title: Biochemical alteration in cerebrospinal fluid precedes behavioral deficits in Parkinsonian rats induced by 6-hydroxydopamine.
abstract: BACKGROUND
  Parkinson's disease, affecting at least 1% of population older than 65 years, is the most common neurodegenerative movement disorder. Up to now, no evidence has demonstrated that biochemical changes in CSF occur preceding the onset of Parkinson's symptoms. In this study, we tested the hypothesis that biochemical changes in CSF precede behavioral deficits in Parkinsonian animals.
  
  
  METHODS
  We infused different doses of 6-OHDA into the MFB of rats bilaterally and examined the animals' movement behaviors, biochemical alterations in CSF, and dopaminergic neuronal number in the SNpc 1 week later.
  
  
  RESULTS
  Our results indicated that animals with over 70% dopaminergic neuronal loss in the SNpc exhibited behavioral bradykinesia and rigidity, and a decrease of HVA in CSF. In contrast, animals with about 42% dopaminergic neuronal loss in the SNpc showed normal movement behaviors, but displayed a drastic decline of HVA in CSF. Furthermore, the number of dopaminergic neurons in the SNpc was positively correlated with the HVA level in CSF.
  
  
  CONCLUSIONS
  Our findings demonstrate that biochemical alteration in CSF foreruns behavioral deficits and the HVA level in CSF is positively correlated with the number of dopaminergic neurons in the SNpc of Parkinsonian rats induced by 6-OHDA. Our results strongly suggest that additional studies are needed to evaluate usefulness of monitoring the HVA level in CSF for early detection of the loss of dopaminergic neurons in the SNpc that precedes the onset of Parkinsonian symptoms in humans.
authors: Graduate Institute of Clinical Medicine, Taipei Medical University, Taipei 110, Taiwan.
authors: Jia-Wei
authors: JW
authors: Lin
authors: Chwen-Ming
authors: CM
authors: Shih
authors: Yen-Chou
authors: YC
authors: Chen
authors: Chien-Min
authors: CM
authors: Lin
authors: Jo-Ting
authors: JT
authors: Tsai
authors: Yung-Hsiao
authors: YH
authors: Chiang
authors: Raymond
authors: R
authors: Shih
authors: Pei-Ling
authors: PL
authors: Chiu
authors: Kuo-Sheng
authors: KS
authors: Hung
authors: Yi-Shian
authors: YS
authors: Yeh
authors: Li
authors: L
authors: Wei
authors: Wen-Ta
authors: WT
authors: Chiu
authors: Liang-Yo
authors: LY
authors: Yang
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000032:analysis / Q000134:cerebrospinal fluid; D002452:Cell Count; D016923:Cell Death / Q000187:drug effects / Q000502:physiology; D004195:Disease Models, Animal; D004298:Dopamine / Q000378:metabolism*; D006719:Homovanillic Acid / Q000134:cerebrospinal fluid*; D018476:Hypokinesia / Q000134:cerebrospinal fluid / Q000139:chemically induced / Q000503:physiopathology; D008297:Male; D009127:Muscle Rigidity / Q000134:cerebrospinal fluid / Q000139:chemically induced / Q000503:physiopathology; D009410:Nerve Degeneration / Q000134:cerebrospinal fluid / Q000139:chemically induced / Q000503:physiopathology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D016627:Oxidopamine / Q000633:toxicity; D020734:Parkinsonian Disorders / Q000134:cerebrospinal fluid* / Q000473:pathology* / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013378:Substantia Nigra / Q000378:metabolism* / Q000473:pathology*; D013565:Sympatholytics / Q000633:toxicity
chemical_list: D015415:Biomarkers; D013565:Sympatholytics; D016627:Oxidopamine; D004298:Dopamine; D006719:Homovanillic Acid