Cerebrospinal fluid GABA levels in chronic migraine with and without depression

Vieira, Domingos Savio; Naffah-Mazacoratti, M.G.; Zukerman, Eliova; Soares, Carlos Augusto Senne; Alonso, Elena O.; Faulhaber, Markus; Cavalheiro, Ésper A.; Peres, Mario F. P.

doi:10.1016/j.brainres.2006.03.051

Cited by 39 publications

(26 citation statements)

References 40 publications

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“…Our search identified 45 studies: 26 studies for the comparison of patients with current MDE versus healthy controls, [8][9][10][11][12][13][14][15][16][17][18]30,[33][34][35][36][37][38][39][40][41][42][43][44][45][46] 12 studies for the comparison of patients with current MDE before treatment versus after treatment, 12,20,23,25,26,28,36,43,[47][48][49][50] and 11 for the comparison of euthymic patients and controls. 18,[21][22][23]27,29,38,[51][52][53][54] Figure 1 depicts the study selection proce...…”

Section: Resultsmentioning

confidence: 99%

Meta-analysis of central and peripheral γ-aminobutyric acid levels in patients with unipolar and bipolar depression

Roméo

Choucha

Fossati

et al. 2018

jpn

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Section: Resultsmentioning

confidence: 99%

Meta-analysis of central and peripheral γ-aminobutyric acid levels in patients with unipolar and bipolar depression

Roméo

Choucha

Fossati

et al. 2018

jpn

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“…Notably, this genomic region contains three GABA A receptor subunit genes. Studies have reported higher GABA levels in blood platelets [Kowa et al, 1992] and saliva [Marukawa et al, 1996] of migraineurs and an increase of GABA levels in the cerebrospinal fluid in migraineurs during headache attacks [Vieira et al, 2006]. Certainly GABAergic drugs can modulate biochemical and physiological events in the disorder as evidenced by the use of GABAergic anticonvulsant medications as efficient therapy for migraine prevention [Silberstein, 2004].…”

Section: Linkage Analysis In Migrainementioning

confidence: 98%

Migraine genetics and prospects for pharmacotherapy

Colson

Fernandez

Griffiths

2007

Drug Development Research

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Migraine is a common complex neurological disorder with a well-known but poorly characterized genetic liability. The search for migraine susceptibility genes has been the focus of intense research. It is now believed that common migraine is not a single gene disorder, but attributable to several potentially interacting genetic variants. These variants may differ in each sufferer and interact with environmental factors to set the individual migraine threshold. This genetic liability may play an important role in the clinical heterogeneity seen in migraine and also in the variability of treatment response. This review will look at genetic loci implicated in migraine to date and consider their current or prospective role in migraine therapy. To elucidate the complex nature of migraine genetic liability, approaches that consider detailed endophenotypic profiles that encompass treatment response may provide much more relevant information than simple end diagnosis. Drug Dev Res 68: 282-293, 2007. r 2007 Wiley-Liss, Inc.

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“…Briefly, VGLUT1+/-and WT mice (n= 8/group) received [1-13 C]glucose (543 mg/kg i.p.) and [1,[2][3][4][5][6][7][8][9][10][11][12][13] C]acetate (504 mg/kg i.p. ).…”

Section: C-mrs Spectroscopymentioning

confidence: 99%

“…Using magnetic resonance spectroscopy, increased glutamate and reduced GABA levels have been observed in the cortex of depressed patients leading to an enhanced excitatory-inhibitory ratio (3)(4)(5)(6)(7). Interestingly, this imbalance is particularly associated with melancholic features in the patients (5) and is reverted by chronic treatment with antidepressants (8).…”

Section: Introductionmentioning

confidence: 99%