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Plasticity Mechanisms (plasticity + mechanism)
Selected AbstractsDevelopment of tinnitus-related neuronal hyperactivity through homeostatic plasticity after hearing loss: a computational modelEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2006Roland Schaette Tinnitus, the perception of a sound in the absence of acoustic stimulation, is often associated with hearing loss. Animal studies indicate that hearing loss through cochlear damage can lead to behavioral signs of tinnitus that are correlated with pathologically increased spontaneous firing rates, or hyperactivity, of neurons in the auditory pathway. Mechanisms that lead to the development of this hyperactivity, however, have remained unclear. We address this question by using a computational model of auditory nerve fibers and downstream auditory neurons. The key idea is that mean firing rates of these neurons are stabilized through a homeostatic plasticity mechanism. This homeostatic compensation can give rise to hyperactivity in the model neurons if the healthy ratio between mean and spontaneous firing rate of the auditory nerve is decreased, for example through a loss of outer hair cells or damage to hair cell stereocilia. Homeostasis can also amplify non-auditory inputs, which then contribute to hyperactivity. Our computational model predicts how appropriate additional acoustic stimulation can reverse the development of such hyperactivity, which could provide a new basis for treatment strategies. [source] Dopamine gating of forebrain neural ensemblesEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2003Patricio O'Donnell Abstract Dopamine may exert different actions depending on a number of factors. A common view is that D1 receptors may be responsible for excitatory actions whereas D2 receptors are involved in inhibitory actions. However, this position cannot be reconciled with several findings indicating otherwise. The role of dopamine on forebrain neural ensembles may be better understood in the light of functional states of the system. Pyramidal cortical neurons and striatal medium spiny neurons alternate between two membrane potential states (,up' and ,down') that could shape dopamine actions. It is proposed that D1 receptors can act as state-stabilizers by sustaining up states and thereby facilitating plasticity mechanisms by providing postsynaptic depolarization and increasing NMDA function. In this way, dopamine can sustain activity in depolarized units. This action is accompanied by a decrease in cell firing (perhaps mediated by D2 receptors), which renders the cells responsive only to strong stimuli. The result would be a net increase in signal-to-noise ratio in a selected assembly of neurons. [source] Late postnatal maturation of excitatory synaptic transmission permits adult-like expression of hippocampal-dependent behaviorsHIPPOCAMPUS, Issue 5 2005Theodore C. Dumas Abstract Sensorimotor systems in altricial animals mature incrementally during early postnatal development, with complex cognitive abilities developing late. Of prominence are cognitive processes that depend on an intact hippocampus, such as contextual,configural learning, allocentric and idiocentric navigation, and certain forms of trace conditioning. The mechanisms that regulate the delayed maturation of the hippocampus are not well understood. However, there is support for the idea that these behaviors come "on line" with the final maturation of excitatory synaptic transmission. First, by providing a timeline for the first behavioral expression of various forms of learning and memory, this study illustrates the late maturation of hippocampal-dependent cognitive abilities. Then, functional development of the hippocampus is reviewed to establish the temporal relationship between maturation of excitatory synaptic transmission and the behavioral evidence of adult-like hippocampal processing. These data suggest that, in rats, mechanisms necessary for the expression of adult-like synaptic plasticity become available at around 2 postnatal weeks of age. However, presynaptic plasticity mechanisms, likely necessary for refinement of the hippocampal network, predominate and impede information processing until the third postnatal week. © 2005 Wiley-Liss, Inc. [source] Co-regulation of ocular dominance plasticity and NMDA receptor subunit expression in glutamic acid decarboxylase-65 knock-out miceTHE JOURNAL OF PHYSIOLOGY, Issue 12 2009Patrick O. Kanold Experience can shape cortical circuits, especially during critical periods for plasticity. In visual cortex, imbalance of activity from the two eyes during the critical period shifts ocular dominance (OD) towards the more active eye. Inhibitory circuits are crucial in this process: OD plasticity is absent in GAD65KO mice that show diminished inhibition. This defect can be rescued by application of benzodiazepines, which increase GABAergic signalling. However, it is unknown how such changes in inhibition might disrupt and then restore OD plasticity. Since NMDA dependent synaptic plasticity mechanisms are also known to contribute to OD plasticity, we investigated whether NMDA receptor levels and function are also altered in GAD65KO. There are reduced NR2A levels and slower NMDA currents in visual cortex of GAD65KO mice. Application of benzodiazepines, which rescues OD plasticity, also increases NR2A levels. Thus it appears as if OD plasticity can be restored by adding a critical amount of excitatory transmission through NR2A-containing NMDA receptors. Together, these observations can unify competing ideas of how OD plasticity is regulated: changes in either inhibition or excitation would engage homeostatic mechanisms that converge to regulate NMDA receptors, thereby enabling plasticity mechanisms and also ensuring circuit stability. [source] | ||||||||||