A requirement for astrocyte IPR2 signaling for whisker experience-dependent depression and homeostatic upregulation in the mouse barrel cortex.

Changes to sensory experience result in plasticity of synapses in the cortex. This experience-dependent plasticity (EDP) is a fundamental property of the brain. Yet, while much is known about neuronal roles in EDP, very little is known about the role of astrocytes.

Time-course and mechanisms of homeostatic plasticity in layers 2/3 and 5 of the barrel cortex.

Recent studies have shown that ocular dominance plasticity in layer 2/3 of the visual cortex exhibits a form of homeostatic plasticity that is related to synaptic scaling and depends on TNFα. In this study, we tested whether a similar form of plasticity was present in layer 2/3 of the barrel cortex and, therefore, whether the mechanism was likely to be a general property of cortical neurons. We found that whisker deprivation could induce homeostatic plasticity in layer 2/3 of barrel cortex, but not in a mouse strain lacking synaptic scaling.

Astrocyte and Neuronal Plasticity in the Somatosensory System.

Changing the whisker complement on a rodent's snout can lead to two forms of experience-dependent plasticity (EDP) in the neurons of the barrel cortex, where whiskers are somatotopically represented. One form, termed coding plasticity, concerns changes in synaptic transmission and connectivity between neurons. This is thought to underlie learning and memory processes and so adaptation to a changing environment.

Stimulus intensity determines experience-dependent modifications in neocortical neuron firing rates.

Although subthreshold inputs of neocortical sensory neurons are broadly tuned, the spiking output is more restricted. These subthreshold inputs provide a substrate for stimulus intensity-dependent changes their spiking output, as well as for experience-dependent plasticity to alter firing properties. Here we investigated how different stimulus intensities modified the firing output of individual neurons in layer 2/3 of the mouse barrel cortex.

Experience-dependent plasticity acts via GluR1 and a novel neuronal nitric oxide synthase-dependent synaptic mechanism in adult cortex.

Synaptic plasticity directs development of the nervous system and is thought to underlie memory storage in adult animals. A great deal of our current understanding of the role of AMPA receptors in synaptic plasticity comes from studies on developing cortex and cell cultures. In the present study, we instead focus on plasticity in mature neurons in the neocortex of adult animals.

Parvalbumin-containing neurons, perineuronal nets and experience-dependent plasticity in murine barrel cortex.

The ability to undergo experience-dependent plasticity in the neocortex is often limited to early development, but also to particular cortical loci and specific experience. In layers II-IV of the barrel cortex, plasticity evoked by removing all but one vibrissae (univibrissa rearing) does not have a time limit except for layer IV barrels, where it can only be induced during the first postnatal week. In contrast, deprivation of every second vibrissa (chessboard deprivation) removes time limits for plasticity.

Rapid, learning-induced inhibitory synaptogenesis in murine barrel field.

The structure of neurons changes during development and in response to injury or alteration in sensory experience. Changes occur in the number, shape, and dimensions of dendritic spines together with their synapses. However, precise data on these changes in response to learning are sparse.

Reliable and precise neuronal firing during sensory plasticity in superficial layers of primary somatosensory cortex.

Neocortical neurons show astonishing variation in the presence and timing of action potentials across stimulus trials, a phenomenon whose function and significance has been the subject of great interest. Here we present data showing that this response variability can be significantly reduced by altered sensory experience. Removal of all but one whisker from the side of the mouse face results in the rapid (within 24 h) potentiation of mean firing rates within the cortical representation of the spared whisker in young postnatal animals (postnatal days 13-16).

Laminar analysis of the role of GluR1 in experience-dependent and synaptic depression in barrel cortex.

Several synaptic depression mechanisms have been described for the hippocampus, cerebellum and neocortex in vitro, but little is known about which, if any, are engaged during experience-dependent depression (EDD). We found that EDD in the mouse barrel cortex depends on the AMPA subunit GluR1 in layers II/III and IV, but not in layer V, and that long-term depression is also GluR1 dependent in the IV-II/III, but not II/III-V, pathway.

Ipsilateral whiskers suppress experience-dependent plasticity in the barrel cortex.

Each cerebral hemisphere processes sensory input from both sides of the body, but the impact of this convergence on shaping and modifying receptive field properties remains controversial. Here we investigated the effect of chronic deprivation of ipsilateral sensory whiskers on receptive field plasticity in primary somatosensory cortex. In the absence of ipsilateral whiskers, cortical receptive fields were significantly larger than control after 1 week.

The origin of cortical surround receptive fields studied in the barrel cortex.

The neocortex is thought to be organized into functional columns of neurons, each of which processes an element of a larger representation. In the barrel cortex, the thalamic input to the column preferentially terminates in a barrel. To study the extent and nature of functional connections between columns, we measured the degree to which whisker responses are relayed between columns in the barrel cortex.

Neocortical long-term potentiation and experience-dependent synaptic plasticity require alpha-calcium/calmodulin-dependent protein kinase II autophosphorylation.

Experience-dependent plasticity can be induced in the barrel cortex by removing all but one whisker, leading to potentiation of the neuronal response to the spared whisker. To determine whether this form of potentiation depends on synaptic plasticity, we studied long-term potentiation (LTP) and sensory-evoked potentials in the barrel cortex of alpha-calcium/calmodulin-dependent protein kinase II (alphaCaMKII)T286A mutant mice. We studied three different forms of LTP induction: theta-burst stimulation, spike pairing, and postsynaptic depolarization paired with low-frequency presynaptic stimulation.

Is there a thalamic component to experience-dependent cortical plasticity?

Sensory deprivation and injury to the peripheral nervous system both induce plasticity in the somatosensory system of adult animals, but in different places. While injury induces plasticity at several locations within the ascending somatosensory pathways, sensory deprivation appears only to affect the somatosensory cortex. Experiments have been performed to detect experience-dependent plasticity in thalamic receptive fields, thalamic domain sizes and convergence of thalamic receptive fields onto cortical cells.