In in vitro mouse hippocampal slices we investigated whether cyclocreatine is capable of entering brain cells independently of the creatine transporter and if it reproduces the neuroprotective effect of creatine. Our study shows that cyclocreatine does not increase the creatine content, but is taken up as such and then phosphorylated to phosphocyclocreatine. This uptake is largely blocked by inactivation of the creatine transporter, however some cyclocreatine is taken up and posphorylated even after such inactivation. Thus, cyclocreatine sets up a cyclocreatine/phosphocyclocreatine system in the brain independently of the creatine transporter. Cyclocreatine did not delay the disappearance of the evoked synaptic potentials during anoxia in hippocampal slices, unlike creatine which exerts a neuroprotective effect.
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http://dx.doi.org/10.1142/S0219635213500155 | DOI Listing |
Neurotox Res
January 2025
Programa de Pós-Graduação em Ciências Biológicas: Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.
Resveratrol, a natural polyphenol, has shown promising neuroprotective effects in several in vivo and in vitro experimental models. However, the mechanisms by which resveratrol mediates these effects are not fully understood. Glutamate is the major excitatory neurotransmitter in the brain; however, excessive extracellular glutamate levels can affect neural activity in several neurological diseases.
View Article and Find Full Text PDFBrain Behav Immun Health
February 2025
Department of Physiology, School of Medicine, University College Cork, Western Road, Cork, Ireland.
Duchenne muscular dystrophy (DMD), an X-linked neuromuscular disorder, characterised by progressive immobility, chronic inflammation and premature death, is caused by the loss of the mechano-transducing signalling molecule, dystrophin. In non-contracting cells, such as neurons, dystrophin is likely to have a functional role in synaptic plasticity, anchoring post-synaptic receptors. Dystrophin-expressing hippocampal neurons are key to cognitive functions such as emotions, learning and the consolidation of memories.
View Article and Find Full Text PDFNeurochem Res
January 2025
Department of Pathophysiology, Medical University of Lublin, 20-090, Lublin, Poland.
Methionine sulfoximine (MSO) is a compound originally discovered as a byproduct of agene-based milled flour maturation. MSO irreversibly inhibits the astrocytic enzyme glutamine synthase (GS) but also interferes with the transport of glutamine (Gln) and of glutamate (Glu), and γ-aminobutyric acid (GABA) synthesized within the Glu/Gln-GABA cycle, in this way dysregulating neurotransmission balance in favor of excitation. No wonder that intraperitoneal administration of MSO has long been known to induce behavioral and/or electrographic seizures.
View Article and Find Full Text PDFNeuroscience
January 2025
Key Laboratory of the Ministry of Education for Medicinal Resources and Natural Pharmaceutical Chemistry, China; National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest China, China; College of Life Science, Shaanxi Normal University, Xi'an, China. Electronic address:
Several studies indicate that fructose can be used as an energy source for subterranean rodents. However, how subterranean rodents utilize fructose metabolism with no apparent physiological drawbacks remains poorly understood. In the present study, we measured field excitatory postsynaptic potentials (fEPSPs) in hippocampal slices from Gansu zokor and SD rats hippocampi before and 60 min after replacement of 10 mM glucose in the artificial cerebrospinal fluid (ACSF) with 10 mM fructose (gassed with 95 % O and 5 % CO).
View Article and Find Full Text PDFF1000Res
January 2025
Faculty of Teaching and Education Sciences, Islamic University of Malang, Malang, East Java, Indonesia.
Background: Neurodegeneration due to neurotoxicity is one of the phenomena in temporal lobe epilepsy. Experimentally, hippocampal excitotoxicity process can occur due to kainic acid exposure, especially in the CA3 area. Neuronal death, astrocyte reactivity and increased calcium also occur in hippocampal excitotoxicity, but few studies have investigated immediate effect after kainic acid exposure.
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