6-羟基多巴脑内注射建立帕金森病大鼠模型的实验研究

目的 探讨6-羟基多巴脑内注射建立稳定的帕金森病大鼠模型的方法.方法 将6-羟基多巴立体定向注入大鼠右侧前脑内侧束和中脑被盖腹侧区,观察大鼠的行为变化和中脑黑质区的形态学变化.结果 注药后2周,动物经阿扑吗啡诱导即出现向健侧的旋转行为,注射效果稳定.在长达3个月的观察中,动物的旋转行为稳定,无明显的差异.形态学显示,毁损侧的黑质致密部和中脑被盖腰侧区的酪氨酸羟化酶阳性神经元的数量明显减少.结论 通过6-羟基多巴脑内注射的方法可以建立起稳定、有效的帕金森病大鼠模型.     

高场强~1H-MRS对帕金森病大鼠模型的应用价值探讨

目的:利用高场强氢质子磁共振波谱(1H-MRS)观察帕金森病大鼠模型纹状体区的神经代谢变化,探讨高场强1H-MRS对PD大鼠模型的应用价值。方法:7只正常大鼠经6-羟基多巴胺(6-OHDA)单侧(右侧)损毁制备偏侧帕金森病模型前后应用1.5T磁共振进行波谱分析。分析造模术前后双侧纹状体区N-乙酰天门冬氨酸/肌酸(NAA/Cr)、胆碱/肌酸(Cho/Cr)比值的变化。并对黑质致密部进行黑质酪氨酸羟化酶免疫组织化学染色。结果:6只大鼠造模成功。损毁侧纹状体内NAA/Cr比值明显低于对侧及造模前同侧(P<0.05),而Cho/Cr比值与对侧及造模前同侧相比无显著性差异(P>0.05)。损毁侧黑质酪氨酸羟化酶阳性神经元较对侧显著减少(P<0.05)。结论:1.5T临床专用型磁共振1H-MRS可以作为帕金森病大鼠模型纹状体区细胞代谢有价值的无创性检测方法。     

脑源性神经营养因子对多巴胺能神经元的影响

目的观察脑源性神经营养因子对帕金森氏病大鼠模型黑质多巴胺能神经元的影响。方法选用Wistar种系大白鼠，体重230～250g，随机分3组，通过左侧中脑黑质立体定向注射法，组1为生理盐水对照组（简称对照组）10只，注射相应量（5μl）的生理盐水；组2为注射6-OHDA制作帕金森氏病模型组（简称6-OHDA组）10只，注射6-OHDA，5μl（2μg／μl）；组3为（6-OHDA＋BDNF组），在制成帕金森氏病模型后再向同侧中脑黑质注射BDNF5μl（3μg／μl），连续6d，qd。分别观察动物的旋转行为，免疫组化染色方法观察黑质酪氨酸羟化酶（TH）阳性神经元的数量，高效液相法测定纹状体部多巴胺（DA）含量的变化。结果单侧黑质内注入6-OHDA制成帕金森氏病大鼠模型后，6-OHDA组与对照组比较，产生旋转行为，（6-OHDA＋BDNF）组在观察旋转行为时，症状明显改善；镜下见TH阳性神经元主要见于对照组的黑质致密部，数量为42．3±7．56个／μm^2，模型组黑质致密部TH阳性神经元数明显减少为2．41±1．07个／μm^2，（6-OHDA＋BDNF）组黑质致密部TH阳性神经元数为15．36±3．04个／μm^2；纹状体部多巴胺含量：生理盐水组为11．4±1．2μg／g，6-OHDA组3．6±0．5μg／g，（6-OHDA＋BDNF）组5．5±0．6μg／g。结论①6-OHDA对黑质多巴胺能神经元有损害作用，制成偏侧帕金森病大鼠模型。②BDNF能改善6-OHDA所致的帕金森氏病大鼠黑质多巴胺能神经元数目的减少；BDNF能明显抑制6-OHDA引起的纹状体部多巴胺含量降低；BDNF可抑制6-OHDA对黑质多巴胺能神经元的毒性作用。     

