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Association Learning (association + learning)
Selected AbstractsOlfactory association learning and brain-derived neurotrophic factor in an animal model of early deprivationDEVELOPMENTAL PSYCHOBIOLOGY, Issue 4 2009Betty Zimmerberg Abstract Animal models can serve to explore neural mechanisms underlying the effects of stressful early experiences on behaviors supporting attachment. Neonatal rats primarily use olfaction for attachment, and Brain-Derived Neurotrophic Factor (BDNF) may be a key transcription target in olfactory association learning. In this experiment, neonatal male and female rats were isolated individually for 3 hr daily in the first week of life while their dams were left with partial litters (Early Deprivation, ED) or remained undisturbed (Control). At 1 week of age, subjects were tested using a 2-day classical conditioning paradigm. The conditioned group (O/M) was exposed to a novel odor paired with a milk infusion. Three additional groups included an unpaired odor and milk exposure group (O/M unP), an odor exposure alone group (O/NM), and neither an odor nor a milk group (NO/NM). Learning the odor association, as revealed in a position preference for the novel odor, was accompanied by an increase in hippocampal BDNF in O/M subjects from undisturbed Control litters. BDNF levels were also positively related to degree of preference for the odor in the O/M Control group. ED subjects did not make the classically conditioned odor association and did not show an increase in hippocampal BDNF. ED increased BDNF levels in the olfactory bulb compared to Controls regardless of training group; individual levels were not correlated with performance because samples were pooled. These results suggest that changes in the transcription of BDNF may underlie some of the long-term consequences of the early stress of maternal separation. © 2009 Wiley Periodicals, Inc. Dev Psychobiol 51: 333,344, 2009. [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] Neurobehavioral abnormalities in the dysbindin-1 mutant, sandy, on a C57BL/6J genetic backgroundGENES, BRAIN AND BEHAVIOR, Issue 4 2009M. M. Cox Sandy mice have a deletion mutation in the gene encoding dysbindin-1, Dtnbp1, with consequent reduction of the protein in heterozygotes and its loss in homozygotes. The sandy mouse thus serves as an animal model of dysbindin-1 function. As this protein is concentrated in synaptic tissue and affects transmitter release, it may affect neuronal processes that mediate behavior. To investigate the neurobehavioral effects of the Dtnbp1 mutation, we studied littermate sandy and wild-type controls on a C57BL/6J genetic background. The three animal groups were indistinguishable in their external physical characteristics, sensorimotor skills and indices of anxiety-like behaviors. In the open field, however, homozygous animals were hyperactive and appeared to show less habituation to the initially novel environment. In the Morris water maze, homozygous animals displayed clear deficits in spatial learning and memory with marginal deficits in visual association learning. Apart from the last mentioned deficits, these abnormalities are consistent with hippocampal dysfunction and in some cases with elevated dopaminergic transmission via D2 dopamine receptors. As similar deficits in spatial learning and memory have been found in schizophrenia, where decreased dysbindin-1 has been found in the hippocampus, the sandy mouse may also model certain aspects of cognition and behavior relevant to schizophrenia. [source] Specific reading disability (dyslexia): what have we learned in the past four decades?THE JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES, Issue 1 2004Frank R. Vellutino We summarize some of the most important findings from research evaluating the hypothesized causes of specific reading disability (,dyslexia') over the past four decades. After outlining components of reading ability, we discuss manifest causes of reading difficulties, in terms of deficiencies in component reading skills that might lead to such difficulties. The evidence suggests that inadequate facility in word identification due, in most cases, to more basic deficits in alphabetic coding is the basic cause of difficulties in learning to read. We next discuss hypothesized deficiencies in reading-related cognitive abilities as underlying causes of deficiencies in component reading skills. The evidence in these areas suggests that, in most cases, phonological skills deficiencies associated with phonological coding deficits are the probable causes of the disorder rather than visual, semantic, or syntactic deficits, although reading difficulties in some children may be associated with general language deficits. Hypothesized deficits in general learning abilities (e.g., attention, association learning, cross-modal transfer etc.) and low-level sensory deficits have weak validity as causal factors in specific reading disability. These inferences are, by and large, supported by research evaluating the biological foundations of dyslexia. Finally, evidence is presented in support of the idea that many poor readers are impaired because of inadequate instruction or other experiential factors. This does not mean that biological factors are not relevant, because the brain and environment interact to produce the neural networks that support reading acquisition. We conclude with a discussion of the clinical implications of the research findings, focusing on the need for enhanced instruction. [source] Symbolic Versus Associative LearningCOGNITIVE SCIENCE - A MULTIDISCIPLINARY JOURNAL, Issue 6 2010John E. Hummel Abstract Ramscar and colleagues (2010, this volume) describe the "feature-label-order" (FLO) effect on category learning and characterize it as a constraint on symbolic learning. I argue that FLO is neither a constraint on symbolic learning in the sense of "learning elements of a symbol system" (instead, it is an effect on nonsymbolic, association learning) nor is it, more than any other constraint on category learning, a constraint on symbolic learning in the sense of "solving the symbol grounding problem." [source] | ||||||||||