Literature DB >> 2597167

Transient depletion of nucleus accumbens dopamine content may contribute to initial akinesia induced by MPTP in common marmosets.

S Rose1, M Nomoto, P Jenner, C D Marsden.   

Abstract

Acute treatment of common marmosets with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) caused an initial profound akinesia and other motor deficits. However, over the following months akinesia gradually disappeared although the animals remained clumsy and poorly coordinated. At 10 days following MPTP treatment there was a profound decrease in the dopamine, HVA and DOPAC content of the caudate nucleus, putamen and nucleus accumbens. By 3-4 months following MPTP treatment the animals had largely recovered from their akinesia, but the caudate nucleus and putamen dopamine, HVA and DOPAC content remained low. In contrast, the dopamine content of the nucleus accumbens had returned towards normal and the metabolite levels were higher than at 10 days. No overall alterations in 5HT or 5HIAA levels were observed at either time point. The transient and reversible nature of dopamine loss in the nucleus accumbens may contribute to the initial profound akinesia exhibited by common marmosets treated with MPTP. The restoration of dopamine levels in the nucleus accumbens may be partially responsible for the subsequent recovery of motor function that occurs in MPTP-treated marmosets.

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Year:  1989        PMID: 2597167     DOI: 10.1016/0006-2952(89)90572-8

Source DB:  PubMed          Journal:  Biochem Pharmacol        ISSN: 0006-2952            Impact factor:   5.858


  6 in total

1.  Short and long-term changes in cerebral [14C]-2-deoxyglucose uptake in the MPTP-treated marmoset: relationship to locomotor activity.

Authors:  K K Gnanalingham; N A Milkowski; L A Smith; A J Hunter; P Jenner; C D Marsden
Journal:  J Neural Transm Gen Sect       Date:  1995

2.  The effects of central aromatic amino acid DOPA decarboxylase inhibition on the motor actions of L-DOPA and dopamine agonists in MPTP-treated primates.

Authors:  S A Treseder; M Jackson; P Jenner
Journal:  Br J Pharmacol       Date:  2000-04       Impact factor: 8.739

3.  Selective dopamine antagonist pretreatment on the antiparkinsonian effects of benzazepine D1 dopamine agonists in rodent and primate models of Parkinson's disease--the differential effects of D1 dopamine antagonists in the primate.

Authors:  K K Gnanalingham; A J Hunter; P Jenner; C D Marsden
Journal:  Psychopharmacology (Berl)       Date:  1995-02       Impact factor: 4.530

4.  The competitive NMDA antagonist CPP protects substantia nigra neurons from MPTP-induced degeneration in primates.

Authors:  K W Lange; P A Löschmann; E Sofic; M Burg; R Horowski; K T Kalveram; H Wachtel; P Riederer
Journal:  Naunyn Schmiedebergs Arch Pharmacol       Date:  1993-12       Impact factor: 3.000

Review 5.  Animal models of Parkinson's disease: a source of novel treatments and clues to the cause of the disease.

Authors:  Susan Duty; Peter Jenner
Journal:  Br J Pharmacol       Date:  2011-10       Impact factor: 8.739

6.  Increased vulnerability of nigral dopamine neurons after expansion of their axonal arborization size through D2 dopamine receptor conditional knockout.

Authors:  Nicolas Giguère; Benoît Delignat-Lavaud; Freja Herborg; Aurore Voisin; Yuan Li; Vincent Jacquemet; Madhu Anand-Srivastava; Ulrik Gether; Bruno Giros; Louis-Éric Trudeau
Journal:  PLoS Genet       Date:  2019-08-26       Impact factor: 5.917

  6 in total

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