Regional distribution and pharmacological characteristics of [3H]N-acetyl-aspartyl-glutamate (NAAG) binding sites in rat brain

Shave, E.; Pliss, Lioudmila; Lawrance, Megan L; FitzGibbon, Thomas; Šťastný, F; Balcar, Vladimír J.

doi:10.1016/s0197-0186(00)00045-0

Cited by 27 publications

(13 citation statements)

References 62 publications

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“…NAAG is a highly abundant neuromodulatory peptide in the brain that is expressed in neuronal terminals (Shave et al, 2001) and to lesser extent in glial cells (Cassidy and Neale, 1993). It is synthesized from NAA under tight regulation and acts on presynaptic metabotropic glutamate receptors mGluR2/3 to down-regulate neurotransmitter release via negative feedback (Zhao et al, 2001) and on N-methyl-D-aspartate (NMDA) receptors either as direct agonist (e.g.…”

Section: Neurotransmitter Metabolismmentioning

confidence: 99%

The neurochemical profile quantified by in vivo 1H NMR spectroscopy

et al. 2012

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Section: Neurotransmitter Metabolismmentioning

confidence: 99%

The neurochemical profile quantified by in vivo 1H NMR spectroscopy

et al. 2012

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“…NAAG is an abundant neuropeptide (0.5–3 mM) in the human brain, and is a highly selective agonist at the group II metabotropic glutamate subtype 3 receptor (mGluR3) that presynaptically inhibits glutamate release (Shave et al, 2001; Tsai, 2005; Wroblewska et al, 1997; Wroblewska et al, 2006; Neale et al, 2011; Bergeron and Coyle, 2012) and a NMDAR antagonist (Bergeron and Coyle, 2012). Post-mortem studies in schizophrenia report alterations in NAAG (Reynolds and Reynolds, 2011; Ghose et al, 2009), indicating that NAAG may play a pivotal role in the pathophysiology of schizophrenia.…”

Section: 0 1h-mrs In Schizophreniamentioning

confidence: 99%

In vivo assessment of neurotransmitters and modulators with magnetic resonance spectroscopy: Application to schizophrenia

Wijtenburg

Yang

Fischer

et al. 2015

Neuroscience & Biobehavioral Reviews

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In vivo measurement of neurotransmitters and modulators is now feasible with advanced proton magnetic resonance spectroscopy (1H-MRS) techniques. This review provides a basic tutorial of MRS, describes the methods available to measure brain glutamate, glutamine, γ-aminobutyric acid, glutathione, N-acetylaspartylglutamate, glycine, and serine at magnetic field strengths of 3Tesla or higher, and summarizes the neurochemical findings in schizophrenia. Overall, 1H-MRS holds great promise for producing biomarkers that can serve as treatment targets, prediction of disease onset, or illness exacerbation in schizophrenia and other brain diseases.

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“…NAAG is a neuroactive endogenous peptide that interacts preferentially with metabotropic glutamate receptors group II (Neale et al. , 2000); however, it is also a weak NMDA receptor agonist (Shave et al. , 2001) interacting with heteromers containing NR2D subunits (Hess et al.…”

Section: Introductionmentioning

confidence: 99%

“…QUIN is a neurotoxic metabolite of tryptophan that exhibits selective affinity for heteromeric NMDA receptors containing NR2B ⁄ 2A subunits (Pliss et al, 2000). NAAG is a neuroactive endogenous peptide that interacts preferentially with metabotropic glutamate receptors group II (Neale et al, 2000); however, it is also a weak NMDA receptor agonist (Shave et al, 2001) interacting with heteromers containing NR2D subunits (Hess et al, 1999). NAAG can also serve as a source of extra-synaptic glutamate (Neale et al, 2000) and, according to its concentration, exerts either a neuroprotective or a neurotoxic effect (Orlando et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

Different transfer of nociceptive sensitivity from rats with postnatal hippocampal lesions to control rats

Yamamotová

Franěk

Vaculín

et al. 2007

Eur J of Neuroscience

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Hippocampal lesions in newborn rats alter the development of mechanisms involved in the processing of nociception. The hippocampal lesion was induced by the bilateral infusion, into the lateral cerebral ventricles, of 0.25 microL of saline containing either 0.25 micromol quinolinic acid (QUIN) and/or 0.25 micromol N-acetyl-L-aspartyl-L-glutamate (NAAG) on postnatal day 12. The same amount of sterile saline was injected into the sham-operated animals (group SHAM). It was expected that the QUIN- and NAAG-lesioned rats would exhibit some differences in thermal pain perception; however, we wanted to know if the control rats would exhibit, at least in part, similar changes in pain perception as their chemically lesioned siblings with which they were housed. Young adult NAAG-injured rats exhibited increased withdrawal latencies in the tail-flick and plantar tests, whereas young adult QUIN-injured animals exhibited only marginally decreased latencies. Nociceptive responses in the SHAM rats paralleled the littermates that had been neonatally treated with QUIN or NAAG, i.e. the responses in the SHAM(QUIN) group decreased, whereas the responses in the SHAM(NAAG) group increased. No significant changes in nociception were observed in intact animals, regardless of which group they were housed with. Our results show that social factors, which were originally demonstrated only for the pain behavior, may also influence basal nociceptive sensitivity in rats. We concluded that the "sham operation" may have had a long-term, nonspecific impact on nociceptive behavior by inducing behavioral mimicry of other animals.

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Regional distribution and pharmacological characteristics of [3H]N-acetyl-aspartyl-glutamate (NAAG) binding sites in rat brain

Cited by 27 publications

References 62 publications

The neurochemical profile quantified by in vivo 1H NMR spectroscopy

The neurochemical profile quantified by in vivo 1H NMR spectroscopy

In vivo assessment of neurotransmitters and modulators with magnetic resonance spectroscopy: Application to schizophrenia

Different transfer of nociceptive sensitivity from rats with postnatal hippocampal lesions to control rats

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