PDF(Pubmed)
Abstract：
UNASSIGNED: The involvement of specific basal ganglia-thalamocortical circuits in response inhibition has been extensively mapped in animal models. However, the pivotal nodes and directed causal regulation within this inhibitory circuit in humans remains controversial.
UNASSIGNED: The main aim of the present study was to determine the causal information flow and critical nodes in the basal ganglia-thalamocortical inhibitory circuits and also to examine whether these are modulated by biological factors (i.e. sex) and behavioral performance.
UNASSIGNED: Here, we capitalize on the recent progress in robust and biologically plausible directed causal modeling (DCM-PEB) and a large response inhibition dataset (n = 250) acquired with concomitant functional magnetic resonance imaging to determine key nodes, their causal regulation and modulation via biological variables (sex) and inhibitory performance in the inhibitory circuit encompassing the right inferior frontal gyrus (rIFG), caudate nucleus (rCau), globus pallidum (rGP), and thalamus (rThal).
UNASSIGNED: The entire neural circuit exhibited high intrinsic connectivity and response inhibition critically increased causal projections from the rIFG to both rCau and rThal. Direct comparison further demonstrated that response inhibition induced an increasing rIFG inflow and increased the causal regulation of this region over the rCau and rThal. In addition, sex and performance influenced the functional architecture of the regulatory circuits such that women displayed increased rThal self-inhibition and decreased rThal to GP modulation, while better inhibitory performance was associated with stronger rThal to rIFG communication. Furthermore, control analyses did not reveal a similar key communication in a left lateralized model.
UNASSIGNED: Together, these findings indicate a pivotal role of the rIFG as input and causal regulator of subcortical response inhibition nodes.
UNASSIGNED: The main aim of the present study was to determine the causal information flow and critical nodes in the basal ganglia-thalamocortical inhibitory circuits and also to examine whether these are modulated by biological factors (i.e. sex) and behavioral performance.
UNASSIGNED: Here, we capitalize on the recent progress in robust and biologically plausible directed causal modeling (DCM-PEB) and a large response inhibition dataset (n = 250) acquired with concomitant functional magnetic resonance imaging to determine key nodes, their causal regulation and modulation via biological variables (sex) and inhibitory performance in the inhibitory circuit encompassing the right inferior frontal gyrus (rIFG), caudate nucleus (rCau), globus pallidum (rGP), and thalamus (rThal).
UNASSIGNED: The entire neural circuit exhibited high intrinsic connectivity and response inhibition critically increased causal projections from the rIFG to both rCau and rThal. Direct comparison further demonstrated that response inhibition induced an increasing rIFG inflow and increased the causal regulation of this region over the rCau and rThal. In addition, sex and performance influenced the functional architecture of the regulatory circuits such that women displayed increased rThal self-inhibition and decreased rThal to GP modulation, while better inhibitory performance was associated with stronger rThal to rIFG communication. Furthermore, control analyses did not reveal a similar key communication in a left lateralized model.
UNASSIGNED: Together, these findings indicate a pivotal role of the rIFG as input and causal regulator of subcortical response inhibition nodes.
摘要：
■在动物模型中广泛绘制了特定的基底神经节-丘脑皮质回路在反应抑制中的参与。然而,人类抑制回路中的关键节点和定向因果调节仍存在争议。
■本研究的主要目的是确定基底神经节-丘脑皮质抑制回路中的因果信息流和关键节点，并检查这些是否受生物因素（即性别）和行为表现的调节。
■这里，我们利用了健壮和生物学似是而非的因果模型（DCM-PEB）的最新进展和伴随功能磁共振成像获得的大反应抑制数据集（n=250）来确定关键节点，它们通过包括右额下回（rIFG）的抑制回路中的生物学变量（性别）和抑制性能的因果调节和调节，尾状核（rCau），苍白球（rGP），和丘脑（rThal）。
■整个神经回路表现出很高的内在连通性，并且反应抑制严重地增加了从rIFG到rCau和rThal的因果预测。直接比较进一步表明，反应抑制可诱导rIFG流入增加，并增加了该区域在rCau和rThal上的因果调节。此外,性别和表现影响了调节回路的功能结构，因此女性表现出增加的rThal自我抑制和减少的rThal对GP的调节，而更好的抑制性能与更强的rThal与rIFG通讯相关。此外，对照分析在左偏侧模型中没有发现类似的关键通信。
■一起，这些发现表明rIFG作为皮质下反应抑制节点的输入和因果调节因子的关键作用。
■本研究的主要目的是确定基底神经节-丘脑皮质抑制回路中的因果信息流和关键节点，并检查这些是否受生物因素（即性别）和行为表现的调节。
■这里，我们利用了健壮和生物学似是而非的因果模型（DCM-PEB）的最新进展和伴随功能磁共振成像获得的大反应抑制数据集（n=250）来确定关键节点，它们通过包括右额下回（rIFG）的抑制回路中的生物学变量（性别）和抑制性能的因果调节和调节，尾状核（rCau），苍白球（rGP），和丘脑（rThal）。
■整个神经回路表现出很高的内在连通性，并且反应抑制严重地增加了从rIFG到rCau和rThal的因果预测。直接比较进一步表明，反应抑制可诱导rIFG流入增加，并增加了该区域在rCau和rThal上的因果调节。此外,性别和表现影响了调节回路的功能结构，因此女性表现出增加的rThal自我抑制和减少的rThal对GP的调节，而更好的抑制性能与更强的rThal与rIFG通讯相关。此外，对照分析在左偏侧模型中没有发现类似的关键通信。
■一起，这些发现表明rIFG作为皮质下反应抑制节点的输入和因果调节因子的关键作用。
