Neuroscience
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Mental rotation is a core indicator of spatial ability, and a threshold for cognitive impairment may exist at approximately 4,000 m above sea level, but the specific thresholds for the severity of hypoxia in Tibetan indigenous populations in mental rotation ability remain largely unknown. To determine whether a threshold for mental rotation impairment exists in indigenous residents, we related a mental rotation task to inter-individual differences in a range of behavioral performance and neuropsychological characteristics across 51 indigenous Tibetan highlanders and 34 matched controls at three different altitudes (sea level, 2,900 m, and 4,200 m). Analyses of reaction time showed delayed behavioral responses in the 4,200 m altitude group. ⋯ Moreover, a time-frequency analysis showed significantly enhanced alpha- and beta-band power values for the 4,200 m altitude participants after stimulus presentation. The impairment in mental rotation ability is related to hypoxia and can be attributed to the absence of sufficient cognitive resources, which demonstrates the existence of a threshold for the effects of high altitude on the brain's mental rotation ability. Taken together, our findings have important implications for exploring the altitude threshold for the influence of high-altitude exposure on brain function, as well as for guiding the development of innovative strategies to optimize the response of the organism against chronic hypoxia-induced under extreme environments.
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Chronic sensory loss is a common and undertreated consequence of many forms of neurological injury. Emerging evidence indicates that vagus nerve stimulation (VNS) delivered during tactile rehabilitation promotes recovery of somatosensation. Here, we systematically varied the timing of VNS relative to tactile rehabilitation to determine the paradigm that yields the greatest degree of somatosensory recovery after peripheral nerve injury (PNI). ⋯ Delivery of VNS during rehabilitative training generates robust, significant recovery compared to rehabilitative training without stimulation (56 ± 14% improvement over sham stimulation). A matched amount of VNS before training, immediately after training, or two hours after training is significantly less effective than VNS during rehabilitative training and fails to improve recovery compared to rehabilitative training alone (5 ± 10%, 4 ± 11%, and -7 ± 22% improvement over sham stimulation, respectively). These findings indicate that concurrent delivery of VNS during rehabilitative training is most effective and illustrate the importance of considering stimulation timing for clinical implementation of VNS therapy.
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The thalamic reticular nucleus (TRN) is a thin sheet of GABAergic neurons surrounding the thalamus, and it regulates the activity of thalamic relay neurons. The TRN has been reported to be involved in sensory gating, attentional regulation, and some other functions. However, little is known about the contribution of the TRN to sequence learning. ⋯ The performance on a task in which mice needed to press an active lever for food reward showed that simple operant learning of lever pressing and learning of win-stay and lose-shift strategies are not affected in Avp-Vgat-/- mice. In contrast, the performance on a task in which mice needed to press three levers in a correct order for food reward showed that learning of the order of lever pressing (action sequence learning) was impaired in Avp-Vgat-/- mice. These results suggest that the TRN plays an important role in action sequence learning.
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At the vertebrate neuromuscular junction (NMJ), presynaptic homeostatic potentiation (PHP) refers to an increase in neurotransmitter release that restores the strength of synaptic transmission following a blockade of nicotinic acetylcholine receptors (nAChRs). Mechanisms informing the presynaptic terminal of the loss of postsynaptic receptivity remain poorly understood. Previous research at the mouse NMJ suggests that extracellular protons may function as a retrograde signal that triggers an upregulation of neurotransmitter output (measured by quantal content, QC) through the activation of acid-sensing ion channels (ASICs). ⋯ In line with this hypothesis, we found that pharmacological inhibition of the PMCA with carboxyeosin induces QC upregulation and that this effect requires functional ASICs. We also demonstrated that muscles pre-treated with carboxyeosin fail to generate PHP. These findings suggest that reduced PMCA activity causes presynaptic homeostatic potentiation by activating ASICs at the mouse NMJ.