Brain-derived neurotrophic factor in cerebrospinal fluid of patients with chronic daily headache: relationship with nerve growth factor and glutamate levels

Sarchielli, Paola; Alberti, Andrea; Gallai, Beatrice; Coppola, Francesca; Baldi, Antonio; Floridi, A.; Gallai, Virgilio

doi:10.1007/s101940200030

Cited by 18 publications

(19 citation statements)

References 31 publications

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“…Based on our findings, it can be hypothesized that the failure of the inhibitory role of AEA can contribute to maintaining central sensitization in chronic head pain, and represents a further mechanism which intervenes in increasing the release of the sensory neuropeptide CGRP and NO production, together with nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) release via glutamatergic transmission (Sarchielli et al, 2001(Sarchielli et al, , 2002.…”

Section: Endocannabinoids In CM P Sarchielli Et Almentioning

confidence: 91%

Endocannabinoids in Chronic Migraine: CSF Findings Suggest a System Failure

Sarchielli

Pini²,

Coppola³

et al. 2006

Neuropsychopharmacol

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120

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Based on experimental evidence of the antinociceptive action of endocannabinoids and their role in the modulation of trigeminovascular system activation, we hypothesized that the endocannabinoid system may be dysfunctional in chronic migraine (CM). We examined whether the concentrations of N-arachidonoylethanolamide (anandamide, AEA), palmitoylethanolamide (PEA), and 2-arachidonoylglycerol (2-AG) in the CSF of patients with CM and with probable CM and probable analgesic-overuse headache (PCM + PAOH) are altered compared with control subjects. The above endocannabinoids were measured by high-performance liquid chromatography (HPLC), and quantified by isotope dilution gas-chromatography/mass-spectrometry. Calcitonin gene-related peptide (CGRP) levels were also determined by RIA method and the end products of nitric oxide (NO), the nitrites, by HPLC. CSF concentrations of AEA were significantly lower and those of PEA slightly but significantly higher both in patients with CM and PCM + PAOH than in nonmigraineur controls (po0.01 and po0.02, respectively). A negative correlation was found between AEA and CGRP levels in CM and PCM + PAOH patients (r ¼ 0.59, po0.01 and r ¼ À0.65, po0.007; respectively). A similar trend was observed between this endocannabinoid and nitrite levels. Reduced levels of AEA in the CSF of CM and PCM + PAOH patients may reflect an impairment of the endocannabinoid system in these patients, which may contribute to chronic head pain and seem to be related to increased CGRP and NO production. These findings support the potential role of the cannabinoid (CB)1 receptor as a possible therapeutic target in CM.

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Section: Endocannabinoids In CM P Sarchielli Et Almentioning

confidence: 91%

Endocannabinoids in Chronic Migraine: CSF Findings Suggest a System Failure

Sarchielli

Pini²,

Coppola³

et al. 2006

Neuropsychopharmacol

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120

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“…In further research we demonstrated a significant correlation between NGF levels in the CSF of CDH patients with a previous history of migraine and those of the other growth factor thought to play a role as central pain modulator, brain-derived neurotrophic factor (BDNF). Levels of both neurotrophins were also correlated to those of glutamate, suggesting their putative intervention in enhancing glutamatergic transmission underlying chronic sensitization in CDH [71].…”

Section: Evidence Of Increased Glutamate Release In Migraine and Fmmentioning

confidence: 86%

Sensitization, glutamate, and the link between migraine and fibromyalgia

Sarchielli

Filippo²,

Nardi³

et al. 2007

Current Science Inc

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101

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Recent advances have shed insight on the pathophysiologic mechanisms of fibromyalgia and migraine, especially in the chronic form. A growing body of evidence supports the involvement of peripheral and central sensitization disturbances of pain-related processes underlying both disorders. They involve increased glutamate transmission through interaction with its ionotropic and metabotropic receptors. Few studies supporting the implication of this excitatory amino acid in chronic migraine and primary fibromyalgia demonstrated increased levels of glutamate in the cerebrospinal fluid of affected patients. These findings have implications for future therapies directed against glutamate receptors (in particular, N-methyl-D-aspartate receptors). Limited clinical experience in this regard, although promising, does not exclude additional mechanisms contributing to the maintenance of pain, which can be the target of therapeutic approaches in both disorders.

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“…Treatment reduced clinical signs, inflammation and apoptosis in EAE mice (Makar et al, 2009). A limitation of the delivery method was that the BDNF production could not be controlled, which could lead to potential undesirable side effects (Sarchielli et al, 2002;Constandil et al, 2011). We have now used a tetracyclineinducible (Tet-on) gene expression system in which BDNF production can be regulated.…”

Section: Introductionmentioning

confidence: 98%