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1.
Figure 2

Figure 2. Cortical cannulation placements. From: Role of the primary motor cortex in L-DOPA-induced dyskinesia and its modulation by 5-HT1A receptor stimulation.

Schematic representation (A) and representative cresyl violet-stained section (B) of M1 sections portraying typical injector placement. Schematic representation of coronal rat brain section taken from . The dashed circle depict the distribution of M1 microinfusion sites in rats used in Experiments 2 and 3. (Relevant anatomical structures: Cc, corpus callosum; Cpu, caudate putamen; M1, primary motor cortex).

Corinne Y Ostock, et al. Neuropharmacology. ;61(4):753-760.
2.
Figure 5

Figure 5. Intracortical ±8-OH-DPAT reduces established ALO AIMs. From: Role of the primary motor cortex in L-DOPA-induced dyskinesia and its modulation by 5-HT1A receptor stimulation.

Sixty min after systemic injections of L-DOPA + Benserazide (12 + 15 mg/kg, sc), VEH or ±8-OH-DPAT (DPAT; 5 & 20mM) were infused continuously into M1 for 60 min using microdialysis. Graphs depict the treatment means for (A) ALO AIMs ± S.E.M., as well as (B) Rotations ± S.E.M. for 6-OHDA-lesioned rats over 3 h of observation. Horizontal white (aCSF) and gray (treatment) bar across graph represents the timecourse of intra-M1 infusion. Treatment effects were analyzed with Kruskal-Wallis ANOVAs and two-way ANOVAs for Rotations. Post hoc comparisons denote significant differences between treatments at the time points indicated (*p < 0.05 for DPAT20 vs. VEH; +p < 0.05 for DPAT20 vs. DPAT5).

Corinne Y Ostock, et al. Neuropharmacology. ;61(4):753-760.
3.
Figure 4

Figure 4. Co-administration of the 5-HT1AR antagonist WAY100635 reverses ±8-OH-DPAT’s anti-dyskinetic effects. From: Role of the primary motor cortex in L-DOPA-induced dyskinesia and its modulation by 5-HT1A receptor stimulation.

Rats received intracortical microinfusions of Vehicle (VEH), the 5-HT1AR antagonist WAY100635 (5 μg; WAY5), the 5-HT1AR agonist ±8-OH-DPAT (10 μg; DPAT10), or ±8-OH-DPAT (10 μg) + WAY100635 (5 μg; DPAT10 + WAY5), followed 5 min later by treatment with the L-DOPA + Benserazide (12 + 15 mg/kg, sc). Graphs depict treatment means for (A) Axial, (B) Forelimb, (C) Orolingual AIMs ± S.E.M., as well as (D) Rotations ± S.E.M. for 6-OHDA-lesioned rats every 10 min for 2 h. Treatment effects were determined by Friedman ANOVAs and two-way repeated-measures ANOVAs for Axial, Forelimb, and Orolingual AIMs and rotations, respectively. Post hoc comparisons indicate significant differences between treatments at the time points indicated (*p < 0.05 for DPAT10 vs VEH; ×p <0.05 for DPAT10 vs. WAY5; +p < 0.05 for DPAT10 vs. DPAT10 + WAY5).

Corinne Y Ostock, et al. Neuropharmacology. ;61(4):753-760.
4.
Figure 3

Figure 3. Intracortical ±8-OH-DPAT attenuates onset of ALO AIMs subtypes. From: Role of the primary motor cortex in L-DOPA-induced dyskinesia and its modulation by 5-HT1A receptor stimulation.

Five min after intracortical microinfusions of Vehicle (VEH) or the 5-HT1AR agonist ±8-OH-DPAT (DPAT; 1 or 10 μg), DA depleted rats received systemic injections of L-DOPA + Benserazide (12 + 15 mg/kg, sc). Graphs depict the treatment means for (A) Axial, (B) Forelimb, and (C) Orolingual AIMs ± S.E.M., as well as (D) Rotations ± S.E.M. for 6-OHDA-lesioned rats over 2 hr of observation. Treatment effects were analyzed with Friedman ANOVAs for Axial, Forelimb, and Orolingual AIMs and two-way repeated-measures ANOVAs for Rotations. Post hoc comparisons denote significant differences between treatments at the time points indicated (*p < 0.05 for DPAT10 vs. VEH; ×p < 0.05 for DPAT1 vs. VEH; +p < 0.05 for DPAT10 vs. DPAT1).

Corinne Y Ostock, et al. Neuropharmacology. ;61(4):753-760.
5.
Figure 1

Figure 1. L-DOPA-induced ALO AIMS and M1 c-fos expression are reduced by ±8-OH-DPAT. From: Role of the primary motor cortex in L-DOPA-induced dyskinesia and its modulation by 5-HT1A receptor stimulation.

Groups of L-DOPA primed, DA depleted rats (n = 3 or 4/group) received either Vehicle followed 5 min later by Vehicle (VEH + VEH) or L-DOPA + Benserazide (12 + 15 mg/kg, ip; VEH + L-DOPA) or ±8-OH-DPAT (1.0 mg/kg, ip) followed by L-DOPA + Benserazide (DPAT + L-DOPA). Rats were rated for abnormal involuntary movements (AIMs) hr after L-DOPA treatment and then immediately perfused, after which 50 μm sections were processed for c-fos immunohistochemistry. (A) Schematic depiction of motor cortex (M1) and prefrontal cortex (PFC) analyzed for c-fos expression and photorepresentations of VEH + VEH, VEH + L-DOPA, DPAT + L-DOPA treatments on M1/PFC c-fos induction in DA- depleted rats. (B) Bars depict mean ALO AIMs ± S.E.M. after treatment with VEH + VEH (white), VEH + L-DOPA (black), and DPAT + L-DOPA (gray). Effects of treatments on (C) M1 and (D) PFC c-fos induction, expressed as mean number of c-fos positive cells/mm2 ± S.E.M.. Treatment effects were determined by one-way ANOVA. Significant differences for each treatment were established by post hoc planned comparisons (*p< 0.05 vs. VEH + VEH; +p < 0.05 vs. VEH + L-DOPA. Relevant anatomical structures: M1, primary motor cortex; PFC, prefrontal cortex; CPu, caudate putamen).

Corinne Y Ostock, et al. Neuropharmacology. ;61(4):753-760.

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