Objective: Glycine transporter-1 (GLYT1) is an early marker of neural development and involved in the excitatory transmission in cortex. The study was designed to investigate the expression of GLYT1 in different parts of the brain by immunohistochemistry in the rat cortical dysplasia model.
Methods: On postnatal day 0, one freeze lesion was carried out on ten rats between bregma and lambda on the skull in the right hemisphere for 5 seconds. Six weeks later, rats were transcardially perfused with fixative and then their brains were removed for both hamotoxylin-eosine (H&E) staining for histopathology and immunohistochemistry staining for glial fibrillary acidic protein (GFAP) for astrocytic activity and GLYT1 in the cortical dysplastic region and other rostral brain regions involving epileptogenesis such as hippocampus, pyriform cortex, amygdala, thalamus and substantia nigra.
Results: GFAP immunoreactivity showed clusters of glial cells in the area of the microgyrus. Dense GLYT1 expression was localized to superficial layer of microgyric cortex and around the microgyrus. GLYT1 immunoreactivity was not detected in the other rostral regions.
Discussion: GLYT1 stained superficial structures might correspond to immature neuron and higher concentrations of GLYT1 around microgyrus might be correlated with increased excitatory mechanisms in these regions.
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http://dx.doi.org/10.1179/174313208X319071 | DOI Listing |
Brain Sci
November 2024
Department of Veterinary Medicine, School of Veterinary Medicine, National Taiwan University, Taipei 10617, Taiwan.
Background: Hypofunction of the glutamate system in the brain is one of the pathophysiological hypotheses for schizophrenia. Accumulating animal and clinical studies show that sarcosine (N-methylglycine), a glycine transporter-1 inhibitor, is effective in ameliorating the negative and cognitive symptoms of schizophrenia. The aims of the present study were to observe the effects of sarcosine on neuronal activity in the dorsal CA1 (dCA1) hippocampal neurons within an NMDA receptor hypofunction model induced by MK801.
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December 2024
Department of Neurology, Neurological Center, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing100045, China.
To analyze the clinical features of creatine transporter(CRTR) deficiency associated with SLC6A8 gene variants. The clinical data (clinical presentation, brain imaging, creatine metabolism test and gene variants) of 5 patients admitted to Beijing Children's Hospital, Capital Medical University and diagnosed with CRTR deficiency associated with SLC6A8 gene variants from January 2016 to June 2024 were retrospectively analyzed. A total of 5 patients, all male, presented with the onset of the disease at 1 year and 1 month old to 1 year and 10 months old, and diagnosis at 1 year and 3 months to 9 years old.
View Article and Find Full Text PDFEcotoxicol Environ Saf
December 2024
Plant Science and Biodiversity Centre, Slovak Academy of Sciences, Bratislava 84523, Slovakia. Electronic address:
Nickel is an essential micronutrient for plant growth and development. However, in excessive amounts caused by accidental pollution of soils, this heavy metal is toxic to plants. Although silicon is a non-essential nutrient, it accumulates in most monocots, particularly the vital crop maize (corn, Zea mays).
View Article and Find Full Text PDFInt J Mol Sci
October 2024
Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Nagyvárad tér 4, H-1085 Budapest, Hungary.
Opioid analgesic tolerance (OAT), among other central side effects, limits opioids' indispensable clinical use for managing chronic pain. Therefore, there is an existing unmet medical need to prevent OAT. Extrasynaptic N-methyl D-aspartate receptors (NMDARs) containing GluN2B subunit blockers delay OAT, indicating the involvement of glutamate in OAT.
View Article and Find Full Text PDFExp Neurol
January 2025
Departamento de Farmacologia, Instituto de Ciências Biológicas, Universidade Federal de Goias, Goiânia, GO, Brazil. Electronic address:
Glycine Transporter Type 1 (GlyT1) inhibition confers neuroprotection against different forms of cerebral damage. This effect occurs through the elevation of synaptic glycine concentrations, which enhances N-methyl-d-aspartate receptor (NMDAR) activation by glutamate. To investigate the neuroprotective mechanism of GlyT1 inhibition, we used the Middle Cerebral Artery Occlusion (MCAO) model in male C57BL/6 mice, aged 10-12 weeks.
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