Mdivi-1对帕金森病大鼠多巴胺能神经元损伤的保护作用研究

目的 研究线粒体分裂引发帕金森病（Parkinson’s disease,PD）大鼠模型中多巴胺能神经元损伤作用及线粒体分裂抑制剂1（mitochondrial division inhibitor 1,Mdivi-1）对神经元损伤的保护作用机制。方法 将大鼠随机分成对照组(生理盐水组)、模型组、美多巴组和Mdivi-1组,采用6-羟基多巴胺(6-hydroxydopamine,6-OHDA)注射大鼠单侧纹状体的方法建立PD动物模型,利用阿朴吗啡（apomorphine,APO）引起的大鼠旋转实验和转棒实验来观察行为学变化。利用免疫组化方法评估酪氨酸羟化酶（tyrosine hydroxylasez,TH）在中脑黑质中阳性细胞比例以及纹状体中TH阳性纤维数量,采用ELISA法检测大鼠黑质和纹状体中超氧化物歧化酶（superoxide dismutase,SOD）、谷胱甘肽过氧化物酶（glutathione peroxidase,GSH-Px）、还原型谷胱甘肽（glutathione,GSH）、过氧化氢酶（catalase,CAT）、丙二醛（malondialdehyde,MDA）、一氧化氮（nitric oxide,NO）及一氧化氮合酶（nitric oxide synthase,NOS）的含量。结果与对照组相比,PD模型组大鼠在APO诱发第3周和6周后旋转圈数均显著增加,同时转棒上停留时间均显著缩短;大脑黑质TH阳性细胞数和纹状体中TH阳性纤维数目显著减少;组织内SOD、GSH Px、CAT的活性显著降低,而NOS 活性显著升高,MDA和NO含量升高,而GSH含量则降低。美多巴及Mdivi-1处理3周和6周后均可显著改善PD大鼠的相关行为学症状,并增加黑质TH阳性细胞数和纹状体中TH阳性纤维数目,同时增加组织内SOD,GSH-Px,CAT,GSH含量,降低NOS 活性,减少MDA和NO含量。结论 Mdivi-1对6-OHDA诱导PD大鼠的多巴胺能神经元损伤具有保护作用,其机制可能与其抗氧化能力有关。     

运动通过上调mGluR2/3表达抑制帕金森病模型大鼠纹状体中等多棘神经元异常电活动

目的：探讨运动通过上调代谢型谷氨酸受体2/3(m GluR2/3)表达对帕金森病（PD）模型大鼠纹状体中等多棘神经元（MSNs）异常电活动的影响。方法：清洁级SD大鼠随机分为假手术安静组（Control组,n=9）和6-羟基多巴胺（6-OHDA）造模组（6-OHDA组,n=40）。6-OHDA造模组采用神经毒素6-OHDA注射于大鼠右脑内侧前脑束（MFB）,建立偏侧损毁PD模型大鼠,假手术组于相同部位给予同等剂量的生理盐水作为对照组。采用阿扑吗啡（APO）诱导旋转行为测试评价PD模型的可靠性。经鉴定符合PD模型的大鼠随机分为6-OHDA安静组（PD组,n=9）、6-OHDA+运动组（PD+Ex组,n=9）和6-OHDA+运动+mGluR2/3拮抗剂组（PD+Ex+APICA组,n=9）。运动组于手术后1周开始进行跑台训练干预（11 m/min,30 min/day,5 d/week,4 weeks）。运动+mGluR2/3拮抗剂组每次运动前,采用微量注射泵将m GluR2/3拮抗剂APICA注射到纹状体内,注射体积为1μL。采用免疫组织化学染色技术检测黑质酪氨酸羟化酶（TH）免疫阳性细...     

乌鸡黑色素对6-OH-DA诱导帕金森病大鼠模型的神经保护作用

目的 探讨乌鸡黑色素对于6-羟多巴胺(6-OH-DA)单侧损毁纹状体诱导的帕金森病模型大鼠的神经保护作用及其机制.方法 将60只SD大鼠造模成功后,随机分为对照组、6-OH-DA诱导的帕金森病单纯模型组和治疗组,治疗组分别按6 mg/kg或20 mg/kg乌鸡黑色素灌胃给药,1次/d,共3w.然后比较各组中脑黑质多巴胺能神经元的数目、纹状体酪氨酸羟化酶(TH)阳性神经纤维的数量、阿朴吗啡诱导的旋转行为以及大鼠自主运动情况的差异.结果 6 mg/kg和20 mg/kg乌鸡黑色素灌胃给药能显著减少6-OH-DA所导致的中脑黑质多巴胺能神经元的死亡,减少纹状体TH阳性神经纤维的丢失,并有效改善阿朴吗啡诱导的旋转行为.结论 乌鸡黑色素能缓解6-OH-DA诱导的中脑黑质多巴胺能神经元的损伤,对于帕金森病有潜在的治疗作用.     

