Journal of neurophysiology
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Visuospatial working memory capacity predicts the organization of acquired explicit motor sequences.
Studies have suggested that cognitive processes such as working memory and temporal control contribute to motor sequence learning. These processes engage overlapping brain regions with sequence learning, but concrete evidence has been lacking. ⋯ We found that visuospatial working memory capacity, but not the CV from the timing task, correlated with the rate of motor sequence learning and the chunking pattern observed in the learned sequence. These results show that individual differences in short-term visuospatial working memory capacity, but not temporal control, predict the temporal structure of explicitly acquired motor sequences.
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Brief radiant laser pulses can be used to activate cutaneous Adelta and C nociceptors selectively and elicit a number of transient brain responses [laser-evoked potentials (LEPs)] in the ongoing EEG. LEPs have been used extensively in the past 30 years to gain knowledge about the cortical mechanisms underlying nociception and pain in humans, by assuming that they reflect at least neural activities uniquely or preferentially involved in processing nociceptive input. ⋯ Indeed, our results indicate that LEPs can be entirely explained by a combination of multimodal neural activities (i.e., activities also elicited by stimuli of other sensory modalities) and somatosensory-specific, but not nociceptive-specific, neural activities (i.e., activities elicited by both nociceptive and non-nociceptive somatosensory stimuli). Regardless of the sensory modality of the eliciting stimulus, the magnitude of multimodal activities correlated with the subjective rating of saliency, suggesting that these multimodal activities are involved in stimulus-triggered mechanisms of arousal or attentional reorientation.
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Afferent A- and C-fibers regenerating into a nerve following peripheral nerve injury are exposed to inflammatory mediators released by Schwann cells, resident and invading macrophages, and other inflammatory cells. Here we tested the hypothesis that ongoing and evoked activity in these afferent fibers are enhanced by a mixture of inflammatory mediators [inflammatory soup (IS)] applied to the injured nerve. Using in vivo electrophysiology, regenerating afferent nerve fibers were studied 7-14 days after sural nerve crush lesion. ⋯ Some initially nonresponsive C- and A-fibers developed new ectopic properties, i.e., were recruited, and exhibited ongoing activity and/or could be activated by physiological stimuli after application of IS. The results suggest that inflammatory mediators may be critical to enhance ectopic excitability of regenerating afferent nerve fibers. These peripheral mechanisms may be important triggering and maintaining neuropathic pain.
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The transient receptor potential vanilloid-1 (TRPV1) receptor is involved in peripheral and spinal nociceptive processing and is a therapeutic target for pain. We have shown previously that TRPV1 in the ventrolateral periaqueductal gray (VL-PAG) tonically contributes to brain stem descending antinociception by stimulating glutamate release into the rostral ventromedial medulla and off neuron activity. Because both opioid and vanilloid systems integrate and transduce pain sensation in these pathways, we studied the potential interaction between TRPV1 and mu-opioid receptors in the VL-PAG-rostral ventromedial medulla (RVM) system. ⋯ These effects were all antagonized by the TRPV1 and opioid receptor antagonists 5'-iodo-resiniferatoxin and naloxone, respectively, thus suggesting the existence of a TRPV1-mu-opioid interaction in the VL-PAG-RVM system. By using double immunofluorescence techniques, we found that TRPV1 and mu-opioid receptors are coexpressed in several neurons of the VL-PAG. These findings suggest that mu-receptor activation not only acts on inhibitory neurons to disinhibit PAG output neurons but also interacts with TRPV1 activation at increasing glutamate release into the RVM, possibly by acting directly on PAG output neurons projecting to the RVM.
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Precise control of synaptic strength is critical for maintaining accurate network activity and normal brain functions. Several major brain diseases are related to synaptic alterations in the adult brain. Detailed descriptions of the normal physiological properties of adult synapses are scarce, mainly because of the difficulties in performing whole cell patch-clamp recording in brain slices from adult animals. ⋯ Changes in synaptic strength were estimated from the ratio of AMPAR to NMDAR evoked and spontaneous EPSCs (AMPAR/NMDAR ratio). Although both AMPAR and NMDAR EPSCs decreased over development, there was an increase of the AMPAR/NMDAR ratio that was linked to changes in NMDAR EPSC. Furthermore, distribution of the AMPAR/NMDAR ratio was more heterogeneous in MSNs from adults, suggesting that synaptic strength is continuously refined during life.