hippocampal formation
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2022 ◽  
Vol 15 ◽  
Author(s):  
Benjamin Jainta ◽  
Sophie Siestrup ◽  
Nadiya El-Sourani ◽  
Ima Trempler ◽  
Moritz F. Wurm ◽  
...  

Intuitively, we assume that we remember episodes better when we actively participated in them and were not mere observers. Independently of this, we can recall episodes from either the first-person perspective (1pp) or the third-person perspective (3pp). In this functional magnetic resonance imaging (fMRI) study, we tested whether agency and perspective modulate neural activity during memory retrieval and subsequently enhance memory performance. Subjects encoded a set of different episodes by either imitating or only observing videos that showed short toy stories. A week later, we conducted fMRI and cued episodic retrieval by presenting the original videos, or slightly modified versions thereof, from 1pp or from 3pp. The hippocampal formation was sensitive to self-performed vs. only observed actions only when there was an episodic mismatch. In a post-fMRI memory test a history of self-performance did not improve behavioral memory performance. However, modified videos were often (falsely) accepted as showing truly experienced episodes when: (i) they were already presented in this modified version during fMRI or (ii) they were presented in their original form during fMRI but from 3pp. While the overall effect of modification was strong, the effects of perspective and agency were more subtle. Together, our findings demonstrate that self-performance and self-perspective modulate the strength of a memory trace in different ways. Even when memory performance remains the same for different agentive states, the brain is capable of detecting mismatching information. Re-experiencing the latter impairs memory performance as well as retrieving encoded episodes from 3pp.


Neuron ◽  
2022 ◽  
Author(s):  
Nils Nyberg ◽  
Éléonore Duvelle ◽  
Caswell Barry ◽  
Hugo J. Spiers

2021 ◽  
Vol 23 (1) ◽  
pp. 204
Author(s):  
Adrienne Mátyás ◽  
Emőke Borbély ◽  
András Mihály

The present experiments reveal the alterations of the hippocampal neuronal populations in chronic epilepsy. The mice were injected with a single dose of pilocarpine. They had status epilepticus and spontaneously recurrent motor seizures. Three months after pilocarpine treatment, the animals were investigated with the Barnes maze to determine their learning and memory capabilities. Their hippocampi were analyzed 2 weeks later (at 3.5 months) with standard immunohistochemical methods and cell counting. Every animal displayed hippocampal sclerosis. The neuronal loss was evaluated with neuronal-N immunostaining, and the activation of the microglia was measured with Iba1 immunohistochemistry. The neuropeptide Y, parvalbumin, and calretinin immunoreactive structures were qualitatively and quantitatively analyzed in the hippocampal formation. The results were compared statistically to the results of the control mice. We detected neuronal loss and strongly activated microglia populations. Neuropeptide Y was significantly upregulated in the sprouting axons. The number of parvalbumin- and calretinin-containing interneurons decreased significantly in the Ammon’s horn and dentate gyrus. The epileptic animals displayed significantly worse learning and memory functions. We concluded that degeneration of the principal neurons, a numerical decrease of PV-containing GABAergic neurons, and strong peptidergic axonal sprouting were responsible for the loss of the hippocampal learning and memory functions.


PLoS Biology ◽  
2021 ◽  
Vol 19 (12) ◽  
pp. e3001127
Author(s):  
Xiaoxiao Lin ◽  
Michelle Amalraj ◽  
Crisylle Blanton ◽  
Brenda Avila ◽  
Todd C. Holmes ◽  
...  

The hippocampal formation (HF) is well documented as having a feedforward, unidirectional circuit organization termed the trisynaptic pathway. This circuit organization exists along the septotemporal axis of the HF, but the circuit connectivity across septal to temporal regions is less well described. The emergence of viral genetic mapping techniques enhances our ability to determine the detailed complexity of HF circuitry. In earlier work, we mapped a subiculum (SUB) back projection to CA1 prompted by the discovery of theta wave back propagation from the SUB to CA1 and CA3. We reason that this circuitry may represent multiple extended noncanonical pathways involving the subicular complex and hippocampal subregions CA1 and CA3. In the present study, multiple retrograde viral tracing approaches produced robust mapping results, which supports this prediction. We find significant noncanonical synaptic inputs to dorsal hippocampal CA3 from ventral CA1 (vCA1), perirhinal cortex (Prh), and the subicular complex. Thus, CA1 inputs to CA3 run opposite the trisynaptic pathway and in a temporal to septal direction. Our retrograde viral tracing results are confirmed by anterograde-directed viral mapping of projections from input mapped regions to hippocampal dorsal CA3 (dCA3). We find that genetic inactivation of the projection of vCA1 to dCA3 impairs object-related spatial learning and memory but does not modulate anxiety-related behaviors. Our data provide a circuit foundation to explore novel functional roles contributed by these noncanonical hippocampal circuit connections to hippocampal circuit dynamics and learning and memory behaviors.


