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This link has been bookmarked by 1 people . It was first bookmarked on 11 Oct 2009, by Sigalon - The Swedish Frog.

  • 11 Oct 09
    sigalon
    Sigalon - The Swedish Frog

    "This establishes yet another means of efficacy for LDN (low dose naltrexone). It may even be
    the case that some of these chronic pain/inflammation syndromes are due
    more to the loss dopaminergic tone, which regulates immunity and
    neurotransmission. It even suggests LDN might work in Parkinson's or
    that CB1 might be deficient in Parkinson's. I'll have more to say when
    my articles are finished. "
    ***********************
    Levodopa is the most commonly prescribed drug for Parkinson's disease
    (PD). Although levodopa improves PD symptoms in the initial stages of
    the disease, its long-term use is limited by the development of side
    effects, including abnormal involuntary movements (dyskinesias) and
    psychiatric complications. The endocannabinoid system is emerging as an
    important modulator of basal ganglia functions and its pharmacologic
    manipulation represents a promising therapy to alleviate
    levodopa-induced dyskinesias. Rats with 6-OHDA lesions that are
    chronically treated with levodopa develop increasingly severe axial,
    limb, locomotor and oro-facial abnormal involuntary movements (AIMs).
    Administration of the cannabinoid agonist WIN 55,212-2 attenuated
    levodopa-induced axial, limb and oral AIMs dose-dependently via a
    CB(1)-mediated mechanism, whereas it had no effect on locomotive AIMs.
    By contrast, systemic administration of URB597, a potent FAAH inhibitor,
    did not affect AIMs scoring despite its ability to increase anandamide
    concentration throughout the basal ganglia. Unlike WIN, anandamide can
    also bind and activate transient receptor potential vanilloid type-1
    (TRPV1) receptors, which have been implicated in the modulation of
    dopamine transmission in the basal ganglia. Interestingly, URB597
    significantly decreased all AIMs subtypes only if co-administered with
    the TRPV1 antagonist capsazepine. Our data indicate that pharmacological
    blockade of TRPV1 receptors unmasks the anti-dyskinetic effects of FAAH
    inhibitors and that CB(1) and TRPV1 receptors play opposite roles in
    levodopa-induced dyskinesias.

    PMID: 17

    pd