Intact Priming for Novel Perceptual Representations in Amnesia

1997 ◽  
Vol 9 (6) ◽  
pp. 699-713 ◽  
Author(s):  
Stephan B. Hamann ◽  
Larry R. Squire
Keyword(s):  
Recognition Memory ◽  
Declarative Memory ◽  
Brain Structures ◽  
Perceptual Identification ◽  
Single Exposure ◽  
Memory Representations ◽  
Perceptual Representations ◽  
The Creation ◽  
And Control ◽  
The Brain

Recent studies have challenged the notion that priming for ostensibly novel stimuli such as pseudowords (REAB) reflects the creation of new representations. Priming for such stimuli could instead reflect the activation of familiar memory representations that are orthographically similar (READ) and/or the activation of subparts of stimuli (RE, EX, AR), which are familar because they occur commonly in English. We addressed this issue in three experiments that assessed perceptual identification priming and recognition memory for novel and familiar letter strings in amnesic patients and control subjects. Priming for words, pseudowords, and orthographically illegal nonwords was fully intact in the amnesic patients following a single exposure, whereas recognition memory was impaired for the same items. Thus, priming can occur for stimuli that are unlikely to have preexisting representations. Words and pseudowords exhibited twice as much priming as illegal nonwords, suggesting that activation may contribute to priming for words and wordlike stimuli. Additional results showed that priming for illegal nonwords resulted from the formation of new perceptual associations among the component letters of each nonword rather than the activation of individual letter representations. In summary, the results demonstrate that priming following a single exposure can depend on the creation of new perceptual representations and that such priming is independent of the brain structures essential for declarative memory.

scholarly journals Increased Aluminum Content in Certain Brain Structures is Correlated with Higher Silicon Concentration in Alcoholic Use Disorder

Molecules ◽  
2019 ◽  
Vol 24 (9) ◽  
pp. 1721 ◽  
Author(s):  
Cezary Grochowski ◽  
Eliza Blicharska ◽  
Jacek Bogucki ◽  
Jędrzej Proch ◽  
Aleksandra Mierzwińska ◽  
...  
Keyword(s):  
Inductively Coupled Plasma ◽  
Optical Emission ◽  
Brain Structures ◽  
Brain Regions ◽  
Protective Role ◽  
Emission Spectrometry ◽  
Inductively Coupled ◽  
Al Content ◽  
And Control ◽  
The Brain

Introduction: Alcohol overuse may be related to increased aluminum (Al) exposure, the brain accumulation of which contributes to dementia. However, some reports indicate that silicon (Si) may have a protective role over Al-induced toxicity. Still, no study has ever explored the brain content of Al and Si in alcoholic use disorder (AUD). Materials and methods: To fill this gap, the present study employed inductively coupled plasma optical emission spectrometry to investigate levels of Al and Si in 10 brain regions and in the liver of AUD patients (n = 31) and control (n = 32) post-mortem. Results: Al content was detected only in AUD patients at mean ± SD total brain content of 1.59 ± 1.19 mg/kg, with the highest levels in the thalamus (4.05 ± 12.7 mg/kg, FTH), inferior longitudinal fasciculus (3.48 ± 9.67 mg/kg, ILF), insula (2.41 ± 4.10 mg/kg) and superior longitudinal fasciculus (1.08 ± 2.30 mg/kg). Si content displayed no difference between AUD and control, except for FTH. Positive inter-region correlations between the content of both elements were identified in the cingulate cortex, hippocampus, and ILF. Conclusions: The findings of this study suggest that AUD patients may potentially be prone to Al-induced neurodegeneration in their brain—although this hypothesis requires further exploration.

scholarly journals The locus of recognition memory signals in human cortex depends on the complexity of the memory representations

2021 ◽  
Author(s):  
D. Merika W. Sanders ◽  
Rosemary A. Cowell
Keyword(s):  
Recognition Memory ◽  
Medial Temporal Lobe ◽  
Declarative Memory ◽  
Memory Task ◽  
Representational Content ◽  
Brain Regions ◽  
Complex Stimuli ◽  
Memory Representations ◽  
Memory Signals ◽  
Feature Memory

