Deep Brain Stimulation: Adenosine is crucial for DBS–mediated attenuation of tremor

Deep brain stimulation is a surgical treatment where electrodes, or brain pacemakers, are implanted into specific areas of the brain to drive an electrical jolt. The mechanism by which DBS results in the treatment of Parkinsons, Dystonia, Tremor, Chronic pain is still not clearly understood. DBS has been also used to treat tourettes, OCD, phantom limb pain, Dystonia. On a biochemical level, one possible mechanism by which DBS results in temporary lesioning – as in the thalamus of mice – is the stimulation of ATP release from Astrocytes. It has been shown that DBS is associated with a marked increase in the release of ATP, resulting in accumulation of its catabolic product, adenosine. A1 receptor activation by adenosine depresses excitatory transmission in the thalamus leading to temporary lesioning.

DBS side effects include: apathy, hallucinations, compulsive gambling, depression and hypersex.

Adenosine is crucial for deep brain stimulation–mediated attenuation of tremor

Nature Medicine 14, 75 – 80 (2008)
Published online: 23 December 2007 | doi:10.1038/nm1693
Lane Bekar1,3, Witold Libionka1,3, Guo-Feng Tian1, Qiwu Xu1, Arnulfo Torres1, Xiaohai Wang1, Ditte Lovatt1, Erika Williams1, Takahiro Takano1, Jurgen Schnermann2, Robert Bakos1 & Maiken Nedergaard1

Deep brain stimulation (DBS) is a widely used neurosurgical approach to treating tremor and other movement disorders. In addition, the use of DBS in a number of psychiatric diseases, including obsessive-compulsive disorders and depression, is currently being tested. Despite the rapid increase in the number of individuals with surgically implanted stimulation electrodes, the cellular pathways involved in mediating the effects of DBS remain unknown. Here we show that DBS is associated with a marked increase in the release of ATP, resulting in accumulation of its catabolic product, adenosine. Adenosine A1 receptor activation depresses excitatory transmission in the thalamus and reduces both tremor- and DBS-induced side effects. Intrathalamic infusion of A1 receptor agonists directly reduces tremor, whereas adenosine A1 receptor–null mice show involuntary movements and seizure at stimulation intensities below the therapeutic level. Furthermore, our data indicate that endogenous adenosine mechanisms are active in tremor, thus supporting the clinical notion that caffeine, a nonselective adenosine receptor antagonist, can trigger or exacerbate essential tremor. Our findings suggest that nonsynaptic mechanisms involving the activation of A1 receptors suppress tremor activity and limit stimulation-induced side effects, thereby providing a new pharmacological target to replace or improve the efficacy of DBS.

More information on DBS http://www.ninds.nih.gov/disorders/deep_brain_stimulation/deep_brain_stimulation.htm

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Comments
2 Responses to “Deep Brain Stimulation: Adenosine is crucial for DBS–mediated attenuation of tremor”
  1. Stan Taylor says:

    I would like your permission to use the above image of a dbi for an article I am writing. I am a freelance writer and I have a dbi for my essential tremor. I do not know at this writing which magazine I’ll submit my article to for publication.

    I sit on the editorial for for the two e-magazines of the Science Teachers Association of Ontario and I have to date 62 published science articles.

    • brainchemist says:

      Hello Stan,

      I check your blog. Interesting stuff. I will spend more time on it on the weekend.

      As for the picture, unfortunately i dont think you can use it for publishing purposes. I found this picture by doing a simple DBS google image search. No owner claimed copyright within the site. It has been used here since the main purpose of this website is to compile and organize specific ideas in the neurosciences and not to generate income.

      Amadeus

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