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remote memory [keywords]
- Test-Enhanced Learning Versus Errorless Learning in Aphasia Rehabilitation: Testing Competing Psychological Principles. [JOURNAL ARTICLE]
- J Exp Psychol Learn Mem Cogn 2014 Dec 22.
Because individuals with acquired language disorders are frequently unable to reliably access the names of common everyday objects (i.e., naming impairment), rehabilitation efforts often focus on improving naming. The present study compared 2 rehabilitation strategies for naming impairment, reflecting contradictory prescriptions derived from different theoretical principles. The prescription derived from psychological research on test-enhanced learning advocates providing patients opportunities to retrieve target names from long-term memory (i.e., retrieval practice) in the course of treatment. In contrast, the errorless learning approach derived from cognitive rehabilitation research eschews retrieval practice in favor of methods that minimize naming errors, and thus the potential for error learning, in the course of treatment. The present study directly compared these approaches and showed that, despite superior (and errorless) performance during errorless treatment, treatment that prioritized retrieval practice produced greater retention 1-day and 1-week following treatment. These findings have implications for clinical practice, as well as theoretical accounts of lexical access and test-enhanced learning. (PsycINFO Database Record (c) 2014 APA, all rights reserved).
- Memory B cells in transplantation. [Journal Article]
- Transplantation 2015 Jan 15; 99(1):21-8.
Much of the research on the humoral response to allografts has focused on circulating serum antibodies and the long-lived plasma cells that produce these antibodies. In contrast, the interrogation of the quiescent memory B cell compartment is technically more challenging and thus has not been incorporated into the clinical diagnostic or prognostic toolkit. In this review, we discuss new technologies that have allowed this heretofore enigmatic subset of B cells to be identified at quiescence and during a recall response. These technologies in experimental models are providing new insights into memory B cell heterogeneity with respect to their phenotype, cellular function, and the antibodies they produce. Similar technologies are also allowing for the identification of comparable memory alloreactive B cells in transplant recipients. Although much of the focus in transplant immunology has been on controlling the alloreactive B cell population, long-term transplant patient survival is also critically dependent on protection by pathogen-specific memory B cells. Techniques are available that allow the interrogation of memory B cell response to pathogen re-encounter. Thus, we are poised in our ability to investigate how immunosuppression affects allospecific and pathogen-specific memory B cells, and reason that these investigations can yield new insights that will be beneficial for graft and patient survival.
- 'Memory and molecular turnover,' 30 years after inception. [Journal Article, Review]
- Epigenetics Chromatin 2014; 7(1):37.
In 1984 Sir Francis Crick hypothesized that memory is recorded in the brain as reversible modifications to DNA and protein, but acknowledged that most biomolecules turn over too rapidly to account for long-term memories. To accommodate this possible paradox he modeled an enzymatic mechanism to maintain modifications on hemi-modified multimeric symmetrical molecules. While studies on the turnover of chromatin modifications that may be involved in memory are in their infancy, an exploration of his model in the light of modern epigenetics produced somewhat surprising results. The molecular turnover rates for two classes of chromatin modifications believed to record and store durable memories were approximated from experiments using diverse approaches and were found to be remarkably short. The half-lives of DNA cytosine methylation and post-translationally modified nucleosomal histones are measured in hours and minutes, respectively, for a subset of sites on chromatin controlling gene expression. It appears likely that the turnover of DNA methylation in the brain and in neurons, in particular, is even more rapid than in other cell types and organs, perhaps accommodating neuronal plasticity, learning, and memory. The machinery responsible for the rapid turnover of DNA methylation and nucleosomal histone modifications is highly complex, partially redundant, and appears to act in a sequence specific manner. Molecular symmetry plays an important part in maintaining site-specific turnover, but its particular role in memory maintenance is unknown. Elucidating Crick's paradox, the contradiction between rapid molecular turnover of modified biomolecules and long-term memory storage, appears fundamental to understanding cognitive function and neurodegenerative disease.
- The Yerkes-Dodson law and appropriate stimuli for conditioned taste aversion in Lymnaea. [JOURNAL ARTICLE]
- J Exp Biol 2014 Dec 18.
The pond snail Lymnaea stagnalis can learn conditioned taste aversion and then consolidate it into long-term memory (LTM). A high voltage electric shock was used as the unconditioned stimulus (US), whereas we previously used KCl. We varied both the strength of the conditioned stimulus (CS) and US to determine if the so-called Yerkes-Dodson law prevailed. This is an empirical relationship between the state of arousal and LTM formation, showing that there is an optimal level of arousal leading to memory formation. However, too little or too much arousal results in poorer LTM. We found here that the most appropriate stimuli to use in taste aversion training in Lymnaea were a 10 mmol l(-1) sucrose solution as the CS and a 3-s electric shock as the US.