Representational theories predict that brain regions contribute to cognition according to the information they represent (e.g., simple versus complex), contradicting the traditional notion that brain regions are specialized for cognitive functions (e.g., perception versus memory). In support of representational accounts, substantial evidence now attests that the Medial Temporal Lobe (MTL) is not specialized solely for long-term declarative memory, but underpins other functions including perception and future-imagining for complex stimuli and events. However, a complementary prediction has been less well explored, namely that the cortical locus of declarative memory may fall outside the MTL if the to-be-remembered content is sufficiently simple. Specifically, the locus should coincide with the optimal neural code for the representations being retrieved. To test this prediction, we manipulated the complexity of the to-be-remembered representations in a recognition memory task. First, participants in the scanner viewed novel 3D objects and scenes, and we used multivariate analyses to identify regions in the ventral visual-MTL pathway that preferentially coded for either simple features of the stimuli, or complex conjunctions of those features. Next, in a separate scan, we tested recognition memory for these stimuli and performed neuroimaging contrasts that revealed two memory signals ‒ feature memory and conjunction memory. Feature memory signals were found in visual cortex, while conjunction memory signals emerged in MTL. Further, the regions optimally representing features via preferential feature-coding coincided with those exhibiting feature memory signals. These findings suggest that representational content, rather than cognitive function, is the primary organizing principle in the ventral visual-MTL pathway.

Word Learning in 6-Month-Olds: Fast Encoding–Weak Retention

2011 ◽  
Vol 23 (11) ◽  
pp. 3228-3240 ◽  
Author(s):  
Manuela Friedrich ◽  
Angela D. Friederici
Keyword(s):  
Semantic Memory ◽  
Word Learning ◽  
Declarative Memory ◽  
Brain Activity ◽  
Brain Structures ◽  
Memory Formation ◽  
Fast Encoding ◽  
Frequent Exposure ◽  
The Brain ◽  
Lexical Mapping

There has been general consensus that initial word learning during early infancy is a slow and time-consuming process that requires very frequent exposure, whereas later in development, infants are able to quickly learn a novel word for a novel meaning. From the perspective of memory maturation, this shift in behavioral development might represent a shift from slow procedural to fast declarative memory formation. Alternatively, it might be caused by the maturation of specific brain structures within the declarative memory system that may support lexical mapping from the very first. Here, we used the neurophysiological method of ERPs to watch the brain activity of 6-month-old infants, when repeatedly presented with object–word pairs in a cross-modal learning paradigm. We report first evidence that infants as young as 6 months are able to associate objects and words after only very few exposures. A memory test 1 day later showed that infants did not fully forget this newly acquired knowledge, although the ERP effects indicated it to be less stable than immediately after encoding. The combined results suggest that already at 6 months the encoding process of word learning is based on fast declarative memory formation, but limitations in the consolidation of declarative memory diminish the long lasting effect in lexical-semantic memory at that age.

scholarly journals In vivo Binding of Nimodipine in the Brain: I. The Effect of Focal Cerebral Ischemia

1991 ◽  
Vol 11 (5) ◽  
pp. 762-770 ◽  
Author(s):  
Antoine M. Hakim ◽  
Matthew J. Hogan
Keyword(s):  
Cerebral Ischemia ◽  
Striate Cortex ◽  
Focal Cerebral Ischemia ◽  
Brain Structures ◽  
Significant Rise ◽  
Secular Equilibrium ◽  
Control Right ◽  
And Control ◽  
The Brain

