Neuroscience Research最新文献_第7页

Formyl peptide receptor 2 antagonist WRW4 ameliorates diabetes-induced cognitive decline in mice 甲酰基肽受体2拮抗剂WRW4改善糖尿病诱导的小鼠认知能力下降。

IF 2.4 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-09-01 Epub Date: 2025-07-05 DOI: 10.1016/j.neures.2025.104932

Hiroki Uno , Takahide Itokazu , Toshihide Yamashita

Cognitive impairment is a significant complication of diabetes. Although the detailed mechanism remains unclear, prolonged neuroinflammation mediated by microglia is recognized as a key contributor to neural dysfunction. Recent studies have shown that Formyl peptide receptor 1 (FPR1), a G protein-coupled chemoattractant receptor, plays a role in microglial activation and brain pathology. However, the involvement of FPR2, another isoform within the FPR family, in microglial activation and cognitive decline has not yet been explored. In this study, we observed an increased expression of FPR2 in microglia within the hippocampus of type 2 diabetes (db/db) mice. Furthermore, we demonstrated that intracerebroventricular administration of WRW4, a selective FPR2 antagonist, alleviates diabetes-related cognitive decline. Histological analysis revealed that WRW4 treatment mitigates morphological alteration and upregulation of a phagocytic marker (CD68) of the microglia in the hippocampus of db/db mice. These results indicate that FPR2 plays a critical role in inducing diabetes-related microglial phenotype. These findings highlight the therapeutic potential of FPR2 signal inhibition as a novel strategy to mitigate cognitive decline associated with diabetes.

认知障碍是糖尿病的一个重要并发症。虽然详细的机制尚不清楚，但由小胶质细胞介导的长期神经炎症被认为是神经功能障碍的关键因素。近年来的研究表明，甲酰基肽受体1 （FPR1）是一种G蛋白偶联的化学引诱剂受体，在小胶质细胞的激活和脑病理中起着重要作用。然而，FPR家族中的另一种亚型FPR2在小胶质细胞激活和认知能力下降中的作用尚未被探索。在本研究中，我们观察到2型糖尿病小鼠海马内小胶质细胞中FPR2的表达增加（db/db）。此外，我们证明了脑室内给药WRW4（一种选择性FPR2拮抗剂）可以减轻糖尿病相关的认知能力下降。组织学分析显示，WRW4处理减轻了db/db小鼠海马小胶质细胞形态改变和吞噬标志物（CD68）的上调。这些结果表明，FPR2在诱导糖尿病相关的小胶质细胞表型中起关键作用。这些发现强调了FPR2信号抑制作为一种缓解糖尿病相关认知能力下降的新策略的治疗潜力。

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引用次数: 0

Effects of MEK1/2 blocker U0126 on the medial preoptic synapse and behavioral selection of male mice MEK1/2阻滞剂U0126对雄性小鼠内侧视前突触和行为选择的影响。

IF 2.4 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-09-01 Epub Date: 2025-06-28 DOI: 10.1016/j.neures.2025.104929

Yumi Hamasaki, Masabumi Minami, Taiju Amano

The central part of the mouse medial preoptic area (cMPOA) is involved in parental behavior because the neurotoxic lesion of the cMPOA disturbed parental behavior and switched to infanticidal behavior. The cMPOA receives projection from many brain regions, including the medial amygdala (Me). We have previously found that optogenetic inhibition of the projection pathway from the Me to the cMPOA in virgin male mice suppressed the infanticidal behavior of virgin mice toward pups. Furthermore, electrophysiological analysis has revealed that intracellular signaling-mediated disinhibition occurs in the cMPOA neurons during the transition from virgin to father in gestation experience (FGE) mice. However, the specific downstream signal transduction pathway remains unclear. In this study, we utilized U0126, a MEK1/2 inhibitor, because U0126 has been reported to modulate GABAergic currents. Therefore, we examined the contribution of U0126 at the synaptic and behavioral levels. Applying U0126 to the cMPOA neurons in FGE mice restored eIPSP as much as that in cMPOA neurons in virgin mice. Furthermore, microinfusion of U0126 into the cMPOA shifted the behavioral pattern of FGE mice toward infanticide. These changes were not observed in the mice that experienced parenting. The results suggest that MEK1/2 mediates neurotransmission in the cMPOA and contributes to the stage transition from virgin to FGE mice after mating with females.

