The Journal of neuroscience : the official journal of the Society for Neuroscience
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The ability to retain information in working memory (WM) requires not only the active maintenance of information about specific items, but also the temporal order in which the items appeared. Although many studies have investigated the neural mechanisms of item maintenance, little is known about the neural mechanisms of temporal order maintenance in WM. Here, we used electroencephalography (EEG) to compare neural oscillations during WM tasks that required maintenance of item or temporal order information. ⋯ EEG analyses indicated that theta (5-7 Hz) oscillations over prefrontal sites were increased during temporal order maintenance, whereas alpha oscillations (9-12 Hz) over posterior parietal and lateral occipital sites were increased during item maintenance. The frontal theta enhancement was primarily evident in high performers on the order WM task, whereas the posterior alpha enhancement was primarily evident in high performers on the item WM task. These results support the idea that frontal theta and posterior alpha oscillations are differentially related to maintenance of item and temporal order information.
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Torpor in hibernating mammals defines the nadir in mammalian metabolic demand and body temperature that accommodates seasonal periods of reduced energy availability. The mechanism of metabolic suppression during torpor onset is unknown, although the CNS is a key regulator of torpor. Seasonal hibernators, such as the arctic ground squirrel (AGS), display torpor only during the winter, hibernation season. ⋯ CHA-induced torpor within the hibernation season was specific to A(1)AR activation; the A(3)AR agonist 2-Cl-IB MECA failed to induce torpor, and the A(2a)R antagonist MSX-3 failed to reverse spontaneous onset of torpor. CHA-induced torpor was similar to spontaneous entrance into torpor. These results show that metabolic suppression during torpor onset is regulated within the CNS via A(1)AR activation and requires a seasonal switch in the sensitivity of purinergic signaling.
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Peripheral nerve lesion triggers alterations in the spinal microenvironment that contribute to the pathogenesis of neuropathic pain. While neurons and glia have been implicated in these functional changes, it remains largely underexplored whether the blood-spinal cord barrier (BSCB) is also involved. The BSCB is an important component in the CNS homeostasis, and compromised BSCB has been associated with different pathologies affecting the spinal cord. ⋯ Interestingly, ZO-1 and occludin, but not caveolin-1, were rescued by TGF-β1. Furthermore, our data provide direct evidence that disrupted BSCB following nerve injury contributed to the influx of inflammatory mediators and the recruitment of spinal blood borne monocytes/macrophages, which played a major role in the development of neuropathic pain. These findings highlight the importance of inflammation in BSCB integrity and in spinal cord homeostasis.
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How do expectations about the identity of a forthcoming visual stimulus influence the neural mechanisms of perceptual decision making in the human brain? Previous investigations into this issue have mostly involved changing the subjects' attentional focus or the behavioral relevance of certain targets but rarely manipulated subjects' prior expectation about the likely identity of the stimulus. Also, because perceptual decisions were often paired with specific motor responses, it has been difficult to dissociate neural activity that reflects perceptual decisions from motor preparatory activity. Here we designed a task in which we induced prior expectations about the direction of a moving-dot pattern and withheld the stimulus-response mapping until the subjects were prompted to respond. ⋯ Furthermore, there was increased effective connectivity between sensory regions (motion-sensitive medial temporal area MT+) and dorsolateral prefrontal cortex when subjects had a prior expectation about the upcoming motion direction. Dynamic causal modeling suggested that stimulus expectation modulated both the feedforward and feedback connectivity between MT+ and prefrontal cortex. These results provide a mechanism of how prior expectations may affect perceptual decision making, namely by changing neural activity in, and sensory drive to, prefrontal areas.
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The nerve growth factor (NGF) and glial cell line-derived neurotrophic factor (GDNF) families of growth factors regulate the sensitivity of sensory neurons. The ion channels transient receptor potential vanilloid 1 (TRPV1) and transient receptor potential channel, subfamily A, member 1 (TRPA1), are necessary for development of inflammatory hypersensitivity and are functionally potentiated by growth factors. We have shown previously that inflamed skin exhibits rapid increases in artemin mRNA with slower, smaller increases in NGF mRNA. ⋯ TRPV1 and TRPA1 responses were potentiated by growth factors in all afferent types, but compared with skin afferents, muscle afferents were twice as likely to exhibit NGF-induced potentiation and one-half as likely to exhibit artemin-induced potentiation of TRPV1. Furthermore, skin afferents showed no GDNF-induced potentiation of TRPA1, but 43% of muscle and 38% of colon afferents exhibited GDNF-induced potentiation. These results show that interpretation of afferent homeostatic mechanisms must incorporate properties that are specific to the target tissue.