We report the regional variation in [3H]nimodipine binding in vivo during focal cerebral ischemia. After intravenous injection, 30 min of circulation of [3H]nimodipine was sufficient to establish a secular equilibrium of distribution in the brain. Rats sustained left middle cerebral and common carotid artery occlusions for 5 min, and 4, 24, and 48 h (n ≥ 6 per group). They were decapitated 30 min after injection of 250 μCi of [3H]nimodipine and their brains were submitted to autoradiography. The concentrations of [3H]nimodipine in plasma and brain structures, corrected for metabolism of nimodipine, were used to calculate the regional volumes of distribution ( V) in the ischemic left (L) and control right (R) hemispheres. Log (VL/VR) was then defined as the group mean of the logarithms of the left-to-right ratio of V of [3H]nimodipine. In the lateral caudate, binding of [3H]nimodipine on the ischemic side was highest within 5 min of occlusion. Log ( VL/ VR) in this region for the combined sham-operated and normal control rats and those after 5 min and 4 and 24 h of ischemia were −0.014 ± 0.025, 0.137 ± 0.056*, −0.201 ± 0.367, and −0.049 ± 0.370 (mean ± SD, *represents p < 0.01 compared with controls). By contrast, in the superior frontal cortex, values for log ( VL/ VR) in the same sequence were −0.016 ± 0.025, 0.028 ± 0.056, 0.284 ± 0.228*, and 0.224 ± 0.069*, thus showing a significant rise in [3H]nimodipine binding only at 4 h. Structures such as the cingulate and striate cortex, sufficiently removed from the ischemic core, showed only small changes in log ( VL/ VR) at all times. Correlating these data with CBF and histologic determinations performed in separate groups of rats, we conclude that [3H]nimodipine binding increases earlier in the more severely ischemic structures than in those with more moderate reductions in perfusion. Furthermore, when binding declines in a region where it was previously increased, infarction is likely. These studies afford new insight into the concept of ischemic penumbra and suggest that this model may allow testing for therapeutic effectiveness.

I was not so

2017 ◽  
Vol 41 (S1) ◽  
pp. S668-S669
Author(s):  
M.J. Gordillo Montaño ◽  
S. Ramos Perdigues ◽  
E. Guillén Guillén ◽  
O. Lopez Berastegui ◽  
M. Guisado Rico ◽  
...  
Keyword(s):  
Unknown Origin ◽  
Brain Structures ◽  
Frontal Lobes ◽  
Point Of View ◽  
Multiple Processes ◽  
Purging Behavior ◽  
Competing Interest ◽  
And Control ◽  
The Brain ◽  
Selection Of

IntroductionThe frontal lobes are the brain structures of latest development and evolution in the human brain. It is considered that the frontal lobes represent the “executive center of the brain”. The frontal tumors represent 16% of all supratentorial tumors. Symptoms are easily confused as psychiatric rather than neurological.ObjectivesCan see the alterations of the executive functions in a case of frontal affectation, for future cases know where to focus our attention and develop concepts associated with frontal lobe.MethodThirty-year-old patient without relevant medical history. Go to the emergency department with major episode of agitation. After performing cranial CT abnormality, it is detected in the front area. Sign up study. It presents amnesia episode before admission, whereupon shown stunned and worried. The patient describes a change in your life 12 months ago, when it begins to be more nervous, increasing their impulsiveness, she has episodes of binge eating, purging behavior with subsequent occasional alcohol abuse. Jealousy. The patient is informed as much as your family of the possible impact of the injury on the behavioral sphere and impulse control when it is still unknown origin.ConclusionsFrom a neuropsychological point of view the frontal lobes represent a system of planning, regulation and control of psychological processes; coordination and allow selection of multiple processes and various behavioral options and strategies available to the human being. Tumour research is important as it provides enough information we cognitive impairment. These patients exhibit symptoms that are easily confused as psychiatric rather than neurological.Disclosure of interestThe authors have not supplied their declaration of competing interest.

SPECIFIC PROPERTIES OF TUBULIN IN THE PREFRONTAL CORTEX IN CONTROL, SCHIZOPHRENIA AND VASCULAR DEMENTIA

2020 ◽  
pp. 65-71
Author(s):  
Burbaeva G.Sh. ◽  
Androsova L.V. ◽  
Vorobyeva E.A. ◽  
Savushkina O.K.
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Prefrontal Cortex ◽  
Vascular Dementia ◽  
Binding Activity ◽  
Nephelometric Method ◽  
Rate Of Polymerization ◽  
Mental Diseases ◽  
And Control ◽  
The Brain

