Volume 12 Issue 10, October 2009

During the day, certain retinal ganglion cells respond specifically to dark, approaching stimuli. A study finds that the retinal circuit that gives rise to this response makes use of an amacrine cell that was previously known for its role in night vision circuitry, demonstrating that some neurons lead double lives.

Laminar neuronal density varies between cortical areas; thus, the developmental specification of areas and layers needs to be coordinated. AP2γ turns out to be an important regulator of upper layer development in occipital cortex.

Fusion of synaptic vesicles upon calcium influx requires precise localization of voltage-gated calcium channels. A new study identifies a previously uncharacterized protein that mediates trafficking of Ca_V2 calcium channels in C. elegans.

A study in this issue found that suppressing expression of TRPM7 in hippocampal CA1 neurons conferred resistance to ischemic cell death, preserved cell function and prevented ischemia-induced deficits in memory.

Recent human imaging work has expanded the view of amygdala function beyond early findings in animals, but two studies of an individual with bilateral amygdala damage now suggest that we should be thinking even more broadly.

This paper shows that synapses between CA1 pyramidal cells in the hippocampus and the tempero-ammonic pathway in the entorhinal cortex undergo spike timing-dependent plasticity.

Sharp wave-ripple (SPW-R) complexes during sleep or rest have yet to be causally linked to memory consolidation. Here, the authors show that suppressing hippocampal SPW-Rs during post-training sleep in rats impairs the consolidation of a hippocampus-dependent spatial memory task.

The amygdala is thought to process fear-related stimuli rapidly and nonconsciously. Here, the authors report that an individual with complete lesion of the amygdala shows normal rapid detection and nonconscious processing of fearful faces, despite being unable to recognize fear from faces.

The amygdala is critical for processing information about emotion, but little is known about what role it might play in human behavioral interactions. Here the authors report that a patient with complete bilateral amydala lesions lacks any sense of personal space, and that in healthy controls the amygdala is activated by close personal proximity.

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 closely related Sox5 and Sox6 turn out to perform distinct functions during brain development. Maintenance of the ventricular zone neuroepithelium requires Sox6 in the dorsal and Sox5 in the ventral telencephalon. A portion of the interneurons born in ventral telencephalon then express Sox6, which is necessary for their correct migration and phenotypic differentiation.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.