小鼠内侧视前区（cMPOA）的中央部分参与亲代行为，因为cMPOA的神经毒性病变扰乱了亲代行为并转变为杀婴行为。cpoa接收来自许多大脑区域的投射，包括内侧杏仁核（Me）。我们之前已经发现，光遗传抑制从Me到cpoa的雄性小鼠的投射途径可以抑制雄性小鼠对幼崽的杀婴行为。此外，电生理分析显示，在妊娠经历（FGE）小鼠从处女到父亲的转变过程中，细胞内信号介导的去抑制发生在cMPOA神经元中。然而，具体的下游信号转导途径尚不清楚。在本研究中，我们使用了MEK1/2抑制剂U0126，因为已有报道称U0126可以调节gaba能电流。因此，我们研究了U0126在突触和行为水平上的贡献。U0126作用于FGE小鼠的cMPOA神经元后，eIPSP的恢复程度与未处理小鼠的相同。此外，将U0126微量注入cpoa可使FGE小鼠的行为模式转向杀婴。这些变化在经历父母抚养的老鼠身上没有观察到。结果表明，MEK1/2介导cpoa中的神经传递，并有助于与雌性交配后从处女小鼠到FGE小鼠的阶段转变。

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引用次数: 0

Role of endogenous NT-3 in neuronal activity and neurogenesis in the hippocampal dentate gyrus 内源性NT-3在海马齿状回神经元活动和神经发生中的作用。

IF 2.4 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-09-01 Epub Date: 2025-06-13 DOI: 10.1016/j.neures.2025.104923

Nanami Kasakura, Yuka Murata, Kanzo Suzuki, Eri Segi-Nishida

Neurotrophin-3 (NT-3) is a neurotrophic factor that regulates neuronal differentiation and synaptic plasticity. In the adult central nervous system, NT-3 is predominantly expressed in the hippocampal dentate gyrus (DG). Chronic antidepressant treatment suppresses Ntf3 expression in the DG; however, its functional significance remains unclear. To investigate the role of NT-3 in the adult DG, an adeno-associated virus (AAV)-mediated knockdown system was employed in mice. Immunohistochemical analysis revealed that TrkC, the high-affinity receptor for NT-3, was highly expressed in the DG. Under basal conditions, NT-3 knockdown significantly reduced the expression of FosB, an activity-dependent marker. Gene expression analysis showed that Arc, Egr1, and Fosb expressions were also significantly decreased. Although NT-3 knockdown did not affect cell proliferation in the DG, it impaired dendritic elongation in immature neurons. Additionally, NT-3 knockdown significantly reduced Npy expression. These findings suggest that endogenous NT-3 in the adult DG regulates both basal neuronal activity and newborn neuronal differentiation, contributing to hippocampal homeostasis. Further research is required to determine whether NT-3 downregulation induced by chronic antidepressant treatment influences neuronal activity and hippocampal plasticity in neuropsychiatric conditions.

神经营养因子-3 （NT-3）是一种调节神经元分化和突触可塑性的神经营养因子。在成人中枢神经系统中，NT-3主要在海马齿状回（DG）中表达。慢性抗抑郁治疗抑制Ntf3在DG中的表达；然而，其功能意义尚不清楚。为了研究NT-3在成年DG中的作用，在小鼠中采用了腺相关病毒（AAV）介导的敲低系统。免疫组化分析显示NT-3高亲和受体TrkC在DG中高表达。在基础条件下，NT-3敲低可显著降低FosB（一种活性依赖性标志物）的表达。基因表达分析显示，Arc、Egr1和Fosb的表达也显著降低。虽然NT-3敲除不影响DG中的细胞增殖，但它会损害未成熟神经元的树突伸长。此外，NT-3敲除显著降低Npy的表达。这些发现表明，成人DG中的内源性NT-3调节基础神经元活动和新生神经元分化，有助于海马稳态。慢性抗抑郁药物治疗诱导的NT-3下调是否会影响神经精神疾病患者的神经元活动和海马可塑性，尚需进一步研究。

