Neuroscience
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Training of a musical skill is known to produce a distributed neural representation of the ability to perceive music and perform musical tasks. In the present study we tested the hypothesis that the audiovisual perception of music involves a wider activation of multimodal sensory and sensorimotor structures in the brain, including those containing mirror neurons. We mapped the activation of brain areas during passive listening and viewing of the first 40 s of "Ode to Joy" being played on the piano by an expert pianist. ⋯ A visual stimulus contrast focusing on the visual motion percept of moving fingers on piano keys revealed selective bilateral activation of a locus corresponding to the V5/MT area, which was significantly more pronounced in trained subjects and showed partial linear dependence on the duration of training on the left side. Quantitative analysis of individual brain volumes confirmed a significantly greater and wider spread of activation in trained compared to untrained subjects. These findings support the view that audiovisual perception of music and musical gestures in trained musicians involves an expanded and widely distributed neural representation formed due to experience-dependent plasticity.
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As voluntary muscle fatigue increases, the perception of the effort required to produce a particular level of force also increases. This occurs because we produce greater neural outputs from the brain to compensate for the fatigue-induced loss of force. Muscle fatigue can also be generated following bouts of neuromuscular electrical stimulation (NMES), a technique widely used for rehabilitation and training purposes. ⋯ Contrary to voluntary muscle fatigue, the sense of effort decreased post-NMES in both tasks despite increased neural outputs to the elbow flexors of the fatigued indicator arm. This shows that the relationship between motor command magnitude and effort perception was completely modified by NMES. It is proposed that NMES alters the sensory structures responsible for effort signal integration.
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The present study was performed to determine neuronal loci and individual molecular mechanisms responsible for remifentanil-induced hyperalgesia. The effect of methylnaltrexone (MNX) on remifentanil-induced behavioral hyperalgesia was assessed to distinguish contributions of the peripheral and/or central nervous system to remifentanil-induced hyperalgesia. Phosphorylation of p38 mitogen-activated protein kinase (p38MAPK) in the dorsal root ganglion (DRG) neurons after remifentanil infusion, and the effect of a p38MAPK inhibitor on remifentanil-induced hyperalgesia were analyzed to investigate involvement of p38MAPK in the peripheral mechanisms of remifentanil-induced hyperalgesia. ⋯ Prodynorphin expression increased in the spinal cord, and a BK2 antagonist inhibited hyperalgesia during the late post-infusion period. Remifentanil-induced exacerbation of incisional hyperalgesia was inhibited by MNX and the BK2 antagonist. The present study demonstrated that remifentanil activates peripheral and spinal neurons to promote chronologically distinctive hyperalgesia. p38MAPK phosphorylation in the DRG neuron leads to peripherally-driven hyperalgesia during the early post-infusion period, while spinal dynorphin-bradykinin signaling promotes hyperalgesia during the late post-infusion period.
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An animal's choice behavior is shaped by the outcome feedback from selected actions in a trial-and-error approach. Tonically active neurons (TANs), presumed cholinergic interneurons in the striatum, are thought to be involved in the learning and performance of reward-directed behaviors, but it remains unclear how TANs are involved in shaping reward-directed choice behaviors based on the outcome feedback. To this end, we recorded activity of TANs from the dorsal striatum of two macaque monkeys (Macaca fuscata; 1 male, 1 female) while they performed a multi-step choice task to obtain multiple rewards. ⋯ Moreover, the feedback responses of TANs were similarly observed in any search trials, without distinctions regarding the predicted probability of rewards and the location of chosen targets. Unambiguously, TANs detected reward and no-reward feedback specifically when the monkeys performed trial-and-error searches, in which the monkeys were learning the value of the targets and adjusting their subsequent choice behavior based on the reward and no-reward feedback. These results suggest that striatal cholinergic interneurons signal outcome feedback specifically during search behavior, in circumstances where the choice outcomes cannot be predicted with certainty by the animals.
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Perinatal exposure to nicotine produces ventilatory and chemoreflex deficits in neonatal mammals. Medullary 5-HT neurons are putative central chemoreceptors that innervate respiratory nuclei and promote ventilation, receive cholinergic input and express nicotinic acetylcholine receptors (nAChRs). Perforated patch clamp recordings were made from cultured 5-HT neurons dissociated from the medullary raphé of 0-3 day old mice expressing enhanced yellow fluorescent protein driven by the enhancer region for PET1 (ePet-EYFP). ⋯ Nicotine exposed neurons exhibited ∼67% of the response to acidosis recorded in neurons given vehicle (p = 0.005), with older neurons exposed to high dose prenatal and postnatal nicotine, exhibiting only 28% of that recorded in the vehicle neurons (p < 0.01). In neurons exposed to low or high dose prenatal and postnatal nicotine, acute nicotine exposure led to a smaller increase in FR (∼+51% vs +168%, p = 0.026) and response to acidosis (+6% vs +67%, p = 0.014) compared to vehicle. These data show that exposure to nicotine during development reduces chemosensitivity of 5-HT neurons as they mature, an effect that may be related to the abnormal chemoreflexes reported in rodents exposed to nicotine in utero, and may cause a greater risk for sudden infant death syndrome (SIDS).