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Ocampo-Garces, A.

Publications and source records attributed to Ocampo-Garces, A..

3 recordsLinked to original sources

Hunger and sleep recruit distinct brain systems to form spatial memory

By demonstrating that hunger consolidates spatial memory via a non-hippocampal mechanism that critically involves the retrosplenial cortex, we identify a mode of memory formation that is distinct from well-known hippocampus-dependent memory formation during sleep. Food-deprived rats encoded object locations and, during a subsequent 2-h consolidation phase, either received food and slept (Sleep-Fed) or stayed awake (Wake-Fed), or remained hungry and stayed awake (Wake-Hungry). At later retrieval testing, both Wake-Hungry and Sleep-Fed rats exhibited robust spatial memory, whereas Wake-Fed rats did not. Blocking neuropeptide-Y (NPY) signaling during the consolidation phase abolished hunger-consolidated memory. Unlike sleep-dependent consolidation, hunger-consolidated memory did not require the hippocampus during consolidation or retrieval, and not even during encoding. In contrast, inhibiting retrosplenial cortex during retrieval abolished hunger-consolidated memory but spared memory formed during sleep. Thus, recruitment of brain systems to form spatial memory is tuned to specific brain states, and fundamentally differs between sleep and hunger.

neuroscience↗

Envelope analysis as a tool for identifying epileptic EEG patterns during the sleep-wake cycle in rats

BackgroundThis research aimed to study electroencephalographic abnormalities in an animal model of temporal lobe epilepsy induced by pilocarpine. By using the coefficient of variation of the envelope (CVE) of electroencephalography (EEG), we characterize and quantify morphological alterations in sleep-wake cycle (SWC) stages. MethodsEpilepsy was induced in 13 rats using a single dose of intraperitoneal pilocarpine injection. A second group of 13 rats served as the control. All the rats underwent polysomnography for at least two days. To do so, three channels were created using four electrodes for EEG and one more for EMG. Channels were built using contralateral lead. ResultsEnvelope analysis revealed global alterations in EEG morphology. Significant differences were observed in the delta and theta bands between the epileptic and control groups. Epileptic animals showed a near-total suppression of theta rhythm activity during REM sleep. Additionally, we identified a novel pattern of synchronized slow waves (sDelta), distinct from the physiological delta waves observed in non-REM sleep. ConclusionIdentifying both subtle and overt morphological abnormalities in EEG is challenging for human experts and computational methods. By applying CVE analysis to the well-known pilocarpine model, we reveal abnormal EEG dynamics with exceptional summarizing capabilities. For example, a 24-hour EEG can be synthesized into a single, easily interpretable visualization of EEG morphology. This technique and its underlying framework may serve as valuable tools for epilepsy research and potential diagnostic applications.

neuroscience↗

Absence seizures and sleep abnormalities in a rat model of GRIN2B neurodevelopmental disorder

Pathogenic mutations in GRIN2B are an important cause of severe neurodevelopmental disorders resulting in epilepsy, autism and intellectual disability. GRIN2B encodes the GluN2B subunit of N-methyl-D-aspartate receptors (NMDARs), which are ionotropic glutamate receptors critical for normal development of the nervous system and synaptic plasticity. Here, we characterized a novel Grin2b heterozygous knockout rat model with 24-hour EEG recordings. We found rats heterozygous for the deletion (Grin2b+/-) had a higher incidence of spontaneous spike and wave discharges, the electrographic correlate of absence seizures, than wild-type rats (Grin2b+/+). Spike and wave discharges were longer in duration and displayed higher overall spectral power in Grin2b+/- when compared to those in Grin2b+/+ animals. Heterozygous mutant rats also had abnormal sleep-wake brain state dynamics over the circadian cycle. Specifically, we identified a reduction in total rapid eye movement sleep and, altered distributions of non-rapid eye movement sleep and wake epochs, when compared to controls. This was accompanied by an increase in overall spectral power during non-rapid eye movement sleep in Grin2b+/-. The sleep-wake phenotypes were largely uncorrelated to the incidence of spike and wave discharges. We then tested the antiseizure efficacy of ethosuximide, a T-type voltage-gated calcium channel blocker used in the treatment of absence seizures, and memantine, a noncompetitive NMDAR antagonist currently explored as a mono or adjunctive treatment option in NMDAR related neurodevelopmental disorders. Ethosuximide reduced the number and duration of spike and wave discharges, while memantine did not affect the number of spike and wave discharges but reduced their duration. These results highlight two potential therapeutic options for GRIN2B related epilepsy. Our data shows the new rat Grin2b haploinsufficiency model exhibits clinically relevant phenotypes. As such, it could prove crucial in deciphering underlying pathological mechanisms and developing new therapeutically translatable strategies for GRIN2B neurodevelopmental disorders.

neuroscience↗