Ask your competent? doctor how this will help connect up your brain regions again post stroke.
And since your doctor was so competent a decade ago they started working with this since you need neurogenesis to recover from your stroke. Oh, I guess you don't have a functioning stroke doctor, do you? Sucks to be stuck with your doctor then!
G-Protein-Coupled Receptors in Adult Neurogenesis May 2012
The latest here:
Xanthurenic acid: A role in brain intercellular signaling
Michel Maitre1 | Omar Taleb1 | Hélène Jeltsch-David1,2 | Christian Klein1 |
Ayikoe-Guy Mensah-Nyagan1
Abbreviations: 3-HK, 3-hydroxykynurenine; AhR, aryl hydrocarbon receptor; BBB, blood–brain barrier; CNS, central nervous system; CSF, cerebrospinal fluid; DA, dopamine; EPSP,
excitatory postsynaptic potential; FICZ, 6-formylindolo-carbazole; GC–MS, gas chromatography–mass spectrometry; GPCR, G-protein-coupled receptor; GTP, guanosine-5′-
triphosphate; IDO1, indolamine 2,3 dioxygenase; I.P., intra-peritoneal; KAT, kynurenine aminotransferase; KMO, kynurenine monooxygenase; KP, kynurenine pathway; KYNA,
kynurenic acid; LATS, large neutral amino acid transporters; NAAG, N-Acetyl-Aspartyl- Glutamate; NADP, nicotinamide adenine dinucleotide phosphate; NADPH, nicotinamide adenine
dinucleotide phosphate hydrogen; NMDA, N-methyl-d-aspartate; OAT, organic anion transporter; PFC, prefrontal cortex; QUIN, quinolinic acid; ROS, reactive oxygen species; SN,
substantia nigra; TDO, tryptophan 2,3 dioxygenase; TH, tyrosine hydroxylase; Trp, tryptophan; TTX, tetrodotoxin; VTA, ventral tegmental area; XA, xanthurenic acid.
1
Biopathologie de la Myéline,
Neuroprotection et Stratégies
Thérapeutiques, INSERM U1119,
Fédération de Médecine Translationnelle
de Strasbourg (FMTS), Université de
Strasbourg, Bâtiment CRBS de la Faculté
de Médecine, Strasbourg, France
2 Biotechnologie et signalisation cellulaire,
UMR 7242 CNRS/Université de
Strasbourg, Illkirch Cedex, France
Correspondence
Michel Maitre, Biopathologie de la
Myéline, Neuroprotection et Stratégies
Thérapeutiques, INSERM U1119,
Fédération de Médecine Translationnelle
de Strasbourg (FMTS), Université de
Strasbourg, Bâtiment CRBS de la Faculté
de Médecine, 1 rue Eugène Boeckel,
67000 Strasbourg, France.
Email: maitre@unistra.fr
dizing properties, its ability to complex certain metal ions, and its detoxifier capac-
ity of 3-hydroxykynurenine (3-HK), its brain precursor. However, little is still known
about the role and mechanisms of action of XA in the central nervous system (CNS).
Therefore, many research groups have recently investigated XA and its central func-
tions extensively. The present paper critically reviews and discusses all major data re-
lated to XA properties and neuronal activities to contribute to the improvement of the
current knowledge on XA's central roles and mechanisms of action. In particular, our
data showed the existence of a specific G-protein-coupled receptor (GPCR) for XA
localized exclusively in brain neurons exhibiting Ca 2+-dependent dendritic release and
specific electrophysiological responses. XA properties and central activities suggest a
role for this compound in brain intercellular signaling. Indeed, XA stimulates cerebral
dopamine (DA) release contrary to its structural analog, kynurenic acid (KYNA). Thus,
KYNA/XA ratio could be fundamental in the regulation of brain glutamate and DA
release. Cerebral XA may also represent an homeostatic signal between the periphery
and several brain regions where XA accumulates easily after peripheral administra-
tion. Therefore, XA status in certain psychoses or neurodegenerative diseases seems
to be reinforced by its brain-specific properties in balance with its formation and pe-
ripheral inputs.
Ayikoe-Guy Mensah-Nyagan1
Abbreviations: 3-HK, 3-hydroxykynurenine; AhR, aryl hydrocarbon receptor; BBB, blood–brain barrier; CNS, central nervous system; CSF, cerebrospinal fluid; DA, dopamine; EPSP,
excitatory postsynaptic potential; FICZ, 6-formylindolo-carbazole; GC–MS, gas chromatography–mass spectrometry; GPCR, G-protein-coupled receptor; GTP, guanosine-5′-
triphosphate; IDO1, indolamine 2,3 dioxygenase; I.P., intra-peritoneal; KAT, kynurenine aminotransferase; KMO, kynurenine monooxygenase; KP, kynurenine pathway; KYNA,
kynurenic acid; LATS, large neutral amino acid transporters; NAAG, N-Acetyl-Aspartyl- Glutamate; NADP, nicotinamide adenine dinucleotide phosphate; NADPH, nicotinamide adenine
dinucleotide phosphate hydrogen; NMDA, N-methyl-d-aspartate; OAT, organic anion transporter; PFC, prefrontal cortex; QUIN, quinolinic acid; ROS, reactive oxygen species; SN,
substantia nigra; TDO, tryptophan 2,3 dioxygenase; TH, tyrosine hydroxylase; Trp, tryptophan; TTX, tetrodotoxin; VTA, ventral tegmental area; XA, xanthurenic acid.
1
Biopathologie de la Myéline,
Neuroprotection et Stratégies
Thérapeutiques, INSERM U1119,
Fédération de Médecine Translationnelle
de Strasbourg (FMTS), Université de
Strasbourg, Bâtiment CRBS de la Faculté
de Médecine, Strasbourg, France
2 Biotechnologie et signalisation cellulaire,
UMR 7242 CNRS/Université de
Strasbourg, Illkirch Cedex, France
Correspondence
Michel Maitre, Biopathologie de la
Myéline, Neuroprotection et Stratégies
Thérapeutiques, INSERM U1119,
Fédération de Médecine Translationnelle
de Strasbourg (FMTS), Université de
Strasbourg, Bâtiment CRBS de la Faculté
de Médecine, 1 rue Eugène Boeckel,
67000 Strasbourg, France.
Email: maitre@unistra.fr
Abstract
Xanthurenic acid (XA) raises a growing multidisciplinary interest based upon its oxi-dizing properties, its ability to complex certain metal ions, and its detoxifier capac-
ity of 3-hydroxykynurenine (3-HK), its brain precursor. However, little is still known
about the role and mechanisms of action of XA in the central nervous system (CNS).
Therefore, many research groups have recently investigated XA and its central func-
tions extensively. The present paper critically reviews and discusses all major data re-
lated to XA properties and neuronal activities to contribute to the improvement of the
current knowledge on XA's central roles and mechanisms of action. In particular, our
data showed the existence of a specific G-protein-coupled receptor (GPCR) for XA
localized exclusively in brain neurons exhibiting Ca 2+-dependent dendritic release and
specific electrophysiological responses. XA properties and central activities suggest a
role for this compound in brain intercellular signaling. Indeed, XA stimulates cerebral
dopamine (DA) release contrary to its structural analog, kynurenic acid (KYNA). Thus,
KYNA/XA ratio could be fundamental in the regulation of brain glutamate and DA
release. Cerebral XA may also represent an homeostatic signal between the periphery
and several brain regions where XA accumulates easily after peripheral administra-
tion. Therefore, XA status in certain psychoses or neurodegenerative diseases seems
to be reinforced by its brain-specific properties in balance with its formation and pe-
ripheral inputs.
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