2021 ◽  
Vol 15 ◽  
Author(s):  
Marta Jelitai ◽  
Albert M. Barth ◽  
Ferenc Komlósi ◽  
Tamás F. Freund ◽  
Viktor Varga

Ascending serotonergic/glutamatergic projection from the median raphe region (MRR) to the hippocampal formation regulates both encoding and consolidation of memory and the oscillations associated with them. The firing of various types of MRR neurons exhibits rhythmic modulation coupled to hippocampal oscillatory activity. A possible intermediary between rhythm-generating forebrain regions and entrained ascending modulation may be the GABAergic circuit in the MRR, known to be targeted by a diverse array of top-down inputs. However, the activity of inhibitory MRR neurons in an awake animal is still largely unexplored. In this study, we utilized whole cell patch-clamp, single cell, and multichannel extracellular recordings of GABAergic and non-GABAergic MRR neurons in awake, head-fixed mice. First, we have demonstrated that glutamatergic and serotonergic neurons receive both transient, phasic, and sustained tonic inhibition. Then, we observed substantial heterogeneity of GABAergic firing patterns but a marked modulation of activity by brain states and fine timescale coupling of spiking to theta and ripple oscillations. We also uncovered a correlation between the preferred theta phase and the direction of activity change during ripples, suggesting the segregation of inhibitory neurons into functional groups. Finally, we could detect complementary alteration of non-GABAergic neurons’ ripple-coupled activity. Our findings support the assumption that the local inhibitory circuit in the MRR may synchronize ascending serotonergic/glutamatergic modulation with hippocampal activity on a subsecond timescale.


2021 ◽  
Vol 118 (51) ◽  
pp. e2119670118
Author(s):  
Lynn Nadel

The question of why our conceptions of space and time are intertwined with memory in the hippocampal formation is at the forefront of much current theorizing about this brain system. In this article I argue that animals bridge spatial and temporal gaps through the creation of internal models that allow them to act on the basis of things that exist in a distant place and/or existed at a different time. The hippocampal formation plays a critical role in these processes by stitching together spatiotemporally disparate entities and events. It does this by 1) constructing cognitive maps that represent extended spatial contexts, incorporating and linking aspects of an environment that may never have been experienced together; 2) creating neural trajectories that link the parts of an event, whether they occur in close temporal proximity or not, enabling the construction of event representations even when elements of that event were experienced at quite different times; and 3) using these maps and trajectories to simulate possible futures. As a function of these hippocampally driven processes, our subjective sense of both space and time are interwoven constructions of the mind, much as the philosopher Immanuel Kant postulated.


2021 ◽  
Vol 15 ◽  
Author(s):  
Sarah Woelfle ◽  
Tobias M. Boeckers

The hippocampal formation consists of the Ammon’s horn (cornu Ammonis with its regions CA1-4), dentate gyrus, subiculum, and the entorhinal cortex. The rough extension of the regions CA1-3 is typically defined based on the density and size of the pyramidal neurons without clear-cut boundaries. Here, we propose the vesicular glutamate transporter 1 (VGLUT1) as a molecular marker for the CA3 region. This is based on its strong labeling of the stratum lucidum (SL) in fluorescently stained human hippocampus sections. VGLUT1 puncta of the intense SL band co-localize with synaptoporin (SPO), a protein enriched in mossy fibers (MFs). Owing to its specific intensity profile throughout all hippocampal layers, VGLUT1 could be implemented as a pendant to Nissl-staining in fluorescent approaches with the additional demarcation of the SL. Furthermore, by high-resolution confocal microscopy, we detected VGLUT2 in the human hippocampus, thus reconciling two previous studies. Finally, by VGLUT1/SPO co-staining, we provide evidence for the existence of infrapyramidal MFs in the human hippocampus and we show that SPO expression is not restricted to MF synapses as demonstrated for rodent tissue.


2021 ◽  
Vol 17 (12) ◽  
pp. e1009681
Author(s):  
Michiel W. H. Remme ◽  
Urs Bergmann ◽  
Denis Alevi ◽  
Susanne Schreiber ◽  
Henning Sprekeler ◽  
...  