雌激素对PD模型大鼠黑质纹状体通路的保护作用及其机制探讨

目的研究雌激素（Estrogen）对6-羟基多巴（6-OHDA）制备的去卵巢（OVX）帕金森病（PD）模型大鼠黑质纹状体通路的保护作用及其可能机制。方法应用6-OHDA两点注射单侧损毁内侧前脑束（MFB）制备OVXPD模型大鼠,侧脑室给予17-β雌二醇（17-βestradiol,1μg/5μl）,观察大鼠旋转行为、黑质酪氨酸羟化酶（TH）基因表达、黑质铁染色阳性细胞数量和纹状体内多巴胺（DA）及其代谢产物含量的变化。结果雌激素用药组可明显减少阿朴吗啡诱导的PD模型大鼠单侧旋转行为（P〈0.01）。在损毁侧黑质,雌激素用药组TH基因的表达较PD模型组明显增加（P〈0.01）;纹状体DA及其代谢产物亦较PD模型组显著升高（P〈0.01）。黑质铁染色阳性细胞数量较PD模型组明显减少（P〈0.01）。结论雌激素对PD模型大鼠黑质DA能神经元有明显的保护作用,其作用机制可能与降低铁负载有关。     

MRI对于恒河猴PD模型建立和治疗的评价

目的：应用MRI评价建立恒河猴帕金森病（PD）模型，以及在中脑黑质受损区进行细胞移植的疗效。材料与方法：选取6只恒河猴，雌性2只，雄性4只，体重6．0－8．5kg。经颈总动脉注射甲基－苯基－四氢吡啶（MPTP）建立PD模型，并行MRI模型。获取横断和冠状位T1WI和T2WI，以单侧注射MPTP的对侧脑组织作为正常对照。建立PD模型后，再对病例中脑黑质区进行细胞移植，并复查MRI。最后应用抗酪氨酸羟化酶免疫组化和Grino染色对猴脑组织切片进行病理检查。结果：MRI的T2WI显示注射MPTP侧中脑黑质缩小，内部有局灶性高信号。细胞移植前后的MPRI所见无显著性差异。免疫组化检查证实注射MPTP侧中脑多巴胺能神经元明显减少，Grino染色显示注射侧黑质内大量胶质细胞增生。经细胞移植症状缓解的猴脑切片显示神经元的减少无明显改变。结论：MRI是恒河猴PD模型建立的一种评价手段，可以用于细胞移植疗效的评价。     

CT引导脑内植入携带人类酪氨酸羟化酶基因腺相关病毒载体治疗实验性帕金森病猴

目的 观察CT引导脑内注射入类酪氨酸羟化酶基因腺相关病毒载体(AAV—hTH)对神经细胞的转染能力，以及对帕金森病(PD)猴的治疗效应。方法 经右侧颈内动脉注射1-甲基4-苯基-1，2，3，6一四氢吡啶(MPTP)制作6只偏侧帕金森病恒河猴模型，经CT引导将AAV—hTH注入5只帕金森病猴右侧尾状核内，观测猴模型的行为学改变6个月以上，以高效液相色谱法(HLPC)测定转染后尾状核内多巴胺(DA)及其代谢产物含量，并以免疫组化检测法及逆转录-聚合酶链式反应(RT—PCR)方法检测酪氨酸羟化酶(TH)基因的表达情况。结果 CT引导定位穿刺有实时操作、定位精确、微创的优点。所有注射AAV—hTH的偏侧PD猴模型术后2周即有帕金森病症状改善，持续6个月以上，其中1只动物阿朴吗啡旋转实验示完全停止了帕金森病旋转现象，其余动物旋转次数较术前减少约42％～70％。实验侧与健侧尾状核区多巴胺及其代谢产物含量比值较未治疗模型增高。免疫组化染色见穿刺针道部位有大量TH阳性细胞；RT—PCR检测到实验侧尾状核区有TH-mRNA存在；而对照侧尾状核区、其他部位脑组织与心、肝、肾组织及未注射模型实验侧尾状核区均未见阳性发现。结论 CT引导立体定向穿刺PD猴尾状核注入AAV—hTH能使TH基因精确地在特定部位有效表达，提高尾状核区DA含量，改善模型猴症状，研究结果提示这是一种有效、安全的治疗PD非人类灵长类动物模型的方法。为临床基因治疗PD的研究提供了实验研究依据。     

