scholarly journals A biophysical computational model for memory trace transfer from hippocampus to neocortex

2018 ◽  
Author(s):  
Xin Liu ◽  
Duygu Kuzum

The hippocampus plays important roles in memory formation and retrieval through sharp-wave-ripples. Recent studies have shown that certain neuron populations in the prefrontal cortex exhibit coordinated reactivations during awake ripple events. Also, the reactivation seems stronger during initial awake learning. These experimental findings suggest that the awake ripple is an important biomarker, through which the hippocampus interacts with the neocortex to assist the memory formation and retrieval. However, the computational mechanisms of this ripple based hippocampal-cortical coordination are still not clear. In this work, we build a biophysical model that includes both CA1 and layer V networks of the prefrontal cortex to investigate the possible mechanisms, by which the memory traces in the hippocampus can be transferred to prefrontal cortex. We first show that the local field potentials generated in the hippocampus and prefrontal cortex exhibit ripple range activities that are consistent with the recent experimental studies. Then, we find that the sequence information stored in the hippocampus can be successfully transferred to the prefrontal cortex recurrent networks through spike-timing dependent plasticity (STDP) and sequence replays. Further, we investigate the mechanisms of memory retrieval in the PFC network. Our findings suggest that the stored memory traces in the prefrontal cortex network can be retrieved through two different mechanisms, namely the cell-specific input and non-specific spontaneous background noise. Finally, we show that more SWRs and an optimal background noise level will both contribute to better sequence reactivations in the PFC network during memory retrieval. Our study presents a possible explanation for the memory trace transfer from the hippocampus to the neocortex through ripple coupling in awake states and reports two different mechanisms by which the stored memory traces can be successfully retrieved.

2020 ◽  
Vol 17 (3) ◽  
pp. 319-326
Author(s):  
Mehmet Bostanciklioğlu

Memory retrieval is mediated by discharges of acetylcholine, glutamate, gammaaminobutyric acid, norepinephrine, and serotonin/5-hydroxytryptamine circuits. These projections and memory interact through engram circuits, neurobiological traces of memory. Increased excitability in engram circuits of the medial prefrontal cortex and hippocampus results in remote and recent memory retrievals, respectively. However, due to degenerated neurotransmitter projections, the excitability state of engram circuits is decreased in the patient with dementia; and thus, acquired- memory cannot be retrieved by natural cues. Here, we suggest that artificial neuropharmacological stimulations of the acquired-memory with an excitation potential higher than a natural cue can excite engram circuits in the medial prefrontal cortex, which results in the retrieval of lost memories in dementia. The neuropharmacological foundations of engram cell-mediated memory retrieval strategy in severe dementia, in line with this has also been explained. We particularly highlighted the close interactions between periaqueductal gray, locus coeruleus, raphe nuclei, and medial prefrontal cortex and basolateral amygdala as treatment targets for memory loss. Furthermore, the engram circuits projecting raphe nuclei, locus coeruleus, and pontomesencephalic tegmentum complex could be significant targets of memory editing and memory formation in the absence of experience, and a well-defined study of the neural events underlying the interaction of brain stem and memory will be relevant for such developments. We anticipate our perspective to be a starting point for more sophisticated in vivo models for neuropharmacological modulations of memory retrieval in Alzheimer’s dementia.


2019 ◽  
Author(s):  
Angela Medvedeva ◽  
Rebecca Saw ◽  
Miroslav Sirota ◽  
Giorgio Fuggetta ◽  
Giulia Galli

ABSTRACTRecent evidence suggests that brain activity following the offset of a stimulus during encoding contributes to long-term memory formation, however the exact mechanisms underlying offset-related encoding are still unclear. Here we used repetitive transcranial magnetic stimulation (rTMS) to investigate offset-related activity in the left ventrolateral prefrontal cortex (VLPFC). rTMS was administered at different points in time around stimulus offset while male and female participants encoded visually-presented words (first rTMS experiment) or pairs of words (second rTMS experiment) and the analyses focused on the effects of the stimulation on subsequent memory performance. The results show that rTMS administered at the offset of the stimuli, but not during online encoding, disrupted subsequent memory performance. In the first experiment we show that rTMS specifically disrupted encoding mechanisms initiated by the offset of the stimuli rather than general, post-stimulus processes. In the second experiment, we show a robust decline in associative memory performance when rTMS was delivered at the offset of the word pairs, suggesting that offset-related encoding may contribute to the binding of information into an episodic memory trace. A meta-analysis conducted on the two studies and on a previously published dataset confirmed that the involvement of the left VLPFC in memory formation is initiated by the offset of the stimulus. The offset of the stimulus may represent an event boundary that promotes the reinstatement of the previously experienced event and episodic binding.SIGNIFICANCE STATEMENTHow well an event is encoded predicts how well it is remembered, and verbal encoding is an important part of everyday memory that, if disrupted, can lead to difficulties and disorders. The timing of encoding processes relative to the presentation of an event is important for successful retrieval, and little is known about the interval immediately after an event’s presentation (post-stimulus offset) which is thought to involve critical encoding processes in the VLPFC and hippocampus. The current studies demonstrate that indeed, verbal encoding processes in the VLPFC that are necessary for memory formation are triggered by the offset of the word, and these processes may involve VLPFC-hippocampal interactions that promote binding of event features into a single, coherent memory trace.


