scholarly journals Speed modulation of hippocampal theta frequency correlates with spatial memory performance

Hippocampus ◽  
2013 ◽  
Vol 23 (12) ◽  
pp. 1269-1279 ◽  
Author(s):  
Gregory R. Richard ◽  
Ali Titiz ◽  
Anna Tyler ◽  
Gregory L. Holmes ◽  
Rod C. Scott ◽  
...  
2020 ◽  
pp. 155005942097310
Author(s):  
Limor Shtoots ◽  
Tom Dagan ◽  
Josh Levine ◽  
Aryeh Rothstein ◽  
Liran Shati ◽  
...  

How can the stability of a recently acquired memory be improved? Recent findings regarding the importance of theta frequency EEG activity in the hippocampus suggest that entraining neural activity in that frequency band might increase post-encoding waking replay, reinforcing learning-related plasticity. Our previous studies revealed that upregulating postlearning theta power using EEG neurofeedback (NFB) significantly benefitted procedural and episodic memory performance (both immediate and delayed), and may provide optimal conditions for stabilization of new memories. We have now explored whether memory benefits of theta NFB generalize to delayed spatial memory, an additional hippocampus-dependent process. Participants learned to associate object images with locations on a computer screen. NFB was used to enable participants to selectively increase scalp EEG theta power for 30 minutes. Visuo-spatial memory was tested one week later, with the theta NFB participants compared with 2 control groups (beta-augmentation NFB as an active control group, and an additional passive control group that did not engage in NFB). Theta upregulation was found to improve visuo-spatial memory, as reflected in reduced error distances in location marking and faster reaction time for correct answers by the theta group. This supports the contention that theta upregulation immediately after learning strengthens early consolidation of visuo-spatial memory. This intervention could potentially benefit various memory-challenged populations, as well as healthy individuals.


2020 ◽  
Author(s):  
Calvin K. Young ◽  
Ming Ruan ◽  
Neil McNaughton

AbstractTheta oscillations in the hippocampus have many behavioural correlates, with the magnitude and vigour of ongoing movement being the most salient. Many consider correlates of locomotion with hippocampal theta to be a confound in delineating theta contributions to cognitive processes. But, theory and empirical experiments suggest theta-movement relationships are important if spatial navigation is to support higher cognitive processes. In the current study, we tested if variations in speed modulation of hippocampal theta can predict spatial learning rates in the water maze. Using multi-step regression, we find the magnitude and robustness of hippocampal theta frequency versus speed scaling can predict water maze learning rates. Using generalised linear models, we also demonstrate that speed and water maze learning are the best predictors of hippocampal theta frequency and power. Theta oscillations recorded from the supramammillary area showed much weaker, or non-existent, relationships, which supports the idea that hippocampal theta has specific roles in speed representation and spatial learning. Our findings suggest movement-speed correlations with hippocampal theta frequency may be actively used in spatial learning.


2021 ◽  
Vol 22 (14) ◽  
pp. 7713
Author(s):  
Alyssa Tidmore ◽  
Sucharita M. Dutta ◽  
Arriyam S. Fesshaye ◽  
William K. Russell ◽  
Vania D. Duncan ◽  
...  

Exposure of rodents to <20 cGy Space Radiation (SR) impairs performance in several hippocampus-dependent cognitive tasks, including spatial memory. However, there is considerable inter-individual susceptibility to develop SR-induced spatial memory impairment. In this study, a robust label-free mass spectrometry (MS)-based unbiased proteomic profiling approach was used to characterize the composition of the hippocampal proteome in adult male Wistar rats exposed to 15 cGy of 1 GeV/n 48Ti and their sham counterparts. Unique protein signatures were identified in the hippocampal proteome of: (1) sham rats, (2) Ti-exposed rats, (3) Ti-exposed rats that had sham-like spatial memory performance, and (4) Ti-exposed rats that impaired spatial memory performance. Approximately 14% (159) of the proteins detected in hippocampal proteome of sham rats were not detected in the Ti-exposed rats. We explored the possibility that the loss of the Sham-only proteins may arise as a result of SR-induced changes in protein homeostasis. SR-exposure was associated with a switch towards increased pro-ubiquitination proteins from that seen in Sham. These data suggest that the role of the ubiquitin-proteome system as a determinant of SR-induced neurocognitive deficits needs to be more thoroughly investigated.


2018 ◽  
Vol 115 (43) ◽  
pp. E10187-E10196 ◽  
Author(s):  
Michael A. van der Kooij ◽  
Tanja Jene ◽  
Giulia Treccani ◽  
Isabelle Miederer ◽  
Annika Hasch ◽  
...  

Stringent glucose demands render the brain susceptible to disturbances in the supply of this main source of energy, and chronic stress may constitute such a disruption. However, whether stress-associated cognitive impairments may arise from disturbed glucose regulation remains unclear. Here we show that chronic social defeat (CSD) stress in adult male mice induces hyperglycemia and directly affects spatial memory performance. Stressed mice developed hyperglycemia and impaired glucose metabolism peripherally as well as in the brain (demonstrated by PET and induced metabolic bioluminescence imaging), which was accompanied by hippocampus-related spatial memory impairments. Importantly, the cognitive and metabolic phenotype pertained to a subset of stressed mice and could be linked to early hyperglycemia 2 days post-CSD. Based on this criterion, ∼40% of the stressed mice had a high-glucose (glucose >150 mg/dL), stress-susceptible phenotype. The relevance of this biomarker emerges from the effects of the glucose-lowering sodium glucose cotransporter 2 inhibitor empagliflozin, because upon dietary treatment, mice identified as having high glucose demonstrated restored spatial memory and normalized glucose metabolism. Conversely, reducing glucose levels by empagliflozin in mice that did not display stress-induced hyperglycemia (resilient mice) impaired their default-intact spatial memory performance. We conclude that hyperglycemia developing early after chronic stress threatens long-term glucose homeostasis and causes spatial memory dysfunction. Our findings may explain the comorbidity between stress-related and metabolic disorders, such as depression and diabetes, and suggest that cognitive impairments in both types of disorders could originate from excessive cerebral glucose accumulation.


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