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| http://dx.doi.org/10.1016/j.ejpn.2019.12.015 | DOI Listing |
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Angiotensin IV Receptors in the Rat Prefrontal Cortex: Neuronal Expression and NMDA Inhibition.
Biomedicines
December 2024
Department of Oral Biology, Semmelweis University, H-1089 Budapest, Hungary.
Background: N-methyl-D-aspartate type glutamate receptors (NMDARs) are fundamental to neuronal physiology and pathophysiology. The prefrontal cortex (PFC), a key region for cognitive function, is heavily implicated in neuropsychiatric disorders, positioning the modulation of its glutamatergic neurotransmission as a promising therapeutic target. Our recently published findings indicate that AT receptor activation enhances NMDAR activity in layer V pyramidal neurons of the rat PFC.
View Article and Find Full Text PDFDistinct changes to hippocampal and medial entorhinal circuits emerge across the progression of cognitive deficits in epilepsy.
Cell Rep
January 2025
Nash Family Department of Neuroscience, The Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address:
Temporal lobe epilepsy (TLE) causes pervasive and progressive memory impairments, yet the specific circuit changes that drive these deficits remain unclear. To investigate how hippocampal-entorhinal dysfunction contributes to progressive memory deficits in epilepsy, we performed simultaneous in vivo electrophysiology in the hippocampus (HPC) and medial entorhinal cortex (MEC) of control and epileptic mice 3 or 8 weeks after pilocarpine-induced status epilepticus (Pilo-SE). We found that HPC synchronization deficits (including reduced theta power, coherence, and altered interneuron spike timing) emerged within 3 weeks of Pilo-SE, aligning with early-onset, relatively subtle memory deficits.
View Article and Find Full Text PDFEarly postnatal NMDA receptor ablation in cortical interneurons impairs affective state discrimination and social functioning.
Neuropsychopharmacology
January 2025
Grupo de Neurociencia de Sistemas, Departamento de Ciencias Fisiológicas, Facultad de Ciencias Médicas, Universidad de Buenos Aires, Buenos Aires, Argentina.
Emotion recognition is fundamental for effective social interactions among conspecifics. Impairments in affective state processing underlie several neuropsychiatric disorders, including schizophrenia, although the neurobiological substrate of these deficits remains unknown. We investigated the impact of early NMDA receptor hypofunction on socio-affective behaviors.
View Article and Find Full Text PDFGABAergic Progenitor Cell Graft Rescues Cognitive Deficits in Fragile X Syndrome Mice.
Adv Sci (Weinh)
January 2025
Department of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510260, China.
Fragile X syndrome (FXS) is an inherited neurodevelopmental disorder characterized by a range of clinical manifestations with no effective treatment strategy to date. Here, transplantation of GABAergic precursor cells from the medial ganglionic eminence (MGE) is demonstrated to significantly improve cognitive performance in Fmr1 knockout (KO) mice. Within the hippocampus of Fmr1-KO mice, MGE-derived cells from wild-type donor mice survive, migrate, differentiate into functionally mature interneurons, and form inhibitory synaptic connections with host pyramidal neurons.
View Article and Find Full Text PDFAnxiety-like behavior and altered hippocampal activity in a transgenic mouse model of Fabry disease.
Neurobiol Dis
February 2025
Institute of Physiology, Medical University of Innsbruck, Innsbruck, Austria. Electronic address:
Background: Fabry disease (FD) patients are known to be at high risk of developing neuropsychiatric symptoms such as anxiety, depression and cognitive deficits. Despite this, they are underdiagnosed and inadequately treated. It is unknown whether these symptoms arise from pathological glycosphingolipid deposits or from cerebrovascular abnormalities affecting neuronal functions in the central nervous system.
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