The European journal of neuroscience
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The primary somatosensory barrel cortex processes tactile vibrissae information, allowing rodents to actively perceive spatial and textural features of their immediate surroundings. Each whisker on the snout is individually represented in the neocortex by an anatomically identifiable 'barrel' specified by the segregated termination zones of thalamocortical axons of the ventroposterior medial nucleus, which provide the primary sensory input to the neocortex. The sensory information is subsequently processed within local synaptically connected neocortical microcircuits, which have begun to be investigated in quantitative detail. ⋯ Prominent reciprocal projections are found between primary somatosensory cortex and secondary somatosensory cortex, motor cortex, perirhinal cortex and thalamus. Primary somatosensory barrel cortex also projects strongly to striatum, thalamic reticular nucleus, zona incerta, anterior pretectal nucleus, superior colliculus, pons, red nucleus and spinal trigeminal brain stem nuclei. These long-range connections of the barrel cortex with other specific cortical and subcortical brain regions are likely to play a crucial role in sensorimotor integration, sensory perception and associative learning.
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Huntington's disease (HD) is a devastating neurodegenerative disorder caused by an expanded polyglutamine repeat within the N-terminus of the huntingtin protein. It is characterized by a selective loss of medium spiny neurons in the striatum. It has been suggested that impaired proteasome function and endoplasmic reticulum (ER) stress play important roles in mutant huntingtin (mHtt)-induced cell death. ⋯ On the other hand, knocking down BimEL expression prevented mHtt-induced cell death. Taken together, these findings suggest that BimEL is a key element in regulating mHtt-induced cell death. A model depicting the role of BimEL in linking mHtt-induced ER stress and proteasome dysfunction to cell death is proposed.
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Previous studies have shown that sensations of burning, stinging or pricking can be evoked by warming or cooling the skin to innocuous temperatures [low-threshold thermal nociception (LTN)] below the thresholds of cold- and heat-sensitive nociceptors. LTN implies that some primary afferent fibers classically defined as warm and cold fibers relay stimulation to the nociceptive system. We addressed this question in humans by determining if different adaptation temperatures (ATs) and rates of temperature change would affect thermal sensation and LTN similarly. ⋯ Thresholds of thermal and nociceptive sensations shifted by similar amounts across the three ATs during cooling, whereas during heating the nociceptive threshold was significantly affected only between ATs of 32 and 34 degrees C. In Experiment 2, increasing the rate of temperature change from 0.5 to 4.0 degrees C/s increased the intensity of thermal and nociceptive sensations significantly but the effect was greatest for nociceptive sensations during heating. The results of both experiments are consistent with the mediation of LTN by low-threshold thermoreceptors, although LTN caused by heating may depend on a subset of fibers that express less sensitive TRP channels than those that serve sensations of warmth at the mildest temperatures.
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Glutamate receptors in the basolateral complex of the amygdala (BLA) are essential for the acquisition, expression and extinction of Pavlovian fear conditioning in rats. Recent work has revealed that glutamate receptors in the central nucleus of the amygdala (CEA) are also involved in the acquisition of conditional fear, but it is not known whether they play a role in fear extinction. Here we examine this issue by infusing glutamate receptor antagonists into the BLA or CEA prior to the extinction of fear to an auditory conditioned stimulus (CS) in rats. ⋯ These results reveal that AMPA and NMDA receptors within the amygdala make dissociable contributions to the expression and extinction of conditioned fear, respectively. Moreover, they indicate that NMDA receptor-dependent processes involved in extinction learning are localized to the BLA. Together with previous work, these results reveal that NMDA receptors in the CEA have a selective role acquisition of fear memory.
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Working memory (WM) tasks require not only distinct functions such as a storage buffer and central executive functions, but also coordination among these functions. Neuroimaging studies have revealed the contributions of different brain regions to different functional roles in WM tasks; however, little is known about the neural mechanism governing their coordination. Electroencephalographic (EEG) rhythms, especially theta and alpha, are known to appear over distributed brain regions during WM tasks, but the rhythms associated with task-relevant regional coupling have not been obtained thus far. ⋯ The alpha amplitudes increased during not only the manipulation but also the maintenance periods in the temporal area for the auditory WM and the parietal area for the visual WM. The phase synchronization analyses indicated that, under the relevant task conditions, the temporal and parietal regions show enhanced phase synchronization in the theta bands with the frontal region, whereas phase synchronization between theta and alpha is significantly enhanced only within the individual areas. Our results suggest that WM task-relevant brain regions are coordinated by distant theta synchronization for central executive functions, by local alpha synchronization for the memory storage buffer, and by theta-alpha coupling for inter-functional integration.