Home About us Contact
|
Home About us Contact | ||
|
|
||
Learning Impairment (learning + impairment)
Selected AbstractsAGE-RELATED SYNAPTIC CHANGES IN THE CA1 STRATUM RADIATUM AND SPATIAL LEARNING IMPAIRMENT IN RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 7 2009Li-Hong Long SUMMARY 1Age-related impairments in hippocampus-dependent spatial learning and memory are not associated with a loss of neurons, but may be related to synaptic changes. In the present study, we analysed the behavioural performance of adult, middle-aged and old Wistar rats using the Morris water maze, as well as the structure of synapses and the expression of autophosphorylated Ca2+/calmodulin-dependent protein kinase II at threonine 286 (pThr286-,CaMKII), a key post-synaptic protein in the CA1 stratum radiatum, in the same rats. 2Old Wistar rats showed significant cognitive deficits. Synaptic density, the area of post-synaptic densities and the total number of synapses in the CA1 stratum radiatum of old rats were significantly decreased compared with adult rats. The decrease in autophosphorylated pThr286-,CaMKII was age dependent. 3These findings reveal that age-related impairments in learning and memory are associated with synaptic atrophy. The decreased expression of pThr286-CaMKII may result in reduced synaptic function with ageing. [source] Impairment of eyeblink conditioning in GluR,2-mutant mice depends on the temporal overlap between conditioned and unconditioned stimuliEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 9 2001Yasushi Kishimoto Abstract Mice lacking the glutamate receptor subunit ,2 (GluR,2) are deficient in cerebellar long-term depression (LTD) at the parallel fibre,Purkinje cell synapses. We conducted delay and trace eyeblink conditioning with these mice, using various temporal intervals between the conditioned stimulus (CS) and unconditioned stimulus (US). During trace conditioning in which a stimulus-free trace interval (TI) of 250, 100 or 50 ms intervened between the 352-ms tone CS and 100-ms US, GluR,2-mutant mice learned as successfully as wild-type mice. Even in the paradigm with TI = 0 ms, in which the end of CS and onset of US are simultaneous, there was no difference between the GluR,2-mutant and wild-type mice in their acquisition of a conditioned response. However, in the delay paradigm in which the 452-ms CS overlapped temporally with the coterminating 100-ms US, GluR,2-mutant mice exhibited severe learning impairment. The present study together with our previous work [Kishimoto, Y., Kawahara, S., Suzuki, M., Mori, H., Mishina, M. & Kirino, Y. (2001) Eur. J. Neurosci.,13, 1249,1254], indicates that cerebellar LTD-independent learning is possible in paradigms without temporal overlap between the CS and US. On the other hand, GluR,2 and cerebellar LTD are essential for learning when there is CS,US temporal overlap, suggesting that the cerebellar neural substrates underlying eyeblink conditioning may change, depending on the temporal overlap of the CS and US. [source] Clinical and Magnetic Resonance Imaging Regression of Progressive Multifocal Leukoencephalopathy in an AIDS Patient After Intensive Antiretroviral TherapyJOURNAL OF NEUROIMAGING, Issue 3 2001Rita A. Shapiro DO ABSTRACT A 36-year-old homosexual man with 6 months of visual symptoms and headaches had right homonymous hemianopia, mild new learning impairment, and alexia with agraphia. The initial brain magnetic resonance imaging (MRI) scan was reported consistent with left occipital infarction. Subsequent MRI demonstrated abnormal demyelination in the subcortical white matter and deep parieto-occipital white matter bilaterally, but primarily left. Human immunodeficiency virus testing and cerebrospinal fluid polymerase chain reaction for JC virus DNA were both positive, consistent with progressive multifocal leukoencephalopathy (PML) with AIDS. His clinical status steadily deteriorated, and MRI white matter abnormalities worsened despite high-dose antiretroviral therapy. After the antiretroviral regimen was intensified by the addition of a protease inhibitor, rapid clinical and radiographic improvement occurred with subsequent MRI studies revealing only residual left parieto-occipital encephalomalacia. PML in AIDS patients has been associated with a nearly uniformly poor prognosis until recent reports of improved outcomes after highly active antiretroviral therapy. This patient with PML and AIDS similarly showed a robust clinical and MRI response to intensive antiretroviral combination therapy, which