Articles in 2010

Just before a rapid eye movement (saccade), attentional performance improves for the targeted position where the saccade will land. This behavioral study finds that attentional performance also improves at the subsequent locations that the target of the saccade will move to, suggesting that attentional remapping occurs at least two steps ahead.

Homeostatic plasticity can be induced by increasing neuronal activity and is mediated, in part, by AMPAR endocytosis. Here Fu et al. describe the involvement of EphA4 in synaptic scaling via ubiquitin-dependent degradation of AMPAR.

Several axonal guidance molecules have a dual function in directing dendritic growth as well. UNC-6 (Netrin) in C. elegans is one such molecule. Here, Teichmann and Shen show how UNC-6's action in axon versus dendrite can be specified.

The auxiliary subunit Cavβ regulates calcium channel density in the plasma membrane, but the mechanism by which this occurs has been poorly defined. Altier et al. find that Cavβ prevents ubiquitination of the Cav1.2 channels by the RFP2 ubiquitin ligase and subsequent targeting of the channels for proteasomal degradation.

Hunger makes Drosophila larvae move faster in search of food. Koon and colleagues show that starvation increases the branching of octopaminergic motoneurons' axonal terminal arbors, driven by octopamine released from these same motoneurons. The increased locomotor activity of starved larvae requires octopaminergic signaling.

Even if it doesn't trigger action potential, a slight somatic depolarization can still spread and modulate the neurotransmitter release at distant sites along axons. Here, the authors find that depolarization in the cerebellar molecular layer interneurons can affect presynaptic neurotransmitter release in a calcium-dependent and voltage-sensitive Ca²⁺ channel–dependent manner.

Anticipation about the timing of an event can improve response speed. Here the authors find that responses of single neurons in primary auditory cortex show enhanced representation of sounds during periods of heightened expectation. Neural activity was also linked to perceptual performance, suggesting that this signal could contribute to the behavioral effects of temporal expectation.

This study finds that thalamic interneurons and downstream projecting relay cells have opposite response properties. Computational modeling suggests that such complementary mechanisms may help preserve more spike-timing information.

In a mouse model of Alzheimer's disease, the authors find that early loss of AMPA receptors at synapses at onset of cognitive dysfunction is a result of activation of the phosphatase calcineurin by caspase-3. Inhibition of caspase activity rescued both synapse density and fear memory in this model.

This electrophysiology study finds that spatial tuning in cat A1 is sharpened when the cats are engaged in a task, as compared with rest. Inhibitory mechanisms are likely to be the source of this sharpening.

The patterns of nociceptive innervation in skin and spinal cord differ in mammals and lower vertebrates. Guo et al. report that nerve growth factor induces the transcription factor Hoxd1 in mouse, but not chick, sensory neurons, and that expression of Hoxd1 is necessary and sufficient for a mammalian-like pattern of nociceptive projections in vivo.

The authors report that, in a subset of rodent hippocampal and neocortical interneurons, evoking hundreds of spikes at normal rates caused persistent firing that outlasted the stimulus by about a minute. Persistent firing was generated in the distal axon, did not require somatic depolarization and could be shared between interneurons via an axo-axonal interaction.

Ca_v1.3 calcium channels are critical for neurotransmitter release in auditory hair cells and cardiac pacemaking. The authors identified a mutation in CACNA1D, which encodes the pore-forming α1-subunit of Ca_v1.3, in deaf humans. These individuals also exhibited bradycardia. The insertion of a glycine residue near the pore resulted in nonconducting channels.

During Drosophila metamorphosis, the γ axons of mushroom bodies are pruned and regrow into their adult morphology. The pruning process requires the ecdysone receptor EcR-B1. The authors find antagonistic transcriptional regulation of EcR-B1 by two closely related nuclear receptors, Ftz-f1 and Hr39.

The authors report a transcriptional profile of the discrete stages of spontaneous remyelination following toxin-induced focal demyelination in rats. They find an enrichment of retinoid X receptor (RXR) signaling pathways over the course of remyelination and show that RXR activation stimulates oligodendrocyte differentiation to enhance remyelination.

Motoneuron recruitment is thought to occur in an orderly matter to generate the appropriate movements. Here, the authors find that recruitment threshold is not dictated by input resistance, as was previously believed, but by a combination of biophysical properties and the strength of the synaptic currents.

The receptor sortilin has been implicated in pro-apoptotic signaling of proneurotrophins. In this study, the authors uncover another role for sortilin in neurotrophin signaling: it interacts with Trk family receptors to promote their anterograde transport to nerve endings, thereby enhancing neurotrophin-dependent cell survival.

Volitional control over object viewing improves subsequent memory for these objects in normal subjects. A comparison between subjects with and without hippocampal damage, as well as fMRI imaging during the task, suggest that the hippocampus is a key locus for changes during volitional versus passive object viewing.

Sensory adaptation is thought to improve perceptual discriminability of sensory stimuli. Using simultaneous recordings in aligned thalamic and cortical cells in the vibrissal pathway, the authors find evidence suggesting that adaptation of cortical signals is not apparent in the firing of individual thalamic neurons, but is reflected in thalamic synchrony.

Using a rat model of PD, the authors find a progressive decline in autonomous globus pallidus pacemaking. This loss was reversed by viral expression of the HCN channel. However, the motor disability induced by DA depletion was not reversed, suggesting that the loss of pacemaking was a consequence, not a cause, of key network pathophysiology.