Elsevier

Neuroscience Letters

Volume 303, Issue 3, 11 May 2001, Pages 165-168
Neuroscience Letters

Striatal dopaminergic metabolism is increased by deep brain stimulation of the subthalamic nucleus in 6-hydroxydopamine lesioned rats

https://doi.org/10.1016/S0304-3940(01)01758-XGet rights and content

Abstract

Deep brain stimulation of the subthalamic nucleus is an established therapeutic strategy for patients with Parkinson's disease. Although the exact mechanisms of action remain unknown, it is noteworthy that dopaminergic medication can be markedly reduced after neurostimulation of the subthalamic nucleus. Previously, we have shown that deep brain stimulation of the subthalamic nucleus is followed by an increase of striatal extracellular dopamine metabolites in naive rats. In the present study we examined the effects of deep brain stimulation on striatal monoamine metabolism in the intrastriatal 6-hydroxydopamine rat model of Parkinson's disease. Deep brain stimulation of the subthalamic nucleus was followed by a delayed increase of extracellular 3,4-dihydroxyphenylacetic and homovanillic whereas dopamine levels were unchanged in stimulated rats and controls. Our results indicate that deep brain stimulation of the subthalamic nucleus affects significantly striatal dopaminergic metabolism in 6-hydroxydopamine lesioned rats.

Section snippets

Acknowledgements

We wish to thank C. Koelske, A. Loechner, R. Winter and M. Witt for their excellent technical assistance. This study was supported by grants of the Deutsche Forschungsgemeinschaft (Ku 830/3–1,3–3) and the European Community (QLK6–1999–02173).

References (18)

There are more references available in the full text version of this article.

Cited by (74)

  • Effects of subthalamic nucleus deep brain stimulation on neuronal spiking activity in the substantia nigra pars compacta in a rat model of Parkinson's disease

    2020, Neuroscience Letters
    Citation Excerpt :

    The findings contrasted to expectations, since others had reported that STN-DBS increased excitatory post-synaptic potentials in the SNc in vitro [12], increased dopamine concentrations in the striatum [11], and increased STN spiking activity in vivo in naïve rats [2]. Others also reported that STN-DBS increased striatal dopamine in urethane-anesthetized [16] and awake, freely-moving hemiparkinsonian rats [15]. These changes were plausibly brought about via enhanced excitatory glutamatergic neurotransmitter signaling from STN to SNc neurons, and indirectly by activating cholinergic and/or glutamatergic pedunculopontine tegmental (PPT) neurons in the STN-PPT-SNc neurocircuitry during STN-DBS [13].

  • The pathophysiological mechanisms of motivational deficits in Parkinson's disease

    2018, Progress in Neuro-Psychopharmacology and Biological Psychiatry
    Citation Excerpt :

    The other mechanism suggested is that apathy observed in STN-DBS patients may be caused by the degeneration of the DA mesolimbic pathway (Thobois et al., 2010). Animal models of PD using in vivo microdialysis have demonstrated that STN-DBS enhanced DA release and metabolism in striatum (Bruet et al., 2001; Lacombe et al., 2007; Meissner et al., 2002, 2003, 2001; Paul et al., 2000; Pazo et al., 2010) improving PD motor symptoms (Zhao et al., 2009). Considering that the STN-DBS is effective only against levodopa-sensitive motor symptoms and the possible reduction of DA-ergic therapy of up to 50% in parkinsonian subjects on chronic STN-DBS application, multiple authors postulated that variation in striatal DA-ergic activity may contribute to the clinical benefits of STN-DBS (Benabid et al., 1998; Krack et al., 2003; Limousin et al., 1995; Moro et al., 1999).

View all citing articles on Scopus
View full text