has been maintained for more than 3 years. [source] Fustin flavonoid attenuates ,-amyloid (1,42)-induced learning impairmentJOURNAL OF NEUROSCIENCE RESEARCH, Issue 16 2009Chun-Hui Jin Abstract Natural flavonoids ameliorate amyloid-, peptide (A,)-induced neurotoxicity. We examined whether the fustin flavonoid affects A,-induced learning impairment in mice. Repeated treatment with fustin significantly attenuated A, (1,42)-induced conditioned fear and passive avoidance behaviors. This effect was comparable to that of EGb761, a standard extract of ginkgo. Fustin treatment significantly prevented decreases in acetylcholine (ACh) levels, choline acetyltransferase (ChAT) activity, and ChAT gene expression induced by A, (1,42). Fustin also consistently suppressed increases in acetyl cholinesterase (AChE) activity and AChE gene expression induced by A, (1,42). In addition, fustin significantly attenuated A, (1,42)-induced selective decreases in muscarinic M1 receptor gene expression and muscarinic M1 receptor binding activity (as determined by [3H]pirenzepine binding) by modulating extracellular signal-regulated kinase 1/2 (ERK 1/2) and cAMP response-element binding protein (CREB) phosphorylation and brain-derived neurotrophic factor (BDNF) expression. These effects of fustin were reversed by treatment with dicyclomine, a muscarinic M1 receptor antagonist, and SL327, a selective ERK inhibitor, but not by chelerythrine, a pan-protein kinase C (PKC) inhibitor. Taken together, our results suggest that fustin attenuates A, (1,42)-impaired learning, and that the ERK/CREB/BDNF pathway is important for the M1 receptor-mediated cognition-enhancing effects of fustin. © 2009 Wiley-Liss, Inc. [source] Intake of Maillard reaction products reduces iron bioavailability in male adolescentsMOLECULAR NUTRITION & FOOD RESEARCH (FORMERLY NAHRUNG/FOOD), Issue 12 2009Marta Mesías García Abstract The effects of diets with different Maillard reaction products (MRPs) content on biological iron utilization were compared using in vitro/in vivo assays. Diets were rich (brown diet, BD) or poor (white diet) in MRP. In vitro studies included iron solubility after in vitro digestion of diets and iron transport across Caco-2 cells. In the human assay 18 healthy adolescent males (11,14 years) participated in a 2-wk randomized two-period crossover trial. Subjects collected urine and faeces on the last 3 days of each dietary period, and fasting blood samples were obtained after periods. In vitro dietary iron availability was significantly lower with the BD than the white diet (9.52 and 12.92%, respectively), as a consequence of the lower iron solubility after the in vitro digestion, but not as a result of decreased transport of the remaining soluble iron. The BD consumption increased iron fecal excretion (,1.4-fold) and significantly decreased its bioavailability (,2.7-fold), mainly due to the effects found at digestive level. Serum biochemical parameters related to iron metabolism remained unaltered. It is concluded the presence of MRP in the diet negatively affects iron bioavailability. As iron deficiency may be related to learning impairment and to reductions of cognitive and physical functions, possible long-term effects of excessive MRP intake during adolescence warrant attention. [source] Open-field Behaviors and Water-maze Learning in the F Substrain of Ihara Epileptic RatsEPILEPSIA, Issue 1 2006Yoko Okaichi Summary:,Purpose: Genetically epileptic model rats, Ihara epileptic rat (IER/F substrain), have neuropathologic abnormalities and develop generalized convulsive seizures when they reach the age of ,5 months. Because the neuromorphologic abnormalities are centered in the hippocampus, we expected to observe spatial cognitive deficits. The present study aimed to evaluate emotionality and learning ability of the F substrain of IER. Methods: To determine whether deficits are caused by inborn neuropathologic abnormalities or by repeated generalized convulsions, we tested nine 6- to 12-week-old IER/F rats that had not yet experienced seizures (experiment 1) and nine 7- to 9-month-old IER/F rats that had repeatedly experienced seizures (experiment 2) with identical tasks: an open-field test and the Morris water-maze place and cue tasks. Results: Both groups of IER/Fs showed behaviors that were different from those of control rats in the open-field test, and extensive learning impairments were seen in both the place task, which requires spatial cognition, and the cue task, which does not require spatial cognition but