The aim of the study was to evaluate the rate of polymerization of tubulin into microtubules and determine the level of colchicine binding (colchicine-binding activity of tubulin) in the prefrontal cortex in schizophrenia, vascular dementia (VD) and control. Colchicine-binding activity of tubulin was determined by Sherlinе in tubulin-enriched extracts of proteins from the samples. Measurement of light scattering during the polymerization of the tubulin was carried out using the nephelometric method at a wavelength of 450-550 nm. There was a significant decrease in colchicine-binding activity and the rate of tubulin polymerization in the prefrontal cortex in both diseases, and in VD to a greater extent than in schizophrenia. The obtained results suggest that not only in Alzheimer's disease, but also in other mental diseases such as schizophrenia and VD, there is a decrease in the level of tubulin in the prefrontal cortex of the brain, although to a lesser extent than in Alzheimer's disease, and consequently the amount of microtubules.

scholarly journals Neuron–Glia Interactions in Tuberous Sclerosis Complex Affect the Synaptic Balance in 2D and Organoid Cultures

Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 134
Author(s):  
Stephanie Dooves ◽  
Arianne J. H. van Velthoven ◽  
Linda G. Suciati ◽  
Vivi M. Heine
Keyword(s):  
Tuberous Sclerosis ◽  
Glial Cells ◽  
Tuberous Sclerosis Complex ◽  
Neuronal Development ◽  
Transmembrane Proteins ◽  
Significant Burden ◽  
Epidermal Growth ◽  
And Control ◽  
Egf Signaling ◽  
The Brain

Tuberous sclerosis complex (TSC) is a genetic disease affecting the brain. Neurological symptoms like epilepsy and neurodevelopmental issues cause a significant burden on patients. Both neurons and glial cells are affected by TSC mutations. Previous studies have shown changes in the excitation/inhibition balance (E/I balance) in TSC. Astrocytes are known to be important for neuronal development, and astrocytic dysfunction can cause changes in the E/I balance. We hypothesized that astrocytes affect the synaptic balance in TSC. TSC patient-derived stem cells were differentiated into astrocytes, which showed increased proliferation compared to control astrocytes. RNA sequencing revealed changes in gene expression, which were related to epidermal growth factor (EGF) signaling and enriched for genes that coded for secreted or transmembrane proteins. Control neurons were cultured in astrocyte-conditioned medium (ACM) of TSC and control astrocytes. After culture in TSC ACM, neurons showed an altered synaptic balance, with an increase in the percentage of VGAT+ synapses. These findings were confirmed in organoids, presenting a spontaneous 3D organization of neurons and glial cells. To conclude, this study shows that TSC astrocytes are affected and secrete factors that alter the synaptic balance. As an altered E/I balance may underlie many of the neurological TSC symptoms, astrocytes may provide new therapeutic targets.

scholarly journals Peptides Derived from Growth Factors to Treat Alzheimer’s Disease

2021 ◽  
Vol 22 (11) ◽  
pp. 6071
Author(s):  
Suzanne Gascon ◽  
Jessica Jann ◽  
Chloé Langlois-Blais ◽  
Mélanie Plourde ◽  
Christine Lavoie ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Growth Factors ◽  
Signaling Pathways ◽  
Brain Structures ◽  
Therapeutic Strategies ◽  
Native Proteins ◽  
Receptor Sites ◽  
The Brain

Alzheimer’s disease (AD) is a devastating neurodegenerative disease characterized by progressive neuron losses in memory-related brain structures. The classical features of AD are a dysregulation of the cholinergic system, the accumulation of amyloid plaques, and neurofibrillary tangles. Unfortunately, current treatments are unable to cure or even delay the progression of the disease. Therefore, new therapeutic strategies have emerged, such as the exogenous administration of neurotrophic factors (e.g., NGF and BDNF) that are deficient or dysregulated in AD. However, their low capacity to cross the blood–brain barrier and their exorbitant cost currently limit their use. To overcome these limitations, short peptides mimicking the binding receptor sites of these growth factors have been developed. Such peptides can target selective signaling pathways involved in neuron survival, differentiation, and/or maintenance. This review focuses on growth factors and their derived peptides as potential treatment for AD. It describes (1) the physiological functions of growth factors in the brain, their neuronal signaling pathways, and alteration in AD; (2) the strategies to develop peptides derived from growth factor and their capacity to mimic the role of native proteins; and (3) new advancements and potential in using these molecules as therapeutic treatments for AD, as well as their limitations.

