Study of the Maturation of the Child’s Brain Using 31P-MRS

Hanaoka, Shigeru; Takashima, Sachio; Morooka, Keiichi

doi:10.1016/s0887-8994(97)00201-4

Cited by 22 publications

(11 citation statements)

References 14 publications

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“…On the other hand, Cr markedly prolongs synaptic transmission during hypoxia in vivo and in brain slices [17,33,34]. The pathogenesis of hypoxia-induced seizures and mechanisms of Cr-induced increase in resistance to these seizures in the rat and rabbit are likely to be relevant to human neonatal seizures in which hypoxia may be an important cause at a developmental stage of increasing brain PCr/NTP concentration ratio [35,36].…”

Section: Discussionmentioning

confidence: 99%

Brain Creatine Kinase and Creatine Transporter Proteins in Normal and Creatine-Treated Rabbit Pups

Kekelidze

Khait²,

Togliatti³

et al. 2000

Dev Neurosci

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Systemic creatine (Cr) supplementation increases brain phosphocreatine (PCr) and prevents hypoxic seizures in 15-day-old rabbits . Between 5 and 30 days of age during normal development, rabbit gray matter mitochondrial creatine kinase (Mi-CK) increases 400% while cytosolic CK (BB-CK) increases 60%. In white matter, both isoenzymes show smaller, similar increases (40%) during this period. The Cr transporter protein decreases 60% between 5 and 15 days in both regions. In vivo CK rate constants measured by ³¹P nuclear magnetic resonance increase 30% between 10 and 20 days, and then fall 50% between 20 and 30 days in predominantly gray matter slices. Similar maturational changes are seen in predominantly white matter slices. Injecting Cr at 15 days does not significantly change BB-CK or Mi-CK isoenzymes or the in vivo CK reaction rate constants. Thus, the largest change in the CK system associated with suppression of hypoxic seizures in Cr-treated rabbits is increased PCr in gray and white matter.

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Section: Discussionmentioning

confidence: 99%

Brain Creatine Kinase and Creatine Transporter Proteins in Normal and Creatine-Treated Rabbit Pups

Kekelidze

Khait²,

Togliatti³

et al. 2000

Dev Neurosci

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“…These results in the rabbit and the rat are relevant to the human newborn. At term, the newborn is approximately midway in the developmental time course of increasing brain PCr/NTP (Azzopardi et al., 1989 ; Hanaoka et al, 1998). As in the rabbit and rat, brain PCr approximately doubles, assuming no changes in NTP concentration during the developmental period from 26 weeks post conception to 3 months post term.…”

Section: Discussionmentioning

confidence: 99%

“…In brain, the reactant concentrations and rate of this one‐step reaction (PCr + MgADP + H [UNK] Cr + MgATP) measured in vivo show developmental changes and regional heterogeneity related to ATP metabolism (Holtzman et al, 1993 ; Tsuji et al, 1996). The brain ratio of PCr to nucleoside triphosphate (NTP) increases from 5 to 25 days of age in rats and mice and from 26 weeks post conception to 3‐6 months post term in the human (Tofts and Wray, 1985 ; Azzopardi et al, 1989 ; Holtzman et al, 1991 ; Hanaoka et al, 1998). This postnatal time course parallels the increase in rat brain aerobic glycolysis (Holtzman and Olson, 1983).…”

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confidence: 99%

In Vivo Development of Brain Phosphocreatine in Normal and Creatine‐Treated Rabbit Pups