鱼藤酮对大鼠中脑黑质神经元多巴胺转运体的影响

目的研究鱼藤酮对大鼠中脑黑质神经元多巴胺转运体的影响。方法雄性健康SD大鼠80只,随机分为正常对照组、溶剂对照组和鱼藤酮注射组(1.0mg/kg和1.5mg/kg)。溶剂对照组和鱼藤酮注射组大鼠分别于背部皮下注射溶剂和鱼藤酮,每日1次,28d后处死动物,取脑,冰上分离中脑黑质组织。采用Western blot和免疫组化染色观察酪氨酸羟化酶及多巴胺转运体的蛋白表达,RT-PCR检测多巴胺转运体和多巴胺受体的基因表达,生化实验分析Na -K -ATP酶活性。结果鱼藤酮注射组大鼠中脑黑质组织酪氨酸羟化酶免疫阳性的多巴胺神经元数量减少,酪氨酸羟化酶蛋白表达降低,多巴胺转运体蛋白和基因表达增加,Na -K -ATP酶活性降低,多巴胺Ⅱ型受体表达增加,1.5mg/kg剂量组变化较1.0mg/kg剂量组变化更为显著。结论鱼藤酮对大鼠中脑黑质组织多巴胺神经元具有毒性作用,多巴胺转运体功能异常在鱼藤酮多巴胺神经元毒性中可能具有重要作用。     

Manganese-enhanced MRI in a rat model of Parkinson's disease

PURPOSE: To measure intra- and inter-hemispheric connectivity within the basal ganglia (BG) nuclei in healthy and in unilateral 6-hydroxydopamine (6-OHDA) Parkinson disease rat model in order to test the BG interhemispheric connectivity hypothesis. MATERIAL AND METHODS: The manganese-enhanced MRI (MEMRI) method with direct injection of manganese chloride into the entopeduncular (EP), substantia nigra (SN), and the Habenula nuclei in unilateral 6-OHDA (N = 22) and sham-operated (N = 16) rat groups was used. MEMRI measurements were applied before, 3, 24, and 48 hours post-manganese injection. Signal enhancements in T1-weighted images were compared between groups. RESULTS: Manganese injection into the EP nucleus resulted with bihemispheric signal enhancements in the habenular complex (Hab) at both groups with stronger enhancements in the 6-OHDA group. It also exhibited lower sensorimotor cortex signal enhancement in the 6-OHDA rat group. SN manganese injection caused enhanced anteroventral thalamic and habenular nuclei signals in the 6-OHDA rat group. Manganese habenula injection revealed enhanced interpeduncular (IP) and raphe nuclei signals of the 6-OHDA rat group. CONCLUSION: Modulations in the effective intra- and interhemispheric BG connectivity in unilateral 6-OHDA Parkinson's disease (PD) rat model support the BG interhemispheric connectivity hypothesis and suggest a linkage between the dopaminergic and serotonergic systems in PD, in line with clinical symptoms.     

MR定量磁化率成像在帕金森病临床诊断中的价值研究

目的 分析帕金森病（PD）患者的中脑黑质及红核的磁化率变化情况,明确MR定量磁化率成像（QSM）技术在PD临床诊断中的价值。 方法 回顾性分析2017年2月至2019年8月于佛山市第一人民医院诊断为PD的患者39例（PD组）,其中男性17例、女性22例,年龄47~80（65.44±9.78）岁。根据改良Hoehn-Yahr分级将患者分为早期PD组（23例）及中晚期PD组（16例）,另选取20名健康体检者作为正常对照组。所有患者及正常对照者均进行QSM扫描,测量各组中脑左右两侧黑质和红核的磁化率,取平均值。采用独立样本t检验分析PD患者的中脑黑质及红核磁化率的变化特征,并与PD的临床诊断、分级和病程进行Pearson相关性分析;采用单因素分析中脑左右侧黑质及红核的磁化率变化与临床肢体运动障碍症状侧的关系。 结果 PD组的中脑黑质及红核的磁化率较正常对照组显著升高 [（0.073±0.017）×10?3对（0.058±0.028）×10?3,t=?2.125,P=0.043;（0.094±0.020）×10?3对（0.072±0.035）×10?3,t=?2.605,P=0.015]。PD组的中脑黑质及红核的磁化率与Hoehn-Yahr分级无显著相关性（r=0.051,P=0.759;r=0.045,P=0.788）;黑质的磁化率与病程呈显著正相关（r=0.420,P=0.008）,红核的磁化率与病程无相关性（r=0.241,P=0.130）。PD组的中脑左右侧黑质、红核的磁化率变化与患者临床发病时肢体运动障碍症状的表现无显著相关性（黑质:F_左=0.661,P_左=0.421;F_右=1.153,P_右=0.290。红核:F_左=0.006,P_左=0.940;F_右=0.109,P_右=0.743）。 结论 QSM技术能够测量中脑黑质及红核的磁化率,并间接反映脑内铁沉积情况,对PD诊断及病程评估具有临床价值。     