2013 ◽  
Vol 110 (7) ◽  
pp. 1631-1645 ◽  
Author(s):  
R. C. Evans ◽  
Y. M. Maniar ◽  
K. T. Blackwell

The striatum of the basal ganglia demonstrates distinctive upstate and downstate membrane potential oscillations during slow-wave sleep and under anesthetic. The upstates generate calcium transients in the dendrites, and the amplitude of these calcium transients depends strongly on the timing of the action potential (AP) within the upstate. Calcium is essential for synaptic plasticity in the striatum, and these large calcium transients during the upstates may control which synapses undergo plastic changes. To investigate the mechanisms that underlie the relationship between calcium and AP timing, we have developed a realistic biophysical model of a medium spiny neuron (MSN). We have implemented sophisticated calcium dynamics including calcium diffusion, buffering, and pump extrusion, which accurately replicate published data. Using this model, we found that either the slow inactivation of dendritic sodium channels (NaSI) or the calcium inactivation of voltage-gated calcium channels (CDI) can cause high calcium corresponding to early APs and lower calcium corresponding to later APs. We found that only CDI can account for the experimental observation that sensitivity to AP timing is dependent on NMDA receptors. Additional simulations demonstrated a mechanism by which MSNs can dynamically modulate their sensitivity to AP timing and show that sensitivity to specifically timed pre- and postsynaptic pairings (as in spike timing-dependent plasticity protocols) is altered by the timing of the pairing within the upstate. These findings have implications for synaptic plasticity in vivo during sleep when the upstate-downstate pattern is prominent in the striatum.


2001 ◽  
Vol 13 (10) ◽  
pp. 2221-2237 ◽  
Author(s):  
Rajesh P. N. Rao ◽  
Terrence J. Sejnowski

A spike-timing-dependent Hebbian mechanism governs the plasticity of recurrent excitatory synapses in the neocortex: synapses that are activated a few milliseconds before a postsynaptic spike are potentiated, while those that are activated a few milliseconds after are depressed. We show that such a mechanism can implement a form of temporal difference learning for prediction of input sequences. Using a biophysical model of a cortical neuron, we show that a temporal difference rule used in conjunction with dendritic backpropagating action potentials reproduces the temporally asymmetric window of Hebbian plasticity observed physiologically. Furthermore, the size and shape of the window vary with the distance of the synapse from the soma. Using a simple example, we show how a spike-timing-based temporal difference learning rule can allow a network of neocortical neurons to predict an input a few milliseconds before the input's expected arrival.


Science ◽  
2018 ◽  
Vol 362 (6415) ◽  
pp. 675-679 ◽  
Author(s):  
Céline Drieu ◽  
Ralitsa Todorova ◽  
Michaël Zugaro

Consolidation of spatial and episodic memories is thought to rely on replay of neuronal activity sequences during sleep. However, the network dynamics underlying the initial storage of memories during wakefulness have never been tested. Although slow, behavioral time scale sequences have been claimed to sustain sequential memory formation, fast (“theta”) time scale sequences, nested within slow sequences, could be instrumental. We found that in rats traveling passively on a model train, place cells formed behavioral time scale sequences but theta sequences were degraded, resulting in impaired subsequent sleep replay. In contrast, when the rats actively ran on a treadmill while being transported on the train, place cells generated clear theta sequences and accurate trajectory replay during sleep. Our results support the view that nested sequences underlie the initial formation of memory traces subsequently consolidated during sleep.


2016 ◽  
Vol 116 (3) ◽  
pp. 920-937 ◽  
Author(s):  
Jennifer Barredo ◽  
Timothy D. Verstynen ◽  
David Badre

Functional magnetic resonance imaging (fMRI) evidence indicates that different subregions of ventrolateral prefrontal cortex (VLPFC) participate in distinct cortical networks. These networks have been shown to support separable cognitive functions: anterior VLPFC [inferior frontal gyrus (IFG) pars orbitalis] functionally correlates with a ventral fronto-temporal network associated with top-down influences on memory retrieval, while mid-VLPFC (IFG pars triangularis) functionally correlates with a dorsal fronto-parietal network associated with postretrieval control processes. However, it is not known to what extent subregional differences in network affiliation and function are driven by differences in the organization of underlying white matter pathways. We used high-angular-resolution diffusion spectrum imaging and functional connectivity analysis in unanesthetized humans to address whether the organization of white matter connectivity differs between subregions of VLPFC. Our results demonstrate a ventral-dorsal division within IFG. Ventral IFG as a whole connects broadly to lateral temporal cortex. Although several different individual white matter tracts form connections between ventral IFG and lateral temporal cortex, functional connectivity analysis of fMRI data indicates that these are part of the same ventral functional network. By contrast, across subdivisions, dorsal IFG was connected with the midfrontal gyrus and correlated as a separate dorsal functional network. These qualitative differences in white matter organization within larger macroanatomical subregions of VLPFC support prior functional distinctions among these regions observed in task-based and functional connectivity fMRI studies. These results are consistent with the proposal that anatomical connectivity is a crucial determinant of systems-level functional organization of frontal cortex and the brain in general.


2018 ◽  
Vol 4 (12) ◽  
pp. eaat3702 ◽  
Author(s):  
E. L. Johnson ◽  
L. Tang ◽  
Q. Yin ◽  
E. Asano ◽  
N. Ofen

Prevailing theories link prefrontal cortex (PFC) maturation to the development of declarative memory. However, the precise spatiotemporal correlates of memory formation in the developing brain are not known. We provide rare intracranial evidence that the spatiotemporal propagation of frontal activity supports memory formation in children. Seventeen subjects (6.2 to 19.4 years) studied visual scenes in preparation for a recognition memory test while undergoing direct cortical monitoring. Earlier PFC activity predicted greater accuracy, and subsecond deviations in activity flow between subregions predicted memory formation. Activity flow between inferior and precentral sites was refined during adolescence, partially explaining gains in memory. In contrast, middle frontal activity predicted memory independent of age. These findings show with subsecond temporal precision that the developing PFC links scene perception and memory formation and underscore the role of the PFC in supporting memory development.


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