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Synaptic clustering influences synaptic efficacy by increasing cooperative interactions among neighboring synaptic inputs, however, the mechanism of synaptm clustrring is unknown. We found that in hippocampal neurons in culture synaptic clustering as well as synaptic strength increase at the point of intersection between dendrites compared to other areas along the dendrites. The clustering in the intersection increases linearly and the strengthening exponentially with an increase in the number<span class="external-identifiers"> <a target="_blank" rel="external noopener noreferrer" href="https://doi.org/10.1155/np.2002.65">doi:10.1155/np.2002.65</a> <a target="_blank" rel="external noopener" href="https://www.ncbi.nlm.nih.gov/pubmed/12516548">pmid:12516548</a> <a target="_blank" rel="external noopener" href="https://pubmed.ncbi.nlm.nih.gov/PMC2565399/">pmcid:PMC2565399</a> <a target="_blank" rel="external noopener" href="https://fatcat.wiki/release/6o7uzh2mtfawdao4mzwue32m2y">fatcat:6o7uzh2mtfawdao4mzwue32m2y</a> </span>
more »... f dendrites crossing the intersection. Intersections containing multiple dendrites are frequent (4 times more than in computer simulations of randomly distributed dendrites) and are formed by direct growth of dendrites toward pre-existing dendritic intersections. This process is disrupted by inhibitors of synaptic activity and of glutamate receptors. Thus, an activity-dependent mechanism exists that causes dendrites to converge to a single intersection, resulting in an increase in synaptm clustering and synaptie activity at the intersection. This may se.rve as a mechanism for activity-dependent pre-.synaptie plasticity. In addition to converging, dendrites in the culture tend to grow in parallel, even when separated over large distances, leiding to formation of areas where specific dendritic orientations are dominant. This order restricts the location of the dendritic intersections and their synaptie dusters. Thus, directed convergence combined with parallel growth of dendrites shapes the synaptie map in cultured neuronal networks. Background: Difficulties in writing is a common complaint amoffg children with attention deficit hyperactivity disorder (ADHD). Objec..ave: To examine whether the problem is one of dysgraphia or attentional problems masquarading as dysgraphia. Meihods: Possible sources of writing difficulty tested Were: "lingual", associated with reading and expressed mainly in spelling mistakes, "peripheral motor-output" designated as the_ orthographic buffer and expressed in omission or repetition of strokes While writing and "attention deficit" expressed as _consistence in production in all domains of graphic production. Participants underwent an extensive reading/writing assessment (Shani & Ben-Dror Pivotal Test, 2000), and a set of lingual and peripheral agraphia tests using a digitizing tablet. General kinematic performance in graphic production was assessed using a 30 sec. repetitious tracing of an ellipse. Participana.': Twelve boys with ADHD, aged 11-13 years (unmedicated for at least 1.week) and controls matched for gender, age I.Q, handedness and socio-economic class. Children were eligi'ble to participate if their IQ was > 85, and had no known reading difficulty. ADHD children and controls did not differ significantly in reading scores or in the speed of letter naming. Results: Lihgual: ADHD children spelling scores were significantly lower than controls in most spelling tests. Motor-peripheral: ADHD children had si.gnifieantly more stroke ormssion/repetition errors than controls when writing repetitiously similar-letter words. Atention deficits: ADHD children were significantly less consistent than controls in a repetitious tracing of an ellipse. One of the digitized tasks was circle drawing, once as a letter, once as a humber, and once as an eye. Duration of writing/drawing did not differ between groups, but variance of duration over repetitions was larger for ADHD children, especially in the Written-letters task. Cbnclusions: Children with ADHD demonstrated deficits in the lingual and peripheral domains of writing as well as attention deficits in the graphic domain. Although ADHD children were less consistent than controls on graphm tests, for Abstracts of the 11 th Annual Meeting of the Israel Society for Neuroscience Eilat, Israel, December 15 17, 2002 very simple tasks this was significant for writing but not drawing. We conclude that children with ADHD have a true dysgraphia that is exacerbated by the attention deficits. Background: Error detection is known to be impaired in Schizophrenia, but less is known about error-correction. Objectives: To examine error-correcting activity and correction of brrors in the verbal and motor domain in these patients. Methods: The neurocognitve process of error monitoring and error-correction in schizophrenic patients was examined by using the verbal and handwritten version of the color-naming Stroop