Behavioral and genetic effects promoted by sleep deprivation in rats submitted to pilocarpine-induced status epilepticus

Matos, Gabriela; Ribeiro, Daniel Araki; Alvarenga, Tathiana A.; Hirotsu, Camila; Sueur-Maluf, Luciana Le; Noguti, Juliana; Cavalheiro, Ésper A.; Tufik, Sérgio; Andersen, Mônica Levy

doi:10.1016/j.neulet.2012.03.030

Cited by 11 publications

(2 citation statements)

References 23 publications

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“…The spatial information processing deficits we observed in TLE rats may precede sequential activity disruptions in memory consolidation during sleep in the hippocampal network, especially when pyramidal cell activity is considered as an ensemble. Following previously reported sleep disruptions observed in the pilocarpine model of TLE (Matos et al, ), we hypothesized that the real‐time reactivation structure as well as the replay of behavior‐driven sequences of place cells would be disrupted in the subsequent sleep period. Moreover, the low spatial fidelity of place fields, as evidenced by significantly lower spatial coherence measures, may point to a disruption specifically in the spatial representation by the place cells in TLE.…”

Section: Discussionmentioning

confidence: 94%

Cognitive impairment in temporal lobe epilepsy: Role of online and offline processing of single cell information

et al. 2014

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Cognitive impairment is a common comorbidity in temporal lobe epilepsy (TLE) and is often considered more detrimental to quality of life than seizures. While it has been previously shown that the encoding of memory during behavior is impaired in the pilocarpine model of TLE in rats, how this information is consolidated during the subsequent sleep period remains unknown. In this study, we first report marked deficits in spatial memory performance and severe cell loss in the CA1 layer of the hippocampus lower spatial coherence of firing in TLE rats. We then present the first evidence that the reactivation of behavior-driven patterns of activity of CA1 place cells in the hippocampus is intact in TLE rats. Using a template-matching method, we discovered that real-time (3–5 s) reactivation structure was intact in TLE rats. Furthermore, we estimated the entropy rate of short time scale (~250 ms) bursting activity using block entropies and found that significant, extended temporal correlations exist in both TLE and Control rats. Fitting a first order Markov Chain model to these bursting time series, we found that long sequences derived from behavior were significantly enriched in the Markov model over corresponding models fit on randomized data confirming the presence of replay in shorter time scales. We propose that the persistent consolidation of poor spatial information in both real-time and during bursting activity may contribute to memory impairments in TLE rats.

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Section: Discussionmentioning

confidence: 94%

Cognitive impairment in temporal lobe epilepsy: Role of online and offline processing of single cell information

et al. 2014

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“…In rats subjected to sleep deprivation or sleep fragmentation, there is reduced anxiety but no change in general locomotor activity (Tartar et al, 2009). Experimental studies used paradigms of sleep deprivation or restriction (Zager et al, 2007; Matos et al, 2012), but few studies have addressed how SF affects physiological function in obesity other than feeding and metabolism.…”

Section: Introductionmentioning

confidence: 99%

Sleep Fragmentation Has Differential Effects on Obese and Lean Mice

Kastin

Wang

et al. 2014

J Mol Neurosci

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Summary Chronic sleep fragmentation (SF), common in patients with sleep apnea, correlates with the development of obesity. We hypothesized that SF differentially affects neurobehavior in lean wildtype (WT) and obese pan-leptin receptor knockout (POKO) mice fed the same normal diet. First we established an SF paradigm by interrupting sleep every 2 min during the inactive light span. The maneuver was effective in decreasing sleep duration and bout length, and in increasing sleep state transition and waking, without significant rebound sleep in the dark span. Changes of sleep architecture were evident in the light span and consistent across days 1–10 of SF. There was reduced NREM, shortened sleep latency, and increased state transitions. During the light span of the first day of SF, there also was reduction of REM and increased delta power of slow wave sleep. Potential effects of SF on thermal pain threshold, locomotor activity, and anxiety were then tested. POKO mice had a lower circadian amplitude of pain latency than WT mice in the hot plate test, and both groups had lowest tolerance at 4 pm (ZT 10) and longest latency at 4 am (ZT 22). SF increased the pain threshold in WT but not POKO mice when tested at 8 am (ZT 2). Both the POKO mutation and SF resulted in reduced physical activity and increased anxiety, but there was no additive effect of these two factors. Overall, SF and the POKO mutation differentially regulate mouse behavior. The results suggest that obesity can blunt neurobehavioral responses to SF.

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Behavioral and genotoxic evaluation of rosmarinic and caffeic acid in acute seizure models induced by pentylenetetrazole and pilocarpine in mice

Coelho

Vieira

Souza

et al. 2016

Naunyn-Schmiedeberg's Arch Pharmacol

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The goal of this study was to investigate the effects of rosmarinic acid (RA) and caffeic acid (CA) in the acute pentylenetetrazole (PTZ) and pilocarpine (PIL) seizure models. We also evaluated the effect of RA and CA on the diazepam (DZP)-induced sleeping time test and its possible neuroprotective effect against the genotoxic damage induced by PTZ and PIL. Mice were treated intraperitoneally (i.p.) with saline, RA (2 or 4 mg/kg), or CA (4 or 8 mg/kg) alone or associated to low-dose DZP. After, mice received a single dose of PTZ (88 mg/kg) or PIL (250 mg/kg) and were monitored for the percentage of seizures and the latency to first seizure (LFS) >3 s. Vigabatrin and DZP were used as positive controls. In the DZP-induced sleeping time test, mice were treated with RA and CA and 30 min after receiving DZP (25 mg/kg, i.p.). The alkaline comet assay was performed after acute seizure tests to evaluate the antigenotoxic profiles of RA and CA. The doses of RA and CA tested alone did not reduce the occurrence of seizures induced by PTZ or PIL. The association of 4 mg/kg RA + low-dose DZP was shown to increase LFS in the PTZ model, compared to the group that received only the DZP. In the DZP-induced sleeping time test, the latency to sleep was reduced by 4 mg/kg RA and 8 mg/kg CA. The PTZ-induced genotoxic damage was not prevented by RA or CA, but the PIL-induced genotoxic damage was decreased by pretreatment with 4 mg/kg RA (in cortex) and 4 mg/kg CA (in hippocampus). In conclusion, RA and CA presented neuroprotective effect against PIL-induced genotoxic damage and reduced the latency to DZP-induced sleep. Of the rosmarinic acid, 4 mg/kg enhanced the DZP effect in the increase of latency to clonic PTZ-induced seizures.

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Behavioral and genetic effects promoted by sleep deprivation in rats submitted to pilocarpine-induced status epilepticus

Cited by 11 publications

References 23 publications

Cognitive impairment in temporal lobe epilepsy: Role of online and offline processing of single cell information

Cognitive impairment in temporal lobe epilepsy: Role of online and offline processing of single cell information

Sleep Fragmentation Has Differential Effects on Obese and Lean Mice

Behavioral and genotoxic evaluation of rosmarinic and caffeic acid in acute seizure models induced by pentylenetetrazole and pilocarpine in mice

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