Intracerebroventricular administration of creatine protects against damage by global cerebral ischemia in rat

Lensman, M.V.; Коржевский, Д. Э.; Mourovets, V. O.; Kostkin, V. B.; Izvarina, N. L.; Perasso, Luisa; Gandolfo, Carlo; Otellin, V. A.; Polenov, S. A.; Balestrino, Maurizio

doi:10.1016/j.brainres.2006.06.103

Cited by 57 publications

(46 citation statements)

References 33 publications

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“…Indeed, Cr administration can exert protective effects in various neurodegenerative processes, including Huntington's and Parkinson's diseases Bender et al 2006;Hersch et al 2006;Klein and Ferrante 2007). Creatine was also demonstrated to exert neuroprotective effects, both in vitro and in vivo, against anoxic and ischemic damage (Balestrino et al 2002;Adcock et al 2002;Lensman et al 2006) as well as against traumatic brain injury (Sullivan et al 2000) and spinal cord injury (Hausmann et al 2002).…”

Section: Models Of Transport Of Cr and Gaa At Bbb And Bcsfbmentioning

confidence: 98%

Creatine and guanidinoacetate transport at blood‐brain and blood‐cerebrospinal fluid barriers

Braissant

2012

J of Inher Metab Disea

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While it was thought that most of cerebral creatine is of peripheral origin, AGAT and GAMT are well expressed in CNS where brain cells synthesize creatine. While the creatine transporter SLC6A8 is expressed by microcapillary endothelial cells (MCEC) at blood-brain barrier (BBB), it is absent from their surrounding astrocytes. This raised the concept that BBB has a limited permeability for peripheral creatine, and that the brain supplies a part of its creatine by endogenous synthesis. This review brings together the latest data on creatine and guanidinoacetate transport through BBB and blood-CSF barrier (BCSFB) with the clinical evidence of AGAT-, GAMT- and SLC6A8-deficient patients, in order to delineate a clearer view on the roles of BBB and BCSFB in the transport of creatine and guanidinoacetate between periphery and CNS, and on brain synthesis and transport of creatine. It shows that in physiological conditions, creatine is taken up by CNS from periphery through SLC6A8 at BBB, but in limited amounts, and that CNS also needs its own creatine synthesis. No uptake of guanidinoacetate from periphery occurs at BBB except under GAMT deficiency, but a net exit of guanidinoacetate seems to occur from CSF to blood at BCSFB, predominantly through the taurine transporter TauT.

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Section: Models Of Transport Of Cr and Gaa At Bbb And Bcsfbmentioning

confidence: 98%

Creatine and guanidinoacetate transport at blood‐brain and blood‐cerebrospinal fluid barriers

Braissant

2012

J of Inher Metab Disea

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“…Previous evidence has suggested that AGS slices suppress ATP-consuming processes in vitro such as the Na + K + ATPase pump (Ross et al, 2006). Alternatively, hibernating brain may contain higher levels of high-energy phosphates, such as phosphocreatine, which has been shown to promote neuronal survival in response to ischemia (Balestrino et al, 2002;Lensman et al, 2006). Brains of hibernating hamsters contain higher concentrations of phosphocreatine than euthermic hamsters (Lust et al, 1989), but the level of phosphocreatine in AGS brain is currently unknown.…”

Section: Ags Tolerate Loss Of Atpmentioning

confidence: 99%

Arctic Ground Squirrel (Spermophilus Parryii) Hippocampal Neurons Tolerate Prolonged Oxygen—Glucose Deprivation and Maintain Baseline ERK1/2 and JNK Activation Despite Drastic ATP Loss

Christian

Ross

Zhao

et al. 2008

J Cereb Blood Flow Metab

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Oxygen-glucose deprivation (OGD) initiates a cascade of intracellular responses that culminates in cell death in sensitive species. Neurons from Arctic ground squirrels (AGS), a hibernating species, tolerate OGD in vitro and global ischemia in vivo independent of temperature or torpor. Regulation of energy stores and activation of mitogen-activated protein kinase (MAPK) signaling pathways can regulate neuronal survival. We used acute hippocampal slices to investigate the role of ATP stores and extracellular signal-regulated kinase (ERK)1/2 and Jun NH 2 -terminal kinase (JNK) MAPKs in promoting survival. Acute hippocampal slices from AGS tolerated 30 mins of OGD and showed a small but significant increase in cell death with 2 h OGD at 371C. This tolerance is independent of hibernation state or season. Neurons from AGS survive OGD despite rapid ATP depletion by 3 mins in interbout euthermic AGS and 10 mins in hibernating AGS. Oxygen-glucose deprivation does not induce JNK activation in AGS and baseline ERK1/2 and JNK activation is maintained even after drastic depletion of ATP. Surprisingly, inhibition of ERK1/2 or JNK during OGD had no effect on survival, whereas inhibition of JNK increased cell death during normoxia. Thus, protective mechanisms promoting tolerance to OGD by AGS are downstream from ATP loss and are independent of hibernation state or season.

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“…Several evidences indicate specific protective effects of Cr in various animal models of neurodegenerative diseases or ischemic stroke [7][8][9]. The neuroprotective effects of Cr has been ascribed to the buffering capacity of cellular ATP levels coupled with mitochondrial targeted antioxidant properties in cell and mammalian models [10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Attenuation of Rotenone-Induced Mitochondrial Oxidative Damage and Neurotoxicty in Drosophila melanogaster Supplemented with Creatine

2010

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Creatine (Cr), an ergogenic nutritional supplement is demonstrated to possess bioenergetic, antiexcitotoxic and antioxidant properties. This study investigated the neuroprotective effects of Cr against rotenone induced oxidative stress, mortality and neurotoxicty in Drosophila melanogaster. We found significant diminution in the endogenous levels of oxidative markers in whole body homogenates of flies exposed to Cr (2-10 mM). Cr supplementation resulted in reduced mortality in flies exposed to rotenone (500 microM) and better performance in a negative geotaxis assay. Further Cr (10 mM) markedly offset rotenone induced mitochondrial oxidative stress, completely restored the GSH levels, nitric oxide levels, activity of Mn-SOD and dopamine depletion. In an oxidative stress bioassay, flies given Cr prophylaxis exhibited marked resistance to paraquat exposure. These data allow us to hypothesize that the neuroprotective action of Cr in Drosophila may be related to its direct antioxidant activity and ability to abrogate rotenone induced mitochondrial oxidative stress.

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Intracerebroventricular administration of creatine protects against damage by global cerebral ischemia in rat

Cited by 57 publications

References 33 publications

Creatine and guanidinoacetate transport at blood‐brain and blood‐cerebrospinal fluid barriers

Creatine and guanidinoacetate transport at blood‐brain and blood‐cerebrospinal fluid barriers

Arctic Ground Squirrel (Spermophilus Parryii) Hippocampal Neurons Tolerate Prolonged Oxygen—Glucose Deprivation and Maintain Baseline ERK1/2 and JNK Activation Despite Drastic ATP Loss

Attenuation of Rotenone-Induced Mitochondrial Oxidative Damage and Neurotoxicty in Drosophila melanogaster Supplemented with Creatine

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