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Nakagawa, Y.

Publications and source records attributed to Nakagawa, Y..

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Phase-amplitude coupling of neural oscillations can be effectively probed with concurrent TMS-EEG

Despite the widespread use of transcranial magnetic stimulation (TMS), knowledge of its neurophysiological mode of action is still incomplete. Recently, TMS has been proposed to synchronise neural oscillators, and to thereby increase the detectability of corresponding oscillations at the population level. As oscillations in the human brain are known to interact within nested hierarchies via phase-amplitude coupling, TMS might also be able to increase the macroscopic detectability of such coupling. In a concurrent TMS-electroencephalography study, we therefore examined the techniques influence on theta-gamma, alpha-gamma and beta-gamma phase-amplitude coupling by delivering single-pulse TMS (sTMS) and repetitive TMS (rTMS) over the left motor cortex and right visual cortex of healthy participants. The rTMS pulse trains were of 5 Hz, 11 Hz and 23 Hz for the three coupling variations, respectively. Relative to sham stimulation, all conditions showed transient but significant increases in phase-amplitude coupling at the stimulation site. In addition, we observed enhanced coupling over various other cortical sites, with a more extensive propagation during rTMS than during sTMS. By indicating that scalp-recorded phase-amplitude coupling can be effectively probed with TMS, these findings open the door to the techniques application in manipulative dissections of such coupling during human cognition and behaviour in healthy and pathological conditions.

neuroscience

The thalamus regulates retinoic acid signaling and development of parvalbumin interneurons in postnatal mouse prefrontal cortex

Abnormal development of GABAergic interneurons in the prefrontal cortex (PFC) is implicated in a number of psychiatric disorders. Yet, developmental mechanisms for these neurons are poorly understood. Here we show that the retinoic acid-degrading enzyme CYP26B1 is temporally expressed specifically in postnatal frontal cortex in mice, and its genetic deletion results in an increased density of parvalbumin (PV)-expressing interneurons in medial PFC during postnatal development. Furthermore, initiation of Cyp26b1 expression in neonatal PFC depends on the connections between the thalamus and the neocortex. Thus, the thalamus has a postnatal role in regulating PV neuron development in PFC by inducing Cyp26b1 and thereby restricting retinoic acid signaling. Prenatally, the lack of thalamic input causes an aberrant radial distribution of medial ganglionic eminence-derived interneurons throughout the cortex. Therefore, the thalamus controls PV neuron development in PFC both by region-specific and cortex-wide mechanisms.

neuroscience

In vivo clonal analysis reveals spatiotemporal regulation of thalamic nucleogenesis

The thalamus, a crucial regulator of cortical functions, is composed of many nuclei arranged in a spatially complex pattern. Thalamic neurogenesis occurs over a short period during mammalian embryonic development. These features have hampered the effort to understand how regionalization, cell divisions and fate specification are coordinated and produce a wide array of nuclei that exhibit distinct patterns of gene expression and functions. Here, we performed in vivo clonal analysis to track the divisions of individual progenitor cells and spatial allocation of their progeny in the developing mouse thalamus. Quantitative analysis of clone compositions revealed evidence for sequential generation of distinct sets of thalamic nuclei based on the location of the founder progenitor cells. Furthermore, we identified intermediate progenitor cells that produced neurons populating more than one thalamic nuclei, indicating a prolonged specification of nuclear fate. Our study reveals an organizational principle that governs the spatial and temporal progression of cell divisions and fate specification, and provides a framework for studying cellular heterogeneity and connectivity in the mammalian thalamus.

neuroscience