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引用次数: 0

Biased thalamic innervation onto the distinct subregion where dopamine receptor 1 is dominantly expressed in the caudal striatum 偏置丘脑神经支配到多巴胺受体1在尾状体中主要表达的独特亚区。

IF 2.4 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-09-01 Epub Date: 2025-06-30 DOI: 10.1016/j.neures.2025.104930

Fuko Kadono , Jingqi Wang , Kenta Kobayashi , Fuyuki Karube , Fumino Fujiyama

In the ventral part of the caudal striatum, the direct and indirect pathway neurons are unevenly distributed, forming zones with a paucity of neurons with dopamine receptor 1 (D1R) or dopamine receptor 2 (D2R), referred as D1R- or D2R-poor zone (D1pz or D2pz, respectively). This contrasts with their uniform distribution in other striatal regions. A key question is whether D1pz and D2pz function as a unit or independently. Since the striatum requires afferent excitatory inputs for activation, investigating biased excitatory inputs to the caudal striatum is essential. Our findings indicate that vesicular glutamate transporter 2 (VGluT2) was concentrated in D2pz, suggesting biased excitatory innervation. Retrograde tracer labeling identified potential sources of subcortical glutamatergic projections. Projection from the paraventricular nucleus of the thalamus (PVT) was visualized using VGluT2-Cre mice. PVT preferentially projected to the ventral caudal region in the striatum. Quantitative analysis of PVT axons revealed preferential localization in the D2pz, with fewer axons in the D1pz. The substantia nigra pars lateralis, innervated by the caudal striatum, did not project to the PVT, suggesting the caudal striatum and PVT may not form a part of the cortico-basal ganglia-thalamic loop. These results imply that D1pz and D2pz may be differentially activated by PVT inputs, selectively recruiting direct pathways.

在尾侧纹状体腹侧，直接和间接通路神经元分布不均匀，形成多巴胺受体1 （D1R）或多巴胺受体2 （D2R）神经元缺乏的区域，称为D1R-或D2R-贫区（分别为D1pz或D2pz）。这与它们在其他纹状体区域的均匀分布形成对比。一个关键问题是D1pz和D2pz是作为一个整体还是独立发挥作用。由于纹状体需要传入兴奋输入来激活，因此研究尾侧纹状体的偏向性兴奋输入是必要的。我们的研究结果表明，水疱性谷氨酸转运蛋白2 （VGluT2）集中在D2pz，提示偏向性兴奋神经支配。逆行示踪标记确定了皮层下谷氨酸能投射的潜在来源。使用VGluT2-Cre小鼠观察丘脑室旁核（PVT）的投影。PVT优先投射到纹状体尾侧腹侧区。定量分析显示PVT轴突优先定位于D2pz，而D1pz轴突较少。由尾状纹状体支配的黑质外侧部没有投射到PVT，这表明尾状纹状体和PVT可能不是皮质-基底神经节-丘脑回路的一部分。这些结果表明，D1pz和D2pz可能被PVT输入不同地激活，选择性地招募直接通路。

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引用次数: 0

The effect of L-alanine on sleep through taste properties in Drosophila melanogaster l -丙氨酸通过果蝇味觉特性对睡眠的影响。

IF 2.4 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-09-01 Epub Date: 2025-06-14 DOI: 10.1016/j.neures.2025.104924

Rabia Garibağaoğlu, Riho Kobayashi , Victoria Hanashiro, Jun Tomita, Kazuhiko Kume

