Journal: The Journal of Neuroscience

Article Title: Rewarding Effects of the Cholinergic Agents Carbachol and Neostigmine in the Posterior Ventral Tegmental Area

doi: 10.1523/JNEUROSCI.22-22-09895.2002

Figure Lengend Snippet: Effects of the D1 antagonist SCH 23390 (SCH) on carbachol (CARB) self-administration into the posterior VTA. The D1antagonist (0.05 mg/kg, i.p.) or saline (1 ml/kg) was administered 30 min before the self-administration session with 0.3 or 1 mmcarbachol. Each session lasted 60 min or until 60 infusions were obtained. The SCH 23390 treatment significantly reduced the rate of self-infusion of intra-VTA 0.3 or 1 mm carbachol (**p < 0.005 or *p < 0.05, respectively). A depicts mean infusion rates with SEM (n = 7). B depicts event records of a representative animal. A vertical line on thehorizontal line indicates the time of an infusion. Thenumber just right of thehorizontal line indicates total infusions per session.C depicts the first six and last six infusion intervals when animals earned 0.3 and 1 mm carbachol. The first six infusion intervals when animals were treated with the D1antagonist did not differ from those when treated with saline for both low (0.3 mm) and high (1 mm) carbachol rewards (F(1,6) = 2.28, p = 0.18 and F(1,6) = 2.32,p = 0.18, respectively). Moreover, animals delivered infusions at similar intervals between the first and last six intervals when treated with saline for both low and high carbachol rewards (F(1,6) = 0.26,p = 0.63 and F(1,6)= 3.55, p = 0.11, respectively). However, when rats were treated with SCH 23390, the last intervals increased more significantly than the first intervals for both low and high carbachol rewards (F(1,6) = 28.53,p < 0.005 andF(1,6) = 12.67, p< 0.05, respectively) and the last intervals of saline treatment (F(1,6) = 40.13, p< 0.001 and F(1,6) = 14.42,p < 0.01, respectively).

Article Snippet: The muscarinic–nicotinic agonist carbachol, the cholinesterase inhibitor neostigmine bromide, the nicotinic antagonist dihydro-β-erythroidine hydrobromide, the muscarinic antagonist (−)-scopolamine methyl bromide, and the dopamine D 1 antagonist R(+)-SCH 23390 hydrochloride, obtained from Research Biochemical International (Natick, MA), were used.

Techniques:

Journal: The Journal of Neuroscience

Article Title: Rewarding Effects of the Cholinergic Agents Carbachol and Neostigmine in the Posterior Ventral Tegmental Area

doi: 10.1523/JNEUROSCI.22-22-09895.2002

Figure Lengend Snippet: Mean latency in seconds (SEM) to self-administer the first infusion as a function of pretreatments (saline vs the dopamine antagonist SCH 23390) ( n = 7)

Article Snippet: The muscarinic–nicotinic agonist carbachol, the cholinesterase inhibitor neostigmine bromide, the nicotinic antagonist dihydro-β-erythroidine hydrobromide, the muscarinic antagonist (−)-scopolamine methyl bromide, and the dopamine D 1 antagonist R(+)-SCH 23390 hydrochloride, obtained from Research Biochemical International (Natick, MA), were used.

Techniques:

Journal: Molecular Neurobiology

Article Title: Dopaminergic Modulation of Forced Running Performance in Adolescent Rats: Role of Striatal D1 and Extra-striatal D2 Dopamine Receptors

