Volume 17 Issue 5, May 2014

It is widely believed that Huntington's disease is driven exclusively by neuronal dysfunction. Work now challenges this view, showing that mutant huntingtin in astrocytes leads to dysregulation of extracellular K⁺.

By eliciting a natural exploratory behavior in rats, head scanning, a study reveals that hippocampal place cells form new, stable firing fields in those locations where the behavior has just occurred.

A study finds that the loss of phasic dopamine signal in ventral, but not dorsal, striatum predicts escalation of cocaine self-administration. We discuss the study's implications for addiction theory and treatment.

The authors review the recently observed relationships between breathing and the sensations of smell and vibrissa-based touch. These data and other experimental evidence are used to support the hypothesis that the breathing rhythm serves not only as a motor drive signal, but also as a common clock that binds these two senses into a common percept.

The author reviews network models of the brain, including models of both structural and functional connectivity. He discusses contributions of network models to cognitive neuroscience, as well as limitations and challenges associated with constructing and interpreting these models.

Many mouse models of Alzheimer's disease (AD) rely on overexpression of amyloid precursor (APP) transgenes, which makes it difficult to tease out which effects are truly disease-relevant and which are induced by the overexpression. In this study, the authors describe several new knock-in AD model mice that express mutant APP at near physiological levels.

The authors identify mutations in the MATR3 gene as a cause of ALS and dementia in several families. MATR3 is known to bind the ALS-associated protein TDP-43, and at least one of these mutations alters the efficiency of this binding.

In this study, the authors show that the heritable behavioral and metabolic changes that are observed in rodents exposed to early life stress are mediated by changes in miRNA levels in the sperm of affected males. Injection of isolated RNA from the sperm of stressed males into donor fertilized oocytes is able to induce these phenotypic changes in the resulting offspring.

Rapid vesicle exocytosis requires the Ca²⁺ sensor synaptotagmin I (syt). Here the AUs manipulate the length and rigidity of the linker connecting the two Ca²⁺ sensing domains of syt. This revealed a set of intra-molecular interactions that determined the ability of the domains to penetrate membranes and drive evoked transmitter release in response to Ca²⁺.

Using time-lapse super-resolution STED imaging of dendritic spines of CA1 pyramidal neurons in mouse, the authors show dynamic structural changes to the spine neck under conditions of synaptic plasticity. The study also shows that such morphological changes can differentially regulate biochemical and electrical compartmentalization of spines and that previous characterizations of dendritic spine subtypes based on static ultrastructural morphologies may not reflect the diversity and plasticity seen in living neurons.

Using subcellular patch-clamp axonal recordings in rat hippocampal slices, this study describes the physiological properties of action potential (AP) initiation and propagation in parvalbumin-expressing GABAergic interneurons/basket cells (BCs). Hu and Jonas also show a gradual increase in Na⁺ conductance along the BC axon away from the soma, and that this differential distribution of sodium conductance along the small-diameter axons can ensure fast and reliable AP propagation to account for the unique functions of these interneurons.

In this study, the authors show that altered medium spiny neuron excitability and symptom onset in Huntington's disease model mice is associated with decreased expression of Kir4.1 and impaired K⁺ handling by astrocytes. Exogenous expression of Kir4.1 could partially rescue motor function and prolong survival in HD mice.

The authors measured striatal dopamine (DA) release in vivo using fast-scan cyclic voltammetry in a model involving escalating self-administration of cocaine in rats. Phasic DA release in ventromedial striatum was negatively correlated with escalation of cocaine intake. The DA precursor L-DOPA restored phasic DA release and reversed escalation of cocaine intake.

Does the spatial tuning of grid cells in the medial entorhinal cortex (MEC) require spatially tuned inhibition? Buetfering and colleagues recorded optogenetically identified parvalbumin (PV) interneurons in the mouse MEC during foraging and found that they were broadly tuned. Moreover, the authors found that stimulating PV cells suppressed firing in grid and head-direction cells but did not alter the spatial tuning of these cells.

Cei and colleagues used a model train to transport rats forward or backward on a circular track while the animals walked on a miniature treadmill. The authors found that the firing fields of hippocampal place cells remained stable across travel directions and that, when the train transported the rat backward, theta sequences of hippocampal cell assemblies and theta phase precession still represented the trajectory and the distance traveled through place fields.

Here the authors find that increased place cell activity during exploratory head-scanning behaviors predicted the formation and potentiation of place fields on the next pass through that location, regardless of environmental familiarity and across multiple days. This place cell activity is a strong candidate mechanism to mediate the one-trial encoding of ongoing experiences necessary for memory.

Here the authors report that repeated presentations of a visual sequence over a course of days causes evoked response potentiation in mouse V1 that is highly specific for stimulus order and timing. After V1 is trained to recognize a sequence, cortical activity regenerates the full sequence even when individual stimulus elements are omitted.

Visual input is often noisy and discontinuous, even though the physical environment is generally stable. The authors show that the visual system trades off change sensitivity to capitalize on physical continuity via serial dependence: present perception is biased toward past visual input. This bias is modulated by attention and governed by a spatiotemporally-tuned operator, a continuity field.