scholarly journals The Brain Resting-State Functional Connectivity Underlying Violence Proneness: Is It a Reliable Marker for Neurocriminology? A Systematic Review

2019 ◽  
Vol 9 (1) ◽  
pp. 11 ◽  
Author(s):  
Ángel Romero-Martínez ◽  
Macarena González ◽  
Marisol Lila ◽  
Enrique Gracia ◽  
Luis Martí-Bonmatí ◽  
...  
Keyword(s):  
Functional Connectivity ◽  
Effective Treatment ◽  
Resting State ◽  
Brain Structures ◽  
Prevention Programs ◽  
Angular Gyrus ◽  
Resting State Functional Connectivity ◽  
Treatment And Prevention ◽  
Reliable Marker ◽  
The Brain

Introduction: There is growing scientific interest in understanding the biological mechanisms affecting and/or underlying violent behaviors in order to develop effective treatment and prevention programs. In recent years, neuroscientific research has tried to demonstrate whether the intrinsic activity within the brain at rest in the absence of any external stimulation (resting-state functional connectivity; RSFC) could be employed as a reliable marker for several cognitive abilities and personality traits that are important in behavior regulation, particularly, proneness to violence. Aims: This review aims to highlight the association between the RSFC among specific brain structures and the predisposition to experiencing anger and/or responding to stressful and distressing situations with anger in several populations. Methods: The scientific literature was reviewed following the PRISMA quality criteria for reviews, using the following digital databases: PubMed, PsycINFO, Psicodoc, and Dialnet. Results: The identification of 181 abstracts and retrieval of 34 full texts led to the inclusion of 17 papers. The results described in our study offer a better understanding of the brain networks that might explain the tendency to experience anger. The majority of the studies highlighted that diminished RSFC between the prefrontal cortex and the amygdala might make people prone to reactive violence, but that it is also necessary to contemplate additional cortical (i.e. insula, gyrus [angular, supramarginal, temporal, fusiform, superior, and middle frontal], anterior and posterior cingulated cortex) and subcortical brain structures (i.e. hippocampus, cerebellum, ventral striatum, and nucleus centralis superior) in order to explain a phenomenon as complex as violence. Moreover, we also described the neural pathways that might underlie proactive violence and feelings of revenge, highlighting the RSFC between the OFC, ventral striatal, angular gyrus, mid-occipital cortex, and cerebellum. Conclusions. The results from this synthesis and critical analysis of RSFC findings in several populations offer guidelines for future research and for developing a more accurate model of proneness to violence, in order to create effective treatment and prevention programs.

scholarly journals Glia Not Neurons: Uncovering Brain Dysmaturation in a Rat Model of Alzheimer’s Disease

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 823
Author(s):  
Ekaterina A. Rudnitskaya ◽  
Tatiana A. Kozlova ◽  
Alena O. Burnyasheva ◽  
Natalia A. Stefanova ◽  
Nataliya G. Kolosova
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Prefrontal Cortex ◽  
Brain Structures ◽  
Time Frame ◽  
Oxys Rats ◽  
Unknown Etiology ◽  
Suitable Model ◽  
Model Of Alzheimer’S Disease ◽  
The Brain

Sporadic Alzheimer’s disease (AD) is a severe disorder of unknown etiology with no definite time frame of onset. Recent studies suggest that middle age is a critical period for the relevant pathological processes of AD. Nonetheless, sufficient data have accumulated supporting the hypothesis of “neurodevelopmental origin of neurodegenerative disorders”: prerequisites for neurodegeneration may occur during early brain development. Therefore, we investigated the development of the most AD-affected brain structures (hippocampus and prefrontal cortex) using an immunohistochemical approach in senescence-accelerated OXYS rats, which are considered a suitable model of the most common—sporadic—type of AD. We noticed an additional peak of neurogenesis, which coincides in time with the peak of apoptosis in the hippocampus of OXYS rats on postnatal day three. Besides, we showed signs of delayed migration of neurons to the prefrontal cortex as well as disturbances in astrocytic and microglial support of the hippocampus and prefrontal cortex during the first postnatal week. Altogether, our results point to dysmaturation during early development of the brain—especially insufficient glial support—as a possible “first hit” leading to neurodegenerative processes and AD pathology manifestation later in life.

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