Current concepts hold that during learning in waking animals, new information is transmitted from the neocortex to the hippocampus, where it leaves a temporary trace in the form of a mosaic of modified synapses. During sleep, reactivation of the neuron population initially activated by the new stimulus has the result that this information is returned to the neocortex, ensuring consolidation of a permanent memory trace. Exchange of information between the neocortex and hippocampal formation is mediated mainly by the entorhinal cortex, whose internal connections, in principle, allow "messages" from the output of the hippocampal formation to return to its inputs. Our experiments in awake and sleeping rabbits demonstrated that waves of excitation can return to hippocampal field CA1 and the dentate gyrus via fibers of the perforant path, these waves having initially entered field CA1 via potentiated synapses of Schäffer collaterals; during sleep, re-entrant waves of excitation reach a maximum and have a high probability of evoking discharges of dentate gyrus neurons. Thus, the new stimulus, potentiating synaptic connections in the hippocampus and, probably, the entorhinal cortex during waking, create conditions for reactivation of the corresponding hippocampal neuron populations during sleep by waves of excitation returning via the entorhinal cortex.
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http://dx.doi.org/10.1007/s11055-010-9258-8 | DOI Listing |
Neuromolecular Med
January 2025
Biochemistry and Molecular Biology Laboratory, Department of Zoology, Institute of Science, Banaras Hindu University, Varanasi, 221 005, India.
Hypoxia is a significant stressor, and stabilized hypoxia-inducible factor-1α (HIF-1α) regulates the expression of numerous genes, leading to various biochemical, molecular, physiological and genomic changes. The body's oxygen-sensing system activates gene expression to protect brain tissues from hypoxia. Gamma-aminobutyric acid, an inhibitory neurotransmitter, regulates brain excitability during hypoxia through the activation of HIF-1 α.
View Article and Find Full Text PDFCureus
December 2024
School of Allied Health Sciences, Manav Rachna International Institute of Research and Studies, Faridabad, IND.
Introduction: Sleep deprivation (SD), stemming from a myriad of aetiologies, is a prevalent health condition frequently overlooked. It typically impairs memory consolidation and synaptic plasticity, potentially through neuroinflammatory mechanisms and adenosinergic signalling. It is still unclear whether the adenosine A1 receptor (A1R) modulates SD-induced neurological deficits in the hippocampus.
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 PDFBr J Pharmacol
January 2025
Institute of Neurobiology, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Background And Purpose: Autophagy-lysosomal pathway dysfunction leads to postoperative cognitive dysfunction (POCD). Dexmedetomidine (Dex) improves POCD, and we probed the effects of Dex on autophagy-lysosomal pathway dysfunction in a POCD model.
Experimental Approach: A POCD mouse model was established and intraperitoneally injected with Dex.
J Neurosci
January 2025
Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, NJ 07102.
We aimed to identify the neuronal correlates of performance errors in a difficult timing task. Male rats were trained to seek ewards and avoid hocks depending on the position of photic conditioned stimuli (CS- and CS-, respectively). Then, they were exposed to conflict trials where they had to time the interval between the CS-R and CS-S to obtain rewards while avoiding footshocks.
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