Systems memory consolidation involves the transfer of memories across brain regions and the transformation of memory content. For example, declarative memories that transiently depend on the hippocampal formation are transformed into long-term memory traces in neocortical networks, and procedural memories are transformed within cortico-striatal networks. These consolidation processes are thought to rely on replay and repetition of recently acquired memories, but the cellular and network mechanisms that mediate the changes of memories are poorly understood. Here, we suggest that systems memory consolidation could arise from Hebbian plasticity in networks with parallel synaptic pathways—two ubiquitous features of neural circuits in the brain. We explore this hypothesis in the context of hippocampus-dependent memories. Using computational models and mathematical analyses, we illustrate how memories are transferred across circuits and discuss why their representations could change. The analyses suggest that Hebbian plasticity mediates consolidation by transferring a linear approximation of a previously acquired memory into a parallel pathway. Our modelling results are further in quantitative agreement with lesion studies in rodents. Moreover, a hierarchical iteration of the mechanism yields power-law forgetting—as observed in psychophysical studies in humans. The predicted circuit mechanism thus bridges spatial scales from single cells to cortical areas and time scales from milliseconds to years.


2021 ◽  
Vol 12 ◽  
Author(s):  
Panlong Li ◽  
Qi Huang ◽  
Shiyu Ban ◽  
Yuan Qiao ◽  
Jing Wu ◽  
...  

Background and Purpose: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy caused by mutations in the NOTCH3 gene is a hereditary cerebral small vessel disease, manifesting with stroke, cognitive impairment, and mood disturbances. Functional or structural changes in the default mode network (DMN), which plays important role in cognitive and mental maintenance, have been found in several neurological and mental diseases. However, it remains unclear whether DMN is altered in patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).Methods: Multimodal imaging methods, including MRI and positron emission tomography (PET), were applied to evaluate the functional, structural, and metabolic characteristics of DMN in 25 patients with CADASIL and 42 healthy controls.Results: Compared with controls, patients with CADASIL had decreased nodal efficiency and degree centrality of the dorsal medial pre-frontal cortex and hippocampal formation within DMN. Structural MRI and diffusion tensor imaging (DTI) showed decreased gray matter volume and fiber tracks presented in the bilateral hippocampal formation. Meanwhile, PET imaging showed decreased metabolism within the whole DMN in CADASIL. Furthermore, correlation analyses showed that these nodal characteristics, gray matter volume, and metabolic signals of DMN were related to cognitive scores in CADASIL.Conclusions: Our results suggested that altered network characteristics of DMN might play important roles in cognitive deficits of CADASIL.


2021 ◽  
Vol 12 ◽  
Author(s):  
Gabriel G. Fernandes ◽  
Karla C. M. Costa ◽  
Davi S. Scomparin ◽  
Juliana B. Freire ◽  
Francisco S. Guimarães ◽  
...  

Inducible nitric oxide synthase (iNOS) is an enzyme upregulated in the brain during neuroimmune stimuli which is associated with an oxidative and pro-inflammatory environment in several brain regions, including the hippocampal formation and the prefrontal cortex. The dentate gyrus of the hippocampal formation is the site of a process known as adult hippocampal neurogenesis (AHN). Although many endogenous and extrinsic factors can modulate AHN, the exact participation of specific proinflammatory mediators such as iNOS in these processes remains to be fully elucidated. Here, we investigated how the total genetic ablation of iNOS impacts the hippocampal neurogenic niche and microglial phenotype and if these changes are correlated to the behavioral alterations observed in iNOS knockout (K.O.) mice submitted or not to the chronic unpredictable stress model (CUS - 21 days protocol). Contrary to our initial hypothesis, at control conditions, iNOS K.O. mice displayed no abnormalities on microglial activation in the dentate gyrus. However, they did exhibit impaired newborn cells and immature neuron survival, which was not affected by CUS. The reduction of AHN in iNOS K.O. mice was accompanied by an increased positive coping response in the tail suspension test and facilitation of anxiety-like behaviors in the novelty suppressed feeding. Next, we investigated whether a pro-neurogenic stimulus would rescue the neurogenic capacity of iNOS K.O. mice by administering in control and CUS groups the antidepressant escitalopram (ESC). The chronic treatment with ESC could not rescue the neurogenic capacity or the behavioral changes observed in iNOS K.O. mice. Besides, in the ventromedial prefrontal (vmPFC) cortex there was no change in the expression or the chronic activation of PV neurons (evaluated by double labeling PV with FOSB) in the prelimbic (PrL) or infralimbic subregions. FOSB expression, however, increased in the PrL of iNOS K.O. mice. Our results suggest that iNOS seems essential for the survival of newborn cells and immature neurons in the hippocampus and seem to partially explain the anxiogenic-like behavior observed in iNOS K.O. mice. On the other hand, the iNOS ablation appears to result in increased activity of the PrL which could explain the antidepressant-like behaviors of iNOS K.O mice.


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