requires simple association learning. Their impaired performance of the cue task indicates that their deficiency was not limited to spatial cognition. Conclusions: Because young IER/F rats without seizure experiences also showed severe learning impairments, genetically programmed microdysgenesis in the hippocampus was suspected as a cause of the severe learning deficits of IER/Fs. [source] Environmental enrichment reverses cognitive and molecular deficits induced by developmental lead exposureANNALS OF NEUROLOGY, Issue 1 2003Tomás R. Guilarte PhD Long-term deficits in cognitive function are the principal effects of lead (Pb2+) exposure in children and can be modeled in experimental animals. Current therapeutic approaches in the treatment of childhood Pb2+ intoxication are not effective in reversing learning deficits once they have occurred. We report that environmental enrichment reverses long-term deficits in spatial learning produced by developmental Pb2+ exposure in rats. Enhanced learning performance of Pb2+ -exposed animals reared in an enriched environment was associated with recovery of deficits in N- methyl- D -aspartate receptor subunit 1 (NR1) mRNA and induction of brain-derived neurotrophic factor (BDNF) mRNA in the hippocampus. The effect of environmental enrichment on NR1 and BDNF gene expression was specific to Pb2+ -exposed animals and was present in the absence of changes in the NR2B subunit of the N- methyl- D -aspartate receptor, GluR1, ,CamKII, or PSD-95 gene expression measured in the same animals. Our findings demonstrate that the learning impairments and NR1 subunit mRNA deficits resulting from developmental Pb2+ exposure are reversible if the animals are provided with an enriched environment even after the exposure has occurred. We propose environmental enrichment as a basis for the treatment of childhood Pb2+ intoxication. [source] Reward processing in autismAUTISM RESEARCH, Issue 2 2010Ashley A. Scott-Van Zeeland Abstract The social motivation hypothesis of autism posits that infants with autism do not experience social stimuli as rewarding, thereby leading to a cascade of potentially negative consequences for later development. While possible downstream effects of this hypothesis such as altered face and voice processing have been examined, there has not been a direct investigation of social reward processing in autism. Here we use functional magnetic resonance imaging to examine social and monetary rewarded implicit learning in children with and without autism spectrum disorders (ASD). Sixteen males with ASD and sixteen age- and IQ-matched typically developing (TD) males were scanned while performing two versions of a rewarded implicit learning task. In addition to examining responses to reward, we investigated the neural circuitry supporting rewarded learning and the relationship between these factors and social development. We found diminished neural responses to both social and monetary rewards in ASD, with a pronounced reduction in response to social rewards (SR). Children with ASD also demonstrated a further deficit in frontostriatal response during social, but not monetary, rewarded learning. Moreover, we show a relationship between ventral striatum activity and social reciprocity in TD children. Together, these data support the hypothesis that children with ASD have diminished neural responses to SR, and that this deficit relates to social learning impairments. [source] Motor-linked implicit learning in persons with autism spectrum disordersAUTISM RESEARCH, Issue 2 2010Brittany G. Travers Abstract Fifteen adolescents and young adults with high-functioning autism spectrum disorders (ASD) and 18 age- and IQ-matched adults with typical development (TD) completed a serial reaction time task (SRT) to examine possible motor-linked implicit learning impairments in persons with ASD. Measures were taken to decrease the role of explicit learning in the SRT. Results showed that participants with ASD demonstrated intact motor-linked implicit learning. Furthermore, the motor-linked implicit learning appeared to take place at a similar rate across trials in the group with ASD compared to the group with TD. These results suggest that persons with ASD are successful in implicit learning of motor-linked behavior. The results of this study, coupled with past findings, suggest that people with ASD may be able to learn motor movements without conscious awareness, especially if the individual is older and is learning fine motor sequences. [source] | |||||||||||||