Accelerated forgetting of contextual details due to focal medio-dorsal thalamic lesion.
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ABSTRACT:
SUBMITTER: Tu S
PROVIDER: S-EPMC4163931 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:We investigated whether the benefit of slow wave sleep (SWS) for memory consolidation typically observed in healthy individuals is disrupted in people with accelerated long-term forgetting (ALF) due to epilepsy. SWS is thought to play an active role in declarative memory in healthy individuals and, furthermore, electrographic epileptiform activity is often more prevalent during SWS than during wakefulness or other sleep stages. We studied the relationship between SWS and the benefit of sleep for memory retention using a word-pair associates task. In both the ALF and the healthy control groups, sleep conferred a memory benefit. However, the relationship between the amount of SWS and sleep-related memory benefits differed significantly between the groups. In healthy participants, the amount of SWS correlated positively with sleep-related memory benefits. In stark contrast, the more SWS, the smaller the sleep-related memory benefit in the ALF group. Therefore, contrary to its role in healthy people, SWS-associated brain activity appears to be deleterious for memory in patients with ALF.
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Project description:Accelerated long-term forgetting (ALF) is a form of memory impairment in which learning and initial retention of information appear normal but subsequent forgetting is excessively rapid. ALF is most commonly associated with epilepsy and, in particular, a form of late-onset epilepsy called transient epileptic amnesia (TEA). ALF provides a novel opportunity to investigate post-encoding memory processes, such as consolidation. Sleep is implicated in the consolidation of memory in healthy people and a deficit in sleep-dependent memory consolidation has been proposed as an explanation for ALF. If this proposal were correct, then sleep would not benefit memory retention in people with ALF as much as in healthy people, and ALF might only be apparent when the retention interval contains sleep. To test this theory, we compared performance on a sleep-sensitive memory task over a night of sleep and a day of wakefulness. We found, contrary to the hypothesis, that sleep benefits memory retention in TEA patients with ALF and that this benefit is no smaller in magnitude than that seen in healthy controls. Indeed, the patients performed significantly more poorly than the controls only in the wake condition and not the sleep condition. Patients were matched to controls on learning rate, initial retention, and the effect of time of day on cognitive performance. These results indicate that ALF is not caused by a disruption of sleep-dependent memory consolidation. Instead, ALF may be due to an encoding abnormality that goes undetected on behavioural assessments of learning, or by a deficit in memory consolidation processes that are not sleep-dependent.
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Project description:One important feature of episodic memory is that it contains fine-grained and vividly recollected details. How to improve and maintain detailed information over time has been one of the central issues in memory research. Previous studies have inconsistent findings on whether detailed memory is forgotten more rapidly than gist memory. In this study, we investigated to what extent different encoding tasks modulated forgetting of gist and detailed information. In three experiments, participants were presented pictures of common objects and were asked to name them (Experiment 1), describe the details about them (Experiment 2) or imagine scenes associated with them (Experiment 3). After intervals of 10 minutes, one day, one week and one month, gist and detailed memories of the pictures were tested and assessed using a remember/know/guess judgement. The results showed that after the naming task, gist and detailed memories were forgotten at a similar rate, but after the description and the imagination tasks, detailed memory was forgotten at a slower rate than gist memory. The forgetting rate of gist memory was the slowest after the naming task, while that of detailed memory was the slowest after the description task. In addition, when three experiments were compared, the naming task enhanced the contributions of recollection and familiarity for gist memory, while the description task enhanced the contribution of familiarity for detailed memory. These results reveal the importance of the encoding task in the forgetting of gist and detailed information, and suggest a possible way to maintain perceptual details of objects at longer intervals.
