Articles in 2009

Using endogenous circadian oscillators, Drosophila can anticipate diurnal light on/off transition and behave accordingly. Here, the authors show that the fly evening oscillator circuit can synchronize to light cycle through the visual system and the molecular components of morning oscillator.

A feeding leech ignores incoming stimuli that would normally cause an avoidance response. This study found that synaptic transmission from mechanosensory neurons to postsynaptic partners was reduced in feeding leeches. This presynaptic depression by feeding could be mimicked by serotonin and was antagonized by a blocker of an unusual serotonin-gated chloride channel.

The nucleus basalis is thought to regulate arousal and attention via release of acetylcholine in the cortex. Here the authors report that nucleus basalis stimulation in rats results in a decorrelation between visual cortical neurons as a result of activation of cortical muscarinic receptors and an increase in the reliability of responses to natural scenes as a result of more distributed changes along the visual pathway.

Activity in the frontal eye fields (FEF) is important for visuospatial processing and is thought to code information in retinal coordinates. This fMRI study finds FEF activity even for auditory locations behind the head, suggesting that extra-retinal space is also coded in this area.

The authors report the conditional deletion of the alpha and beta forms of glycogen synthase kinase 3 (GSK-3) in mouse neural progenitors. This deletion is associated with dysregulations in β-catenin, Sonic Hedgehog, Notch and fibroblast growth factor signaling pathways and leads to markedly increased proliferation of neural progenitors.

Silva et al. show that CREB modulates allocation of fear memory to specific cells in the lateral amygdala. Reversibly inactivating a subset of CREB-expressing neurons disrupted memory for tone conditioning. Neurons with higher CREB levels were more excitable than their neighbors and showed larger synaptic efficacy changes following tone conditioning.

Spinal cord injury disrupts input from the brain to the spinal motor circuitry, but that circuitry and pattern generator circuits still exist below the lesion. A regime combining electrical and serotonergic agonist stimulation of the lesioned spinal cord with intensive treadmill training enabled rats to recover weight-bearing stepping that was very similar to normal walking.

Trace conditioning in humans is thought to require explicit knowledge of the temporal contingency between the conditioned and unconditioned stimuli. Bekinschtein et al. demonstrate that such conditioning can occur in individuals with disorders of consciousness, suggesting the possibility that these individuals may have partially preserved conscious processing that cannot be measured by behavioral assessment.

When our actions conflict with our prior attitudes, we often change our attitudes to be more consistent with our actions, a phenomenon that is known as cognitive dissonance. Here the authors report that activity during cognitive dissonance in the dorsal anterior cingulate cortex and anterior insula predicts subsequent attitude changes.

The thickness of cortical layers varies among cortical areas. This study reports that the transcription factor AP2γ is specifically required for the generation of layer II/III neurons in the caudal primary visual cortex. Mice lacking AP2γ show impaired spatial resolution in visual cortex, whereas other parameters of visual cortex function remain close to normal.

The authors recorded neural activity in grid cells while rats ran through a hairpin maze. Their results demonstrate that spatial environments are represented in the entorhinal cortex and hippocampus as a mosaic of discrete submaps corresponding to the geometric structure of the space.

The authors use voltage-sensitive dye imaging and multielectrode recordings to show that the average population response to rapid sequences of orientations can largely be predicted by summation of the responses to each of the individual elements in the sequence. However, they find that following stimulus removal the population response is more persistent than expected.

Topical application of nicotine, as used in nicotine replacement therapies, causes irritation of the mucosa and skin. This reaction had previously been attributed to the activation of nicotinic acetylcholine receptors in chemosensory neurons. However, the Talavera et al. now demonstrate that TRPA1 may be crucial for nicotine-induced irritation.

Deleting the transcription factor SOX2 in mouse embryonic brain causes a loss of neural stem cells and neurogenesis in the hippocampus. An SHH pharmacological agonist partially rescues the hippocampal defect and SHH was found to be a SOX2 target.

This study shows that Epac2, a cAMP-activated Rap-GEF, acts downstream of D1/D5 dopamine receptor signaling to regulate dendritic spines and synaptic transmission. The authors also show that rare mutations of the EPAC2 gene that are associated with autism cause defects in Epac2-mediated spine remodeling.

This study identifies EFHC1 as a microtubule-associated protein that regulates neuronal cell division and migration. Mutations in EHC1 have been linked to juvenile myoclonic epilepsy.

The authors show long-term potentiation at the hippocampal CA3–CA1 synapse is modulated by EphA4 in the postsynaptic CA1 neuron and by ephrin-A3, an EphA4 ligand, in astrocytes, through their regulation of glial glutamate transporters. These results suggest EphA4/ephrin-A3 signaling as a mechanism for astrocytic regulation of synaptic plasticity.

Using genetic labeling of cell types, two-photon microscopy, electrophysiology and theoretical modeling, the authors identify an approach-sensitive ganglion cell type in the mouse retina. They show that it is incorporated into a circuit that serves different purposes during daytime and night-time vision.

In a model of stroke, the authors show that suppressing the expression of TRPM7 in hippocampal CA1 neurons conferred resistance to ischemic death, preserving function and morphology. Also, TRPM7 suppression prevented ischemia-induced deficits in LTP and fear-associated and spatial navigational memory tasks.

In C. elegans, the unc-2 gene encodes the pore-forming subunit of a voltage-gated Ca²⁺ channel (CaV2) involved in neurotransmitter release. Here, the authors identify a protein, CALF-1, that regulates the presynaptic trafficking of UNC-2. The α₂δ subunit UNC-36 is also required for ER exit and synaptic localization of UNC-2.