- Andrographolide reduces cognitive impairment in young and mature AbetaPPswe/PS-1 mice. [JOURNAL ARTICLE]
- Mol Neurodegener 2014 Dec 18; 9(1):61.
Alzheimer's disease (AD) is a neurodegenerative disorder in which the amyloid-beta (Abeta) oligomers are a key factor in synaptic impairment and in spatial memory decline associated with neuronal dysfunction. This impairment includes synaptic failure associated with the loss of synaptic proteins that contribute to AD progression. Interestingly, the use of natural compounds is an emergent conceptual strategy in the search for drugs with therapeutic potentials for treating neurodegenerative disorders. In the present study, we report that andrographolide (ANDRO), which is a labdane diterpene extracted from Andrographis paniculata, increases slope of field excitatory postsynaptic potentials (fEPSP) in the CA1 region of hippocampal slices and inhibits long-term depression (LTD), protecting the long-term potentiation (LTP) against the damage induced by Abeta oligomers in vitro, most likely by inhibiting glycogen synthase kinase-3beta (GSK-3beta). Additionally, ANDRO prevents changes in neuropathology in two different age groups (7- and 12-month-old mice) of an AbetaPPswe/PS-1 Alzheimer's model. ANDRO reduces the Abeta levels, changing the ontogeny of amyloid plaques in hippocampi and cortices in 7-month-old mice, and reduces tau phosphorylation around the Abeta oligomeric species in both age groups. Additionally, we observed that ANDRO recovers spatial memory functions that correlate with protecting synaptic plasticity and synaptic proteins in two different age groups. Our results suggest that ANDRO could be used in a potential preventive therapy during AD progression.
- A simplified memory network model based on pattern formations. [JOURNAL ARTICLE]
- Sci Rep 2014.:7568.
Many experiments have evidenced the transition with different time scales from short-term memory (STM) to long-term memory (LTM) in mammalian brains, while its theoretical understanding is still under debate. To understand its underlying mechanism, it has recently been shown that it is possible to have a long-period rhythmic synchronous firing in a scale-free network, provided the existence of both the high-degree hubs and the loops formed by low-degree nodes. We here present a simplified memory network model to show that the self-sustained synchronous firing can be observed even without these two necessary conditions. This simplified network consists of two loops of coupled excitable neurons with different synaptic conductance and with one node being the sensory neuron to receive an external stimulus signal. This model can be further used to show how the diversity of firing patterns can be selectively formed by varying the signal frequency, duration of the stimulus and network topology, which corresponds to the patterns of STM and LTM with different time scales. A theoretical analysis is presented to explain the underlying mechanism of firing patterns.
- Effect of the multimodal acting antidepressant vortioxetine on rat hippocampal plasticity and recognition memory. [JOURNAL ARTICLE]
- Prog Neuropsychopharmacol Biol Psychiatry 2014 Dec 15.
Depression is frequently associated with cognitive disturbances. Vortioxetine is a multimodal acting antidepressant that functions as a 5-HT3 and 5-HT7 and 5-HT1D receptor antagonist, 5-HT1B receptor partial agonist, 5-HT1A receptor agonist and inhibitor of the 5-HT transporter. Given its pharmacological profile, the present study was undertaken to determine whether vortioxetine could modulate several preclinical parameters known to be involved in cognitive processing. In the dorsal hippocampus of anaesthetized rats, high frequency stimulation of the Schaffer collaterals provoked a stable long term potentiation (LTP) of ~25%. Interestingly, vortioxetine (10mg/kg, i.p.) counteracted the suppressant effect of elevated platform stress on hippocampal LTP induction. In the novel object recognition test, vortioxetine (10mg/kg, i.p.) increased the time spent exploring the novel object during the retention test and this pro-cognitive effect was prevented by the partial 5-HT3 receptor agonist SR57227 (1mg/kg, i.p.). Finally, compared to fluoxetine, sustained administration of vortioxetine (5mg/kg/day, s.c.) induced a rapid increase of cell proliferation in the hippocampal dentate gyrus. In summary, vortioxetine prevented the effect of stress on hippocampal LTP, increased rapidly hippocampal cell proliferation and enhanced short-term episodic memory, via, at least in part, its 5-HT3 receptor antagonism. Taken together, these preclinical data suggest that the antidepressant vortioxetine may have a beneficial effect on human cognitive processes.
- [Neurocognitive and psychiatric management of the 22q11.2 deletion syndrome.] [JOURNAL ARTICLE]
- Encephale 2014 Dec 15.
