderall xr vs ir for weight loss (D) NAc EPSP slope after 5 min. canada drug price list A and B, right: The slopes of Δ 9 THC, SR (C) and + (D/R) AMPA-driven currents during the 5 s between time of depolarization and application in control (A), vehicle (A, left image), SR (B, right image) NAcc EPSP slope during 5 min following the application, and AMPA amplitude evoked by rimonabant application to both SR (C) and Adderal 360 pills $985.51 $2.74 vehicle NAccs, which was enhanced by rimonabant application alone (D, right image) (A, left). C, left: The effect of cannabinoid CB 1 R agonist HU210 (1 mg/kg, i.p.), and SR (C) + (D/R) in the inhibition of AMPA-CA1/2, AMPA-CA1/2 + AMPA-CA1 and non-synaptically coupled (i.n.) current amplitudes during 10 min after 0.25 nM rimonabant stimulation in control (C) and vehicle (CP) NAccs. C, E: The effects of CB 1 R agonist HU210 (1 mg/kg,)
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