阿扑吗啡阻抗6-羟基多巴胺毁损纹状体的实验研究

 目的 探讨阿扑吗啡是否对6-羟基多巴胺毁损纹状体帕金森病鼠模型有神经保护作用.方法 6-羟基多巴胺毁损大鼠左侧纹状体,在毁损前15 min阿扑吗啡(10mg/kg,皮下注射),连续注射11 d.毁损2周后,分别进行行为学(苯丙胺引起的旋转数目)和神经化学(高压液相测定纹状体多巴胺及代谢物含量)的研究.结果 阿扑吗啡能降低苯丙胺引起的向损伤侧旋转的数目.而且,显著减低多巴胺的损耗使其恢复到正常,并使DOPAC/DA比率恢复到正常.结论 在6-羟基多巴胺毁损纹状体模型中,阿扑吗啡不仅改善运动功能,而且,恢复纹状体的多巴胺含量.     

Proton MRS of the unilateral substantia nigra in the human brain at 4 tesla: detection of high GABA concentrations.

Parkinson's disease (PD) is characterized by loss of dopaminergic neurons in the substantia nigra (SN), the cause of which is unknown. Characterization of early SN pathology could prove beneficial in the treatment and diagnosis of PD. The present study shows that with the use of short-echo (5 ms) Stimulated-Echo Acquisition Mode (STEAM) spectroscopy and LCModel, a neurochemical profile consisting of 10 metabolites, including gamma-aminobutyric acid (GABA), glutamate (Glu), and glutathione (GSH), can be measured from the unilateral SN at 4 tesla. The neurochemical profile of the SN is unique and characterized by a fourfold higher GABA/Glu ratio compared to the cortex, in excellent agreement with established neurochemistry. The presence of elevated GABA levels in SN was validated with the use of editing, suggesting that partial volume effects were greatly reduced. These findings establish the feasibility of obtaining a neurochemical profile of the unilateral human SN by single-voxel spectroscopy in small volumes.     

Transcranial Sonography of the Substantia Nigra: Digital Image Analysis

BACKGROUND AND PURPOSE:Increased echogenicity of the substantia nigra is a typical transcranial sonography finding in Parkinson disease. Experimental software for digital analysis of the echogenic substantia nigra area has been developed. The aim of this study was to compare the evaluation of substantia nigra echogenicity by using digital analysis with a manual measurement in patients with Parkinson disease and healthy volunteers.MATERIALS AND METHODS:One hundred thirteen healthy volunteers were enrolled in the derivation cohort, and 50 healthy volunteers and 30 patients with Parkinson disease, in the validation cohort. The substantia nigra was imaged from the right and left temporal bone window by using transcranial sonography. All subjects were examined twice by using different sonographic machines by an experienced sonographer. DICOM images of the substantia nigra were encoded; then, digital analysis and manual measurement of the substantia nigra were performed. The 90th percentile of the derivation cohort values was used as a cut-point for the evaluation of the hyperechogenic substantia nigra in the validation cohort. The Spearman coefficient was used for assessment of the correlation between both measurements. The Cohen κ coefficient was used for the assessment of the correlation between both measurements and Parkinson disease diagnosis.RESULTS:The Spearman coefficient between measurements by using different machines was 0.686 for digital analysis and 0.721 for manual measurement (P < .0001). Hyperechogenic substantia nigra was detected in the same 26 (86.7%) patients with Parkinson disease by using both measurements. Cohen κ coefficients for digital analysis and manual measurement were 0.787 and 0.762, respectively (P < .0001).CONCLUSIONS:The present study showed comparable results when measuring the substantia nigra features conventionally and by using the developed software.