task. Eighteen medicated open-ward Schizophrenic patients and controls, matched for gender, h, andedness, age and education, were asked to 'name the color and to 'write the color' in two blocks of 24 randomly ordered congruent, incongruent and neutral stimuli. The timing of error correction, if occurred, was recorded in both modalities. In the handwritten version of the task, a digitized tablet recorded spatial and kinematic data. Results: Error correction activi of schizophrenic patients depends on the modality (verbal/written): The propoRion of corrected errors in the verbal domain for patients and controls was similar whereas the handwritten version shows marked differences between the two groups. The corrected handwritten responses in schizophrenic patients persisted significantly longer and appearing at later stages of words. Clinical positive and negative symptoms analyss shows that higher positive symptoms correlate with longer response duration, less accuracy and higher variability in both modalities. Anxiety and poor attention are correlated with less accuracy in handwritten responses (all r's >.4). Conclusions: Error correcting activity in Schizophrenia differs between modalities. We hypnotize that the difference between speech and writing feedback processes results in different correcting activity. For handwriting we found an ever-lasting correction. This suggests that in schizophrenia there is a continuous burdened on the thought process by it inability to conclude, especially in the motor domain. We relate these results also to the differentiated function of the anterior cingulated cortex in the verbal and motor domain. Basolateral amygdala (BLA) activation by emotional arousal modulates memory-related processes in the hippoeampus. We have shown (Aldrav and Richter-Levin, dNeurosci 19:10530-5 ) that activating the BLA prior to perforant path (PP) tetanization has a bi-phasie effect on hippocampal plasticity; priming the BLA immediately before PP tetanization results m the, enfianeement of dentate gyrus (DG)-LTP (an 'emotional tag ), whereas stimulation in a spaced interval results in the suppression of DG-LTP. Here, we aimed to elucidate the mechanisms underlying BLA modulation of DG-LTP and specifically to examme whether the stress hormones norepinephrine (NE) and corticosterone (CORT) are main medmtors of the BLA bi-phasic effects. We found that the BLA affects hippoeampal plasticity in a complex manner; BLA priming enhanced DG:LTP, and both NE and CORT mediated this effect. Furthermore, we found that ipsilateral BLA spaced activation (2hrs prior to PP tetanization) suppressed DG-LTP, and that this suppressive effect was also mediated by NE and CORT. Priming the contralateral BLA enhanced DG-LTP similarly to the ipsilateral enhancement, but neither NE nor CORT mediated this effect. The spaced activation of the contralateral BLA did not suppress DG-LTP. Thus differential mechanisms underlie the ipsilateral and eontralateral BLA effects on hippocampal plasticity. 66 The BLA modulates hippocampal memory processes, presumably via the mediation of the stress hormones NE and CORT, to establish a diverse memory of the experience. Possibly, at the onset of an emotional event the stress hormones permissively mediate plasticity. However, their prolonged presence in the system may suppress the cognitive response to stress. Changes in sleep-wake patterns appear to be one of the hallmarks of biological aging. Elderly persons complain of da_ime drowsiness and difficulties in initiating and maintaining sleep. Likewise, aging has a clear effect on learning and memory processes. However, the interaction between sleep disturbances and memory among elderly people remains unclear. This study aims to assess whether insomnia is associated with memory decline in the elderly. Seventy-three elderly (45 males and 28 females) aged 65-80 (70.4+/-5.9 years) Who were living independently in the community participated in this study. Sleep was assessed using Mini Sleep Questionnaire, and memory processes were evaluated via the Rey Auditory Verbal Learning Test. Twenty-three of the 73 subjects (32%) had nsomnia index greater than 4 in sub-scale of insomnia, indicating insomnia. Performance of the two groups (insomniacs and good sleepers) in the Rey AVLT was compared in order to assess the relationships between insomnia and memory. Generally, the results demonstrated that in almost all categories of episodic memory elderly people who do not have sleep disorders displayed better performance results compared to insonmiacs. More spe.cifically, results revealed siggificant differences between nsomniacs and good sleepers n learning, and in resistance to proactive interference, and close to significant in temporal memory. These findings suggest that insomnia is significantly associated with some aspects of memory decline in the elderly. These aspects include learning, resistance to proactive interference, and temporal memory.
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