doi: 10.1007/s12035-020-02252-2

Figure Lengend Snippet: Systemic blockade of D1 and D2 receptors during the incremental exercise test and open field. ( a ) Mean running time during the incremental test after systemic (i.p.) injection of the D1 antagonist SCH23390 (0.1 and 0.2 mg/kg). Data: SCH23390: 0 mg/kg: 36.75 ± 2.52 min ( n = 14, blue bar), 0.1 mg/kg: 16.67 ± 3.74 min ( n = 11, red bar), and 0.2 mg/kg: 5.23 ± 0.23 min, ( n = 5, red bar). * p < 0.0001 vs 0 mg/kg, Tukey post hoc test after significant one-way ANOVA, F 2,27 = 23.2, p < 0.0001. ( b ) Mean running time during the incremental test after systemic (i.p.) injection of the D2 antagonist raclopride (0.5 and 1 mg/kg). Data: 0 mg/kg: 36.75 ± 2.52 min ( n = 14, blue bar), 0.5 mg/kg: 17.19 ± 3.99 min ( n = 12, white bar), and 1 mg/kg: 8.78 ± 0.78 min ( n = 5, white bar). * p < 0.001 vs 0 mg/kg, Tukey post hoc test after significant one-way ANOVA, F 2,28 = 17, p < 0.0001. ( c ) Mean running time during the incremental test after systemic (i.p.) injection of SCH23390 (0.1 mg/kg) plus raclopride (0.5 mg/kg). Data: 0 mg/kg: 36.75 ± 2.52 min ( n = 14, blue bar) and SCH23390 + raclopride: 5 ± 0 min ( n = 8, red bar). t 20 = 9.4, * p < 0.0001, unpaired t test. ( d ) Locomotor activity during an open field test, comparing the effects of systemic (i.p.) injections of vehicle (blue bar), SCH23390 (0.1 mg/kg, light red bar), raclopride (0.5 mg/kg, white bar), and SCH23390 (0.1 mg/kg) plus raclopride (0.5 mg/kg, dark red bar). Data: vehicle: 313 ± 23.86 ( n = 6), SCH23390: 67.67 ± 31.85 ( n = 6), and raclopride: 130 ± 21.25 ( n = 6), SCH23390 + raclopride: 7.14 ± 1.95 ( n = 7). * p < 0.0001 vs vehicle, # p = 0.0027 vs raclopride, Tukey post hoc test after significant one-way ANOVA, F 3,21 = 37.6, p < 0.0001. Diamonds represent individual values

Article Snippet: To evaluate whether the dopaminergic system plays a role in mediating the motor performance, dopamine receptors were pharmacologically blocked during the incremental test by systemic and intrastriatal administration of the dopamine D1 receptor antagonist SCH23390 (Hello Bio, HB1643) and the D2 receptor antagonist raclopride (Sigma, 98185-20-7).

Techniques: Injection, Activity Assay

Journal: Molecular Neurobiology

Article Title: Dopaminergic Modulation of Forced Running Performance in Adolescent Rats: Role of Striatal D1 and Extra-striatal D2 Dopamine Receptors

doi: 10.1007/s12035-020-02252-2

Figure Lengend Snippet: Intrastriatal blockade of D1 and D2 receptors during the incremental exercise test and open field. ( a ) Examples of Nissl-stained coronal sections showing the site of injection. The image above shows an example of a rat injected with raclopride and the image below a rat injected with SCH23390. ( b ) Mean running time during the incremental exercise test after intrastriatal administration of aCSF (blue bar), SCH23390 (red bar, 10 μM, and 100 μM, ), or raclopride (white bar, 20 μM, 200 μM, and 5 mM, ). Data from the different concentrations were pooled for treatment comparison. Data: aCSF: 33.87 ± 1.7 min ( n = 6), SCH23390, 10 and 100 μM: 26.64 ± 1.39 min ( n = 8), and raclopride, 20 μM, 200 μM, and 5 mM ( n = 10): 33.01 ± 1.62. * p < 0.02 vs aCSF, Tukey post-hoc test after significant one-way ANOVA, F 2,21 = 5.9, p < 0.01. Diamonds represent individual values. ( c ) Locomotor activity during an open field test, comparing the effects of intrastriatal administration (i.s.) of aCSF and SCH23390 (100 μM). Data: aCSF (i.s.): 344.8 ± 28.14 ( n = 5, blue bar) and SCH23390 (i.s.): 354.6 ± 17.51 ( n = 5, red bar). t 8 = 0.3, p = 0.775, unpaired t test

Article Snippet: To evaluate whether the dopaminergic system plays a role in mediating the motor performance, dopamine receptors were pharmacologically blocked during the incremental test by systemic and intrastriatal administration of the dopamine D1 receptor antagonist SCH23390 (Hello Bio, HB1643) and the D2 receptor antagonist raclopride (Sigma, 98185-20-7).

Techniques: Staining, Injection, Activity Assay