Parkinson disease (PD) is a progressive neurodegenerative disorder. Postmortem and neuroimaging studies showed that PD-associated neuronal dysfunction, cell loss, and α-synuclein pathology begin years before clinical symptoms appear and clinical diagnosis is possible.^1–4 This preclinical period may be the most promising time window for successful neuroprotective interventions in PD.⁵Increased echogenicity of the substantia nigra (SN) is a typical transcranial sonography (TCS) finding in patients with PD. Recent studies reported an enlarged hyperechogenic SN in approximately 90% of patients with PD, by using cutoff values between 0.20 and 0.25 cm², depending on the specific sonography system used.^6,7 In contrast, a hyperechogenic enlarged SN is detectable in only approximately 10% of healthy volunteers.⁸ Moreover, this feature is already present in prediagnostic disease stages and persists during the course of PD without significant changes.^9,10 Approximately 60% of healthy volunteers with hyperechogenic SN show a decrease in ¹⁸F-DOPA uptake in the striatum,⁸ and hyperechogenic SN is more frequently observed in subjects prone to develop extrapyramidal symptoms after neuroleptic therapy.¹¹However, the main limitation of TCS in the evaluation of SN hyperechogenicity is the dependence of image quality on both the sonographer''s experience and the quality of the bone window.^12–14 Digital analysis of TCS images of the SN could eliminate this limitation. We developed an experimental application B-mode Assist System with a graphic user interface in Matlab (MathWorks, Natick, Massachusetts), an integrated development environment with a plug-in Image Processing Toolbox, for digital analysis of SN echogenicity.^15,16The aim of the study was to compare the manual measurement of SN with digital analysis of SN echogenicity by using the developed software obtained by 2 different sonography machines in patients with PD and healthy volunteers.     

天麻对帕金森病模型大鼠行为学、生物化学的影响

 目的 探讨天麻剂量对帕金森病模型大鼠行为学及生物化学的影响及防治的机制.方法 采用6-羟基多巴胺大鼠模拟帕金森病,治疗2周后,分别进行行为学(阿朴吗啡引起的旋转数目)和神经化学(高压液相测定纹状体多巴胺及代谢物含量)的研究.结果 天麻小剂量组能降低阿朴吗啡引起的向损伤对侧旋转的数目,而且显著减少多巴胺的损耗,使其它含量恢复正常.结论 在6-羟基多巴胺毁损纹状体模型中,天麻小剂量组不仅运动功能改善,而且,可恢复纹状体的多巴胺含量.     

Metabolic–dopaminergic mapping of the 6-hydroxydopamine rat model for Parkinson’s disease

Purpose The unilateral 6-hydroxydopamine (6-OHDA) lesion rat model is a well-known acute model for Parkinson’s disease (PD). Its validity has been supported by invasive histology, behavioral studies and electrophysiology. Here, we have characterized this model in vivo by multitracer imaging [glucose metabolism and dopamine transporter (DAT)] in relation to behavioral and histological parameters. Methods Eighteen female adult Wistar rats (eight 6-OHDA-lesioned, ten controls) were investigated using multitracer [¹⁸F]-fluoro-2-deoxy-D-glucose (FDG) and [¹⁸F]-FECT {2′-[¹⁸F]-fluoroethyl-(1R-2-exo-3-exe)-8-methyl-3-(4-chlorophenyl)-8-azabicyclo(3.2.1)-octane-2-carboxylate} small animal positron emission tomography (PET). Relative glucose metabolism and parametric DAT binding images were anatomically standardized to Paxinos space and analyzed on a voxel-basis using SPM2, supplemented by a template-based predefined volumes-of-interest approach. Behavior was characterized by the limb-use asymmetry test; dopaminergic innervation was validated by in vitro tyrosine hydroxylase staining. Results In the 6-OHDA model, significant glucose hypometabolism is present in the ipsilateral sensory-motor cortex (−6.3%; p = 4 × 10⁻⁶). DAT binding was severely decreased in the ipsilateral caudate-putamen, nucleus accumbens and substantia nigra (all p < 5 × 10⁻⁹), as confirmed by the behavioral and histological outcomes. Correlation analysis revealed a positive relationship between the degree of DAT impairment and the change in glucose metabolism in the ipsilateral hippocampus (p = 3 × 10⁻⁵), while cerebellar glucose metabolism was inversely correlated to the level of DAT impairment (p < 3 × 10⁻⁴). Conclusions In vivo cerebral mapping of 6-OHDA-lesioned rats using [¹⁸F]-FDG and [¹⁸F]-FECT small animal PET shows molecular–functional correspondence to the cortico-subcortical network impairments observed in PD patients. This provides a further molecular validation supporting the validity of the 6-OHDA lesion model to mimic multiple aspects of human PD.