Non-Spatial Correlates of Hippocampal Activity

2002 ◽  
pp. 81-96
Author(s):  
Paul A. Dudchenko ◽  
Emma R. Wood ◽  
Howard Eichenbaum
Keyword(s):  
Hippocampal Activity

scholarly journals MEG detects abnormal hippocampal activity in amyloid‐positive MCI

2020 ◽  
Vol 16 (S4) ◽  
Author(s):  
Janne Luppi ◽  
Deborah N Schoonhoven ◽  
Anne M van Nifterick ◽  
Hillebrand Arjan ◽  
Alida A Gouw ◽  
...  
Keyword(s):  
Hippocampal Activity

scholarly journals Cortical amyloid burden and age moderate hippocampal activity in cognitively-normal adults

2016 ◽  
Vol 12 ◽  
pp. 78-84 ◽  
Author(s):  
Zhuang Song ◽  
Ian M. McDonough ◽  
Peiying Liu ◽  
Hanzhang Lu ◽  
Denise C. Park
Keyword(s):  
Amyloid Burden ◽  
Cognitively Normal ◽  
Hippocampal Activity ◽  
Normal Adults

scholarly journals Interactions between hippocampal activity and striatal dopamine in people at clinical high risk for psychosis: relationship to adverse outcomes

2021 ◽  
Author(s):  
Gemma Modinos ◽  
Anja Richter ◽  
Alice Egerton ◽  
Ilaria Bonoldi ◽  
Matilda Azis ◽  
...  
Keyword(s):  
High Risk ◽  
Functional Outcomes ◽  
Mental States ◽  
Adverse Outcomes ◽  
Striatal Dopamine ◽  
Psychotic Symptoms ◽  
Dopamine Synthesis ◽  
Clinical High Risk ◽  
Hippocampal Activity ◽  
The Relationship

AbstractPreclinical models propose that increased hippocampal activity drives subcortical dopaminergic dysfunction and leads to psychosis-like symptoms and behaviors. Here, we used multimodal neuroimaging to examine the relationship between hippocampal regional cerebral blood flow (rCBF) and striatal dopamine synthesis capacity in people at clinical high risk (CHR) for psychosis and investigated its association with subsequent clinical and functional outcomes. Ninety-five participants (67 CHR and 28 healthy controls) underwent arterial spin labeling MRI and 18F-DOPA PET imaging at baseline. CHR participants were followed up for a median of 15 months to determine functional outcomes with the global assessment of function (GAF) scale and clinical outcomes using the comprehensive assessment of at-risk mental states (CAARMS). CHR participants with poor functional outcomes (follow-up GAF < 65, n = 25) showed higher rCBF in the right hippocampus compared to CHRs with good functional outcomes (GAF ≥ 65, n = 25) (pfwe = 0.026). The relationship between rCBF in this right hippocampal region and striatal dopamine synthesis capacity was also significantly different between groups (pfwe = 0.035); the association was negative in CHR with poor outcomes (pfwe = 0.012), but non-significant in CHR with good outcomes. Furthermore, the correlation between right hippocampal rCBF and striatal dopamine function predicted a longitudinal increase in the severity of positive psychotic symptoms within the total CHR group (p = 0.041). There were no differences in rCBF, dopamine, or their associations in the total CHR group relative to controls. These findings indicate that altered interactions between the hippocampus and the subcortical dopamine system are implicated in the pathophysiology of adverse outcomes in the CHR state.

scholarly journals Neural Circuitry–Neurogenesis Coupling Model of Depression

2021 ◽  
Vol 22 (5) ◽  
pp. 2468
Author(s):  
Il Bin Kim ◽  
Seon-Cheol Park
Keyword(s):  
Entorhinal Cortex ◽  
Coupling Model ◽  
Neural Circuitry ◽  
Hippocampal Neurogenesis ◽  
Pattern Separation ◽  
Dependent Process ◽  
Hippocampal Activity ◽  
Mechanistic Understanding ◽  
Activity Dependent ◽  
Memory Pattern

Depression is characterized by the disruption of both neural circuitry and neurogenesis. Defects in hippocampal activity and volume, indicative of reduced neurogenesis, are associated with depression-related behaviors in both humans and animals. Neurogenesis in adulthood is considered an activity-dependent process; therefore, hippocampal neurogenesis defects in depression can be a result of defective neural circuitry activity. However, the mechanistic understanding of how defective neural circuitry can induce neurogenesis defects in depression remains unclear. This review highlights the current findings supporting the neural circuitry-regulated neurogenesis, especially focusing on hippocampal neurogenesis regulated by the entorhinal cortex, with regard to memory, pattern separation, and mood. Taken together, these findings may pave the way for future progress in neural circuitry–neurogenesis coupling studies of depression.

Recollection-related Hippocampal Activity during Continuous Recognition: a High-resolution fMRI Study

NeuroImage ◽  
2009 ◽  
Vol 47 ◽  
pp. S53
Author(s):  
M. Suzuki ◽  
J.D. Johnson ◽  
M.D. Rugg
Keyword(s):  
High Resolution ◽  
Fmri Study ◽  
Hippocampal Activity

Abstract P730: MCA Stroke Chronically Disrupts Hippocampal Activity and Cortico-Hippocampal Communication

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Zachary Ip ◽  
Gratianne Rabiller ◽  
Jiwei He ◽  
Shivalika Chavan ◽  
Yasuo Nishijima ◽  
...  
Keyword(s):  
Structural Integrity ◽  
Memory Function ◽  
Brain Regions ◽  
Male Rats ◽  
Brain State ◽  
Signal Power ◽  
Hippocampal Function ◽  
Electrode Arrays ◽  
Mca Occlusion ◽  
Hippocampal Activity

Introduction: Cognition and memory deficits are common sequelae following middle cerebral artery (MCA) stroke, one of the most common strokes in humans. However MCA stroke does not compromise the structural integrity of the hippocampus, which is highly involved in memory function, because the MCA does not supply blood flow to the hippocampus. We previously reported on the acute effect of MCA stroke, where we observed increased hippocampal activity and cortico-hippocampal communication. Here we investigate chronic changes to local oscillations and cortico-hippocampal communication following MCA occlusion in rats two weeks and one month following stroke. Hypothesis: Cortical stroke affects remote brain regions, disrupting hippocampal function and cortico-hippocampal communication. Methods: We subjected male rats (n=28) to distal MCA occlusion compared to controls (n=19). We recorded local field potentials simultaneously from cortex and hippocampus two weeks and one month following stroke using 16-site linear electrode arrays under urethane anesthesia. We analyzed signal power, brain state, CFC, and sharp wave SPW-Rs to assess hippocampal function and cortico-hippocampal communication. Results: Our results show disruptions to local oscillations; lowered delta (1-3 Hz) signal power in the cortex and hippocampus, increased signal power in gamma (30-60 Hz) and high gamma (60-200 Hz) in cortex and hippocampus. Theta/delta brain state is disrupted, and SPW-Rs increase in power at two weeks, before returning to baseline levels at one month. Communication is also disrupted; Theta-gamma coupling, a measure of information being communicated between regions, breaks down after stroke. Conclusions: These results suggest that chronic stroke causes significant changes to hippocampal function, which can be characterized by these electrophysiological biomarkers, establishing putative targets for targeted stimulation therapies.

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