Sleep and nutrition are important for the survival of organisms. This study focuses on the effects of amino acids, specifically L-alanine, on sleep of Drosophila melanogaster. Some amino acids including L-alanine are shown to be attractive to flies. To assess their effect on sleep, either sucrose (sweet) or sorbitol (non-sweet) was used as a base sugar of the food. Sleep was measured using monitors with infrared beams, and feeding behavior was examined by food intake and proboscis extension response tests. L-alanine supplementation in a sweet diet did not alter sleep, but supplementation in a non-sweet diet increased sleep. The addition of non-nutritive sweetener, sucralose to a non-sweet diet also increased sleep, but combining sucralose with L-alanine did not produce additive effects. L-alanine also increased the lifespan of aged flies when supplemented in a non-sweet diet. These findings suggest that the attractive taste properties of L-alanine induced sleep and offer new insights into the relationship between sleep and taste.

睡眠和营养对生物体的生存至关重要。本研究主要研究氨基酸，特别是l -丙氨酸对黑腹果蝇睡眠的影响。包括l -丙氨酸在内的一些氨基酸对苍蝇很有吸引力。为了评估它们对睡眠的影响，研究人员使用蔗糖（甜味）或山梨醇（非甜味）作为食物的基础糖。研究人员使用红外线光束监测睡眠，并通过食物摄入和喙伸反应测试来检查进食行为。在甜的饮食中补充l -丙氨酸不会改变睡眠，但在非甜的饮食中补充l -丙氨酸会增加睡眠。在不吃甜食的饮食中加入非营养性甜味剂三氯蔗糖也会增加睡眠，但三氯蔗糖和l -丙氨酸的结合不会产生附加效应。在不含糖的饮食中补充l -丙氨酸也能延长年老果蝇的寿命。这些发现表明，l -丙氨酸吸引人的味觉特性诱导了睡眠，并为睡眠和味觉之间的关系提供了新的见解。

引用次数: 0

Alteration of perineuronal nets and parvalbumin interneurons in prefrontal cortex and hippocampus, and correlation with blood corticosterone in activity-based anorexia model mice 活动性厌食症模型小鼠前额皮质和海马神经元周围网和小白蛋白中间神经元的改变及其与血皮质酮的相关性。

IF 2.4 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-09-01 Epub Date: 2025-06-14 DOI: 10.1016/j.neures.2025.104922

Hoang Duy Nguyen , Haruko Miyazaki , Hiroki Kawai , Ziyi Wang , Shinji Sakamoto , Manabu Takaki , Toshitaka Oohashi

Anorexia nervosa (AN) is an eating disorder characterized by restricted energy intake, severely underweight status, and frequent hyperactivity. Previous research has shown structural and functional alterations in the medial prefrontal cortex (mPFC) and hippocampus of AN patients. To investigate the pathological mechanism of AN, we analyzed the expression and distribution of parvalbumin (PV) interneurons and perineuronal nets (PNNs), which are implicated in the pathology of neuropsychiatric disorders, in the mPFC and hippocampus dorsal (HPCd) and ventral (HPCv) using an activity-based anorexia (ABA) mouse model. We found that PNN expression and density increased in the mPFC, with minor alterations in the HPCd and HPCv of ABA mice. The expression and distribution of PV neurons were unchanged in the brains of ABA mice, except for a regional decrease in PV-expressing neuron density in the HPCd. Co-localization analysis showed an increased number of PNNs enwrapping PV-negative neurons in the mPFC of ABA mice. Furthermore, the upregulation of PNN expression in the mPFC was positively correlated with elevated blood corticosterone levels, a well-known stress indicator, in ABA mice. Our findings suggest that the increased expression and distribution of PNNs surrounding PV-negative neurons in the mPFC may indicate the pathological mechanisms of AN.