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Project description:The present study in rats was conducted to identify brain regions affected by the interruption of vestibular transmission and to explore selected aspects of their functional connections. We analyzed, by positron emission tomography (PET), the regional cerebral glucose metabolism (rCGM) of cortical, and subcortical cerebral regions processing vestibular signals after an experimental lesion of the left laterodorsal thalamic nucleus, a relay station for vestibular input en route to the cortical circuitry. PET scans upon galvanic vestibular stimulation (GVS) were conducted in each animal prior to lesion and at post-lesion days (PLD) 1, 3, 7, and 20, and voxel-wise statistical analysis of rCGM at each PLD compared to pre-lesion status were performed. After lesion, augmented metabolic activation by GVS was detected in cerebellum, mainly contralateral, and in contralateral subcortical structures such as superior colliculus, while diminished activation was observed in ipsilateral visual, entorhinal, and somatosensory cortices, indicating compensatory processes in the non-affected sensory systems of the unlesioned side. The changes in rCGM observed after lesion resembled alterations observed in patients suffering from unilateral thalamic infarction and may be interpreted as brain plasticity mechanisms associated with vestibular compensation and substitution. The second set of experiments aimed at the connections between cortical and subcortical vestibular regions and their neurotransmitter systems. Neuronal tracers were injected in regions processing vestibular and somatosensory information. Injections into the anterior cingulate cortex (ACC) or the primary somatosensory cortex (S1) retrogradely labeled neuronal somata in ventral posteromedial (VPM), posterolateral (VPL), ventrolateral (VL), posterior (Po), and laterodorsal nucleus, dorsomedial part (LDDM), locus coeruleus, and contralateral S1 area. Injections into the parafascicular nucleus (PaF), VPM/VPL, or LDDM anterogradely labeled terminal fields in S1, ACC, insular cortex, hippocampal CA1 region, and amygdala. Immunohistochemistry showed tracer-labeled terminal fields contacting cortical neurons expressing the ?-opioid receptor. Antibodies to tyrosine hydroxylase, serotonin, substance P, or neuronal nitric oxide-synthase did not label any of the traced structures. These findings provide evidence for opioidergic transmission in thalamo-cortical transduction.
| S-EPMC7256190 | biostudies-literature
Project description:The Medio-Dorsal Nuclei (MDN) including the thalamic magnocellular and parvocellular thalamic regions has been implicated in verbal memory function. In a 77 year old lady, with a prior history of a clinically silent infarct of the left MDN, we observed the acute onset of spontaneous confabulations when an isolated new infarct occurred in the right MDN. The patient and five age-matched healthy subjects underwent Magnetic Resonance Imaging (MRI) and Diffusion Tensor Imaging (DTI). The thalamic lesions were localized by overlapping Morel Thalamic Atlas with structural MRI data. DTI was used to assess: i) white matter alterations (Fractional Anisotropy, FA) within fibers connecting the ischemic areas to cortex; ii) the micro-structural damage (Mean Diffusivity) within the thalamic sub-regions defined by their structural connectivity to the Anterior Cingulate Cortex (ACC) and to the temporal lobes. These target regions were chosen because their damage is considered associated with the appearance of confabulations. Thalamic lesions were localized within the parvocellular regions of the right and left MDNs. The structural connectivity study showed that the fiber tracts, connecting the bilaterally damaged thalamic regions with the frontal cortex, corresponded to the anterior thalamic radiations (ATR). FA within these tracts was significantly lower in the patient as compared to controls. Mean diffusivity within the MDNs projecting to Broadman area (BA) 24, BA25 and BA32 of ACC was significantly higher in the patient than in control group. Mean diffusivity values within the MDN projecting to temporal lobes in contrast were not different between patient and controls. Our findings suggest the involvement of bilateral MDNs projections to ACC in the genesis of confabulations and help provide clarity to the longstanding debate on the origin of confabulations.
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Project description:Aversively established contextual fear memory manifests itself in robust freezing behavior, often lasting several weeks or months. Therefore, this approach is amenable to investigate the underlying neural circuitries by lesion or inactivation of specific brain regions or to test efficacy of substances that disrupt either the ability to acquire the association or to retrieve memories. In contrast, investigation of memory enhancement using this technique is time intensive since the non-treated control group naturally forgets the learned association only weeks after acquisition. Pharmacological interventions have been used to overcome this time span by disrupting memory at any time point, however, limiting it a mechanistic model of reversal of impairments instead of studying memory enhancement. Here, we investigated several parameters of the cued and contextual fear conditioning (CFC) protocol such that, while memory acquisition is established, loss of fear association occurs within a shorter time frame, allowing studies of memory enhancement in the context of natural forgetting. We found that three predictive tone-cues, each separated from a 0.3 mA foot shock by an interstimulus interval of 2 s and a pre-exposure to the context enables the investigation of enhanced contextual memory 7 d post training without the necessity of inducing pharmacological lesions.
