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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

Putamen

 
 
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Disease relevance of Putamen

 

Psychiatry related information on Putamen

 

High impact information on Putamen

 

Chemical compound and disease context of Putamen

 

Biological context of Putamen

  • Using a genetic approach, we show that mice lacking dopamine (DA-deficient, or DD, mice) are resistant to the hypophagic effects of a moderate dose of AMPH (2 microg/g) but manifest normal AMPH-induced hypophagia after restoration of DA signaling in the caudate putamen by viral gene therapy [20].
  • Dopamine receptors, evaluated as 3H-spiperone binding sites, were unchanged in the putamen but decreased to 30% of control values in the caudate [21].
  • In the antitumor necrosis factor-alpha neutralizing antibody-treated rats, infarct volume was significantly reduced (P=0.014, n=7; respectively), and cerebral specific gravity was dramatically increased in the cortex and caudate putamen (P<0.001, n=7; respectively) in association with a reduction in MMP-9 and membrane type 1-MMP upregulation [22].
  • Ascorbate induces lipid peroxidation in human caudate and putamen, an effect that is further enhanced by guanyl and inosine nucleotides [23].
  • All of the compounds inhibited dopamine uptake in rat caudate putamen (IC50 = 24-4456 nM) which correlated significantly (r = 0.907; p > 0.0001) with binding affinities at the dopamine transporter [24].
 

Anatomical context of Putamen

 

Associations of Putamen with chemical compounds

  • We found that in the putamen there was a nearly complete depletion of dopamine in all subdivisions, with the greatest reduction in the caudal portions (less than 1 percent of the dopamine remaining) [30].
  • In the brains of deceased schizophrenics who underwent long-term treatment with antipsychotic drugs, the concentration of homovanillic acid (a dopamine metabolite) was significantly increased in the orbital frontal, cingulate, and temporal tip areas of the cortex, but not in the putamen or the nucleus accumbens [31].
  • CONCLUSIONS: Patients with SPD showed reduced volume and elevated relative glucose metabolic rate of the putamen compared with both schizophrenic patients and controls [32].
  • Using positron emission tomography and the carbon 11-labeled ligand raclopride, central D2-dopamine receptor occupancy in the putamen was determined in psychiatric patients treated with clinical doses of psychoactive drugs [33].
  • RESULTS: Subjects with MDD had a hypersensitive response to the rewarding effects of dextroamphetamine (2-fold increase; t(21) = 2.74, P = .01), with altered brain activation in the ventrolateral prefrontal cortex and the orbitofrontal cortex and the caudate and putamen (F(1,44) = 11.93, P = .001) [34].
 

Gene context of Putamen

  • Citrate synthase-corrected complex II-III activity was markedly reduced in both HD caudate (-29%) and putamen (-67%), and complex IV activity was reduced in HD putamen (-62%) [35].
  • 125I-NT-3 binding to sections of human basal ganglia resembled that seen in rat or cat, including high densities in the caudate, putamen, and superficial neocortex [36].
  • In the autopsied putamen of an asymptomatic GCH1 mutation carrier, we found that brain biopterin loss (-82%) paralleled that reported in dopa-responsive dystonia patients (-84%) [37].
  • In human tissue, LRRK2 mRNA was found in the corresponding brain areas caudatus and putamen at lower levels and dopamine neurons were also devoid of LRRK2 mRNA [38].
  • Although the caudate/putamen (CPu) expresses mPer1 and/or mPer2 mRNA, the function of these genes in this nucleus has not yet been elucidated [39].
 

Analytical, diagnostic and therapeutic context of Putamen

References

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