Coordination of hippocampal theta and gamma oscillations relative to spatial active avoidance reflects cognitive outcome after febrile status epilepticus.
Coordination of hippocampal theta and gamma oscillations relative to spatial active avoidance reflects cognitive outcome after febrile status epilepticus.
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DOI:
10.1037/bne0000388
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发表时间:
2020-12
影响因子:
1.9
通讯作者:
Holmes GL
中科院分区:
文献类型:
--
作者:
Barry JM;Mahoney JM;Holmes GL
Cognitive deficits may arise from a variety of genetic alterations and neurological insults that impair neural coding mechanisms and the routing of neural information underpinning learning and memory. Slow and medium gamma oscillations underpin memory recall and sensorimotor processing and represent dynamic inputs at CA1 synapses. Febrile status epilepticus (FSE) can lead to increased risk for temporal lobe epilepsy and enduring cognitive impairments. In a rodent model, we assessed how FSE alters hippocampal CA1 signals relative to spatial task performance and serve as a readout of synaptic input efficacy. The power of theta (5–12 Hz), slow gamma (30–50 Hz), and medium gamma (70–90 Hz) differentially interact with respect to cognitive demands during active avoidance behavior on a rotating arena. Successful avoidance was characterized by slow gamma that was largest several seconds before or after peak acceleration. Peak acceleration coincides with peak theta oscillations, followed within approximately 1 s by peak medium gamma. FSE animals showing impairment in the task maintained the profiles of theta and medium gamma associated with increased sensorimotor processing following peak acceleration but did not exhibit the same slow gamma profile associated with epochs of memory retrieval. While CA1 synapses from entorhinal cortex were functionally unaffected by FSE, communication via synapses from CA3 may have been impaired, leading to both temporal discoordination and poor memory retrieval. These findings demonstrate theta/gamma profiles can serve as both physiological biomarkers for memory retrieval or encoding deficits and synapse level treatment targets that could attenuate cognitive comorbidities associated with early life seizures.
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影响因子:
16.2
作者:
Fries P
通讯作者:
Fries P
影响因子:
5.4
作者:
Brennan GP;Baram TZ;Poolos NP
通讯作者:
Poolos NP
影响因子:
13.9
作者:
Buzsáki G;Wang XJ
通讯作者:
Wang XJ
DOI:
10.1523/jneurosci.5110-11.2012
发表时间:
2012-05-23
期刊:
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子:
--
作者:
Ahmed OJ;Mehta MR
通讯作者:
Mehta MR
影响因子:
5.3
作者:
Barry, Jeremy M.;Choy, ManKin;Dube, Celine;Robbins, Ashlee;Obenaus, Andre;Lenck-Santini, Pierre Pascal;Scott, Rod C.;Baram, Tallie Z.;Holmes, Gregory L.
通讯作者:
Holmes, Gregory L.