| S-EPMC6706144 | biostudies-literature
Project description:OBJECTIVE:Accelerated long-term forgetting (ALF) occurs when newly learned information decays faster than normal over extended delays. It has been recognised most frequently in temporal lobe epilepsy, including Transient Epileptic Amnesia (TEA), but can also be drug-induced. Little is known about the evolution of ALF over time and its impacts upon other memory functions, such as autobiographical memory (ABM). Here we investigate the long-term outcome of ALF and ABM in a group of patients with TEA and a single case of baclofen-induced ALF. METHODS:Study 1 involved a longitudinal follow-up of 14 patients with TEA over a 10-year period. Patients repeated a neuropsychological battery, three ALF measures (with free recall probed at 30-min and 1-week), and a modified Autobiographical Memory Interview (MAMI). Performance was compared with a group of healthy age-matched controls. In Study 2, patient CS, who previously experienced baclofen-induced ALF, was followed over 4 years, and re-tested now, 18 months after ceasing baclofen. CS repeated a neuropsychological battery, three ALF experimental tasks (each probed after 30?min and 1 week), and a modified autobiographical interview (AI). Her performance was compared with healthy age-matched controls. RESULTS:On ALF measures, the TEA group performed significantly below controls, but when analysed individually, 4 of the 7 patients who originally showed ALF no longer did so. In two, this was accompanied by improvements in ABM for recent but not remote memory. Patient CS no longer demonstrated ALF on standard lab-based tests and now appeared to retain new episodic autobiographical events with a similar degree of episodic richness as controls. CONCLUSION:Long-term follow up suggests that ALF can resolve, with improvements translating to recent ABM in some cases.
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Project description:Episodic memory entails the storage of events together with their spatio-temporal context and retrieval comprises the subjective experience of a link between the person who remembers and the episode itself. We used an encoding procedure with mobile-phones to generate experimentally-controlled episodes in the real world: object-images were sent to the participants' phone, with encoding durations up to 3 weeks. In other groups of participants, the same objects were encoded during the exploration of a virtual town (45 min) or using a standard laboratory paradigm, with pairs of object/place-images presented in a sequence of unrelated trials (15 min). At retrieval, we tested subjective memory for the objects (remember/familiar) and memory for the context (place and time). We found that accurate and confident context-memory increased the likelihood of "remember" responses, in all encoding contexts. We also tested the participants' ability to judge the temporal-order of the encoded episodes. Using a model of temporal similarity, we demonstrate scale-invariant properties of order-retrieval, but also highlight the contribution of non-chronological factors. We conclude that the mechanisms governing episodic memory retrieval can operate across a wide range of spatio-temporal contexts and that the multi-dimensional nature of the episodic traces contributes to the subjective experience of retrieval.
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Project description:The mammalian visual system is one of the most well-studied brain systems. Visual information from the retina is relayed to the dorsal lateral geniculate nucleus of the thalamus (LGd). The LGd then projects topographically to primary visual cortex (VISp) to mediate visual perception. In this view, the VISp is a critical network hub where visual information must traverse LGd-VISp circuits to reach higher order "extrastriate" visual cortices, which surround the VISp on its medial and lateral borders. However, decades of conflicting reports in a variety of mammals support or refute the existence of extrastriate LGd connections that can bypass the VISp. Here, we provide evidence of bidirectional extrastriate connectivity with the mouse LGd. Using small, discrete coinjections of anterograde and retrograde tracers within the thalamus and cortex, our cross-validated approach identified bidirectional connectivity between LGd and extrastriate visual cortices. We find robust reciprocal connectivity of the medial extrastriate regions with LGd neurons distributed along the "ventral strip" border with the intergeniculate leaflet. In contrast, LGd input to lateral extrastriate regions is sparse, but lateral extrastriate regions return stronger descending projections to localized LGd areas. We show further evidence that axons from lateral extrastriate regions can overlap onto medial extrastriate-projecting LGd neurons in the ventral strip, providing a putative subcortical LGd pathway for communication between medial and lateral extrastriate regions. Overall, our findings support the existence of extrastriate LGd circuits and provide novel understanding of LGd organization in rodent visual system.
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