Late-phase long-term potentiation (L-LTP) plays a very important role in the maintenance of long-term memory in hippocampus. However, studies have shown that L-LTP can be reversed by subsequent neuronal activity. The aim of the present study is to investigate whether the presynaptic mechanism and the change of AMPARs expressions are involved in the reversal of L-LTP in hippocampal CA1 area. Standard extracellular recording technique was used to record the potential change in the stratum radiatum of CA1 area of adult rat hippocampal slices. Two hours after LTP induction, which was induced by high-frequency stimulation (HFS), two episodes of high-intensity paired-pulse low-frequency stimulation (HI-PP-LFS) were delivered to induce L-LTP reversal. Paired-pulse ratios (PPR) were obtained before LTP induction, 2 h after LTP induction and 30 min after LTP reversal. On the other hand, immunofluorescence histochemistry was used to detect AMPARs expressions before and after L-LTP reversal. The results showed that, after 2 h of induction, L-LTP was partially reversed by two episodes of HI-PP-LFS, and the percentage of depotentiation was 61.79%+/-14.51%. PPR obtained before and after LTP induction, and as well that after LTP reversal, are all more than 1, showing paired-pulse facilitation (PPF). Multiple comparison indicated PPR before LTP induction was the greatest one, and PPR after LTP induction was the smallest. In addition, no significant difference was observed in the intensity of AMPAR/GluR2 immunoreactivity in CA1 area among control group, LTP group and LTP reversal group. These results suggest that the presynaptic mechanism is involved in both the maintenance and reversal of L-LTP and there is no change in AMPAR/GluR2 expression before and after the reversal of L-LTP.
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Pharmaceuticals (Basel)
December 2024
School of Pharmacy, University of Reading, Whiteknights, Reading RG6 6AJ, UK.
Recent studies, typically using patient cerebrospinal fluid (CSF), have suggested that different autoantibodies (Aabs) acting on their respective receptors, may underlie neuropsychiatric disorders. The GluN1 (NR1) subunit of the N-methyl-D-aspartate receptor (NMDAR) has been identified as a target of anti-NMDAR Aabs in a number of central nervous system (CNS) diseases, including encephalitis and autoimmune epilepsy. However, the role or the nature of Aabs responsible for effects on neuronal excitability and synaptic plasticity is yet to be established fully.
View Article and Find Full Text PDFFront Synaptic Neurosci
December 2024
Laboratory of Physiology, Department of Medicine, University of Patras, Patras, Greece.
β-adrenergic receptors (β-ARs) play a critical role in modulating learning, memory, emotionality, and long-term synaptic plasticity. Recent studies indicate that β-ARs are necessary for long-term potentiation (LTP) induction in the ventral hippocampus under moderate synaptic activation conditions that do not typically induce LTP. To explore potential dorsoventral differences in β-AR-mediated effects, we applied the β-AR agonist isoproterenol (10 μM, 30 min) to dorsal and ventral hippocampal slices, recording field excitatory postsynaptic potentials (fEPSPs) and population spikes (PSs) from the CA1 region.
View Article and Find Full Text PDFSci Rep
January 2025
Departamento de Medicina Genómica y Toxicología Ambiental, Instituto de Investigaciones Biomédicas, Universidad Nacional Autónoma de México, 04510, Mexico City, Mexico.
Autism spectrum disorder (ASD) comprises alterations in brain anatomy and physiology that ultimately affect information processing and behavior. In most cases, autism is considered idiopathic, involving alterations in numerous genes whose functions are not extensively documented. We evaluated the C58/J mouse strain as an idiopathic model of ASD, emphasizing synaptic transmission as the basis of information processing.
View Article and Find Full Text PDFAdv Biomed Res
November 2024
Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
Background: Escitalopram, a pharmacological compound, and crocin, the active compound of saffron, influence brain functions and serotonin levels. This study examined the efficacy of escitalopram with and without crocin in restoring the input-output (I/O) functions and long-term potentiation (LTP) within the hippocampal cornu ammonis 1 (CA1) region of stressed rats.
Materials And Methods: Rats were divided into six groups: control (Co), sham (Sh), stress-recovery (St-Rec), stress-escitalopram (St-Esc), stress-crocin (St-Cr), and stress-escitalopram-crocin (St-Esc-Cr) groups.
Mol Neurobiol
December 2024
Department of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences, Hamedan, Iran.
There is no acquiesced remedy for the treatment of traumatic brain injury (TBI)-associated impairment, especially cognitive decline. The first 24 h after TBI is a golden time for preventing the progress of the impairments. The present study aimed to examine the acute effects of fucoidan on neurological outcomes and memory performance and investigate its potential mechanisms in rats with TBI.
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