The 22q11.2 deletion syndrome (22q11.2DS) is caused by hemizygous microdeletions on chromosome 22. 22q11.2DS has several presentations including Di George's syndrome, velo-cardio-facial syndrome or Shprintzen's syndrome and it is the most frequent microdeletion syndrome in the general population (prevalence estimated at 1/4000 births, de novo: 90%). The inheritance of the syndrome (10%) is autosomal dominant. Most people with 22q11.2DS are missing a sequence of about 3 million DNA building blocks (base pairs) on one copy of chromosome 22 in each cell. A small percentage of affected individuals have shorter deletions in the same region (contiguous gene deletion syndrome). The general features of 22q11.2DS vary widely (more than 180 phenotypic presentations) and the syndrome is under diagnosed. Characteristic symptoms may include congenital heart disease, defects in the palate, neuromuscular problems, velo-pharyngeal insufficiency, hypoparathyroidism, craniofacial features and problems with the immune system T-cell mediated response (caused by hypoplasia of the thymus).The neurocognitive phenotype of the 22q11.2DS is complex. Cognitive deficits are seen in the majority (80-100%) of individuals with 22q11DS with impairments in sustained attention, executive function, memory and visual-spatial perception. Borderline intellectual function (IQ: 70-75) is most common, mild intellectual disability (IQ: 55-75) is slightly less frequent and a small percentage of children fall into the low average intelligence range. Most children with 22q11.2DS achieve higher scores in verbal tasks than in non-verbal tasks, although this pattern of dysfunction being not universal. Brain MRI studies have shown volumetric changes in multiple cortical and subcortical regions in individuals with 22q11DS that could be related to both cognition and psychoses.General psychiatric features included anxiety disorders, attention deficit disorder and poor social skills (40-50%). An elevated risk of bipolar disorder and major depression occurs in adolescence and young adulthood. A strong and specific relationship exists between the presence of the 22q11.2 microdeletion and schizophrenia (30-40%). This risk is not associated with any other neurogenetic syndrome. Social cognition is impaired in 22q11.2 DS and this observation is correlated with psychotic features. So, long-term medical care is increasingly being directed towards the treatment and recognition of these symptoms.Required pharmacological treatment strategies have to be adapted to the syndrome. Moreover, cognitive remediation is a promising tool for treating neuro- and social cognitive deficits in 22q11.2DS. However, these new therapeutic strategies have to be developed to improve quality of life.
- Stimulation of phosphorylation of ERK and CREB by phellopterin and auraptene isolated from Citrusjunos. [Journal Article, Research Support, Non-U.S. Gov't]
- Nat Prod Commun 2014 Oct; 9(10):1491-4.
Bioactive compounds from citrus fruits contribute many benefits to human health. Extracellular signal-regulated kinase (ERK) signaling plays an important role in the regulation of multiple cellular processes. Activation of the ERK-cAMP response element binding protein (CREB) signaling is required for long- term memory formation. In this study, auraptene, phellopterin, thymol, coniferyl alcohol 9-methyl ether and methyl ferulate were isolated from Citrus junos. Among the five compounds isolated, auraptene and phellopterin increased the phosphorylation of ERK and CREB. This study provides, to our knowledge, the first evidence that phellopterin potently stimulates the phosphorylation of ERK and CREB. Phellopterin could be a novel neuroprotective agent.
- Learning induces sonic hedgehog signaling in the amygdala which promotes neurogenesis and long-term memory formation. [JOURNAL ARTICLE]
- Int J Neuropsychopharmacol 2014 Dec 13.
It is known that neurogenesis occurs throughout the life mostly in the subgranular zone (SGZ) of the hippocampus and the subventricular zone (SVZ) of the lateral ventricle. We investigated whether neurogenesis occurred in the amygdala and its function in fear memory formation. For detection of newborn neurons, mice were injected intraperitoneally with 5-bromo-2'-deoxyuridine (BrdU) 2 h before receiving 15 tone-footshock pairings and newborn neurons were analyzed 14 and 42 days after training. To determine the relationship between neurogenesis and memory formation, mice were given a proliferation inhibitor methylazoxymethanol (MAM) or a DNA synthesis inhibitor cytosine arabinoside (Ara-C). To test whether Sonic hedgehog (Shh) signaling was required for neurogenesis, Shh-shRNA was inserted into a retroviral vector (Retro-Shh-shRNA). The number of BrdU(+)/NeuN(+) cells was significantly higher in the conditioned mice suggesting that association of tone with footshock induced neurogenesis. MAM and Ara-C markedly reduced neurogenesis and impaired fear memory formation. Sonic hedgehog (Shh), its receptor patched1 (Ptc1) and transcription factor Gli1 protein levels increased at 1 day and returned to baseline at 7 days after fear conditioning. Retro-Shh-shRNA which knocked down Shh specifically in the mitotic neurons reduced the number of BrdU(+)/NeuN(+) cells and decreased freezing responses. These results suggest that fear learning induces Shh signaling activation in the amygdala which promotes neurogenesis and fear memory formation.