Holtzman

Khait²,

Mulkern³

et al. 1999

Journal of Neurochemistry

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Abstract:To study the effects of creatine (Cr) on brain energy metabolism and on hypoxia-induced seizures, 5-to 30-day-old rabbit pups were given subcutaneous Cr (3 g/kg) for 3 days before exposure to 4% O 2 for 8 min. In saline-treated controls, hypoxic seizures were most frequent at 15 days (80% of pups) and 20 days (60%) of age. Seizures were prevented at 15 days and reduced 60% at 20 days in Cr-treated pups. In surface coil-localized brain 31 P nuclear magnetic resonance spectra, with signal from both cerebral gray (GM) and white (WM) matter, the phosphocreatine (PCr)/nucleoside triphosphate (NTP) ratio doubled between 5 and 30 days of age in controls. In all Cr-injected pups, brain PCr/NTP increased to values seen in 30-day-old controls. When spectra were acquired in predominantly GM and WM slices in vivo, the PCr/NTP ratio was very low in GM at 5 days but reached adult levels by 15 days in controls. In WM, the ratio increased steadily from 5 to 30 days of age. In Cr-injected pups, PCr/NTP increased to mature levels in WM and in GM at all ages. In conclusion, hypoxic seizures occur midway in the time course of brain PCr/NTP increase in rabbit pups as previously described in rat pups. In both altricial pups, systemic Cr increases brain PCr/NTP ratio and prevents hypoxic seizures. These results suggest that mature levels of PCr and/or Cr in brain limit EEG activation either directly or indirectly by preventing hypoxic metabolic changes. Key Words: Creatine-Development-Seizures-Brain phosphocreatine-HypoxiaNuclear magnetic resonance spectroscopy.

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“…Early in postnatal brain development, levels of membrane phospholipid precursors are high and breakdown products are low; this is followed by dramatic decreases in precursor levels and increases in breakdown products, which then plateau, as the brain reaches late adolescence. [17][18][19][20][21][22] In vivo 31 P MRS studies have shown lower PME levels and higher PDE levels in the PF 7,[23][24][25] and temporal lobe 26 of first-episode, neuroleptic naïve schizophrenia subjects, compared to matched controls. Reduced PME correlate with Wisconsin Cart Sorting test performance 27 and negative symptoms 28 in schizophrenia, implicating the PF in the pathogenesis of this disorder (for a review, see Keshavan et al…”

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confidence: 99%

Prefrontal membrane phospholipid metabolism of child and adolescent offspring at risk for schizophrenia or schizoaffective disorder: an in vivo 31P MRS study

et al. 2003

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In vivo31 P magnetic resonance spectroscopy ( 31 P MRS) studies have shown abnormal membrane phospholipid metabolism in the prefrontal cortex (PF) in the early course of schizophrenia. It is unclear, however, whether these alterations also represent premorbid risk indicators in schizophrenia. In this paper, we report in vivo 31 P MRS data on children and adolescents at high risk (HR) for schizophrenia. In vivo 31 P MRS studies of the PF were conducted on 16 nonpsychotic HR offspring of parents with schizophrenia or schizoaffective disorder, and 37 age-matched healthy comparison (HC) subjects. While 11 of the HR subjects had evidence of Axis I psychopathology (HR-P), five HR subjects had none (HR-NP). We quantified the freely mobile phosphomonoester (PME) and phosphodiester (PDE) levels reflecting membrane phospholipid precursors and breakdown products, respectively, and the relatively broad signal underlying PDE and PME peaks, comprised of less mobile molecules with PDE and PME moieties (eg, synaptic vesicles and phosphorylated proteins). Compared to HC subjects, HR subjects had reductions in freely mobile PME; the differences were accounted for mainly by the HR-P subjects. Additionally, HR-P subjects showed increases in the broad signal underlying the PME and PDE peaks in the PF. To conclude, these data demonstrate new evidence for decreased synthesis of membrane phospholipids and possibly altered content or the molecular environment of synaptic vesicles and/or phosphoproteins in the PF of young offspring at risk for schizophrenia. Follow-up studies are needed to examine the predictive value of these measures for future emergence of schizophrenia in at-risk individuals.

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Study of the Maturation of the Child’s Brain Using 31P-MRS

Cited by 22 publications

References 14 publications

Brain Creatine Kinase and Creatine Transporter Proteins in Normal and Creatine-Treated Rabbit Pups

Brain Creatine Kinase and Creatine Transporter Proteins in Normal and Creatine-Treated Rabbit Pups

In Vivo Development of Brain Phosphocreatine in Normal and Creatine‐Treated Rabbit Pups

Prefrontal membrane phospholipid metabolism of child and adolescent offspring at risk for schizophrenia or schizoaffective disorder: an in vivo 31P MRS study

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