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Tonic pain, a chief clinical problem, is difficult to study in rodent models that measure threshold changes of evoked reactions to acutely applied stimuli. These authors used conditioned place preference to assess tonic pain in rats and measure the efficacy of agents that relieve it.
The instinctual attachment of young animals to their mothers is crucial for survival. Demonstrating the overriding importance of attachment, very young rat pups learn to prefer an odor coupled to electrical shock if the mother is present. This paper shows that low amygdalar dopamine signaling in very young pups is essential for their paradoxical response to odor/shock conditioning.
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.
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 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.
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.
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.
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.