神经性厌食症（AN）是一种以能量摄入受限、体重严重不足和频繁多动为特征的饮食失调。先前的研究表明，AN患者的内侧前额叶皮层（mPFC）和海马结构和功能发生改变。为了探讨AN的病理机制，我们利用活动性厌食症（ABA）小鼠模型，分析了与神经精神疾病病理有关的mPFC和海马背侧（HPCd）和腹侧（HPCv）的小白蛋白（PV）中间神经元和神经周围网络（pnn）的表达和分布。我们发现PNN的表达和密度在ABA小鼠的mPFC中增加，而在HPCd和HPCv中有轻微的变化。ABA小鼠脑内PV神经元的表达和分布没有变化，但在HPCd中表达PV神经元的密度出现了局部下降。共定位分析显示ABA小鼠mPFC中包裹pv -阴性神经元的pnn数量增加。此外，在ABA小鼠中，mPFC中PNN表达的上调与血皮质酮水平升高呈正相关，皮质酮是一种众所周知的应激指标。我们的研究结果表明，mPFC中pv -阴性神经元周围pnn的表达和分布增加可能提示了AN的病理机制。

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引用次数: 0

Corrigendum to “Time-window of offline long-term potentiation in anterior cingulate cortex during memory consolidation and recall” [Neurosci. Res. 212 (2025) 75–83] “记忆巩固和回忆过程中前扣带皮层离线长期增强的时间窗口”的勘误[神经科学]。Res. 212 (2025) 75-83]

IF 2.4 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-08-01 Epub Date: 2025-06-21 DOI: 10.1016/j.neures.2025.104926

Junyu Liu , Akihiro Goto , Yasunori Hayashi

引用次数: 0

Possible role of mosaic mutations of neurodevelopmental disorder-related genes in bipolar disorder: Lessons from Kmt2c chimeric heterozygous knockout mice 神经发育障碍相关基因镶嵌突变在双相情感障碍中的可能作用：来自Kmt2c嵌合敲除小鼠的经验教训。

IF 2.4 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-08-01 Epub Date: 2025-05-23 DOI: 10.1016/j.neures.2025.05.005

Takumi Nakamura , Kazuo Nakajima , Noriko Fujimori-Tonou , Takaoki Kasahara , Takashi Tsuboi , Tadafumi Kato

We recently found a loss of function mosaic mutation of KMT2C, a causative gene for autism spectrum disorder and Kleefstra syndrome, in a patient with bipolar disorder and reported that somatic mutations in neurodevelopmental disorder-related genes are increased in bipolar disorder by deep exome sequencing analysis. However, causal roles of neurodevelopmental disorder-related mutations in bipolar disorder, a qualitatively different mental disorder, are not known. In this study, we focused on a loss of function mutation of Kmt2c, that causes autism-like phenotypes in mice. To simulate a mosaic mutation found in the patient, we generated mosaic Kmt2c knockout mice using conventional chimera mice technology. We showed that the mosaic Kmt2c knockout mice did not show autism-like behavior but presented anxiety disorder-like symptom, which is avoidance to a corner where the mice previously experienced air puff. The rate of depression-like episodes measured by wheel running recording did not differ from control mosaic mice. These results suggest that mosaic mutations of neurodevelopmental disorder-related genes can cause qualitatively different anxiety disorder-like phenotypes. Because anxiety is one of symptomatic spectrum of bipolar disorder, these findings support the role of mosaic mutations of neurodevelopmental disorder-related genes as a component of the genetic architecture of bipolar disorder.

我们最近在一名双相情感障碍患者中发现了自闭症谱系障碍和Kleefstra综合征的致病基因KMT2C的功能缺失镶嵌突变，并报道了通过深度外显子组测序分析，神经发育障碍相关基因的体细胞突变在双相情感障碍中增加。然而，神经发育障碍相关突变在双相情感障碍（一种性质不同的精神障碍）中的因果作用尚不清楚。在这项研究中，我们关注的是导致小鼠自闭症样表型的Kmt2c功能缺失突变。为了模拟在患者身上发现的嵌合体突变，我们使用传统的嵌合体小鼠技术产生了嵌合体Kmt2c敲除小鼠。我们发现马赛克Kmt2c基因敲除小鼠没有表现出自闭症样的行为，但表现出焦虑障碍样的症状，即回避小鼠以前经历过的一个角落。通过滚轮跑步记录测量的抑郁样发作率与对照马赛克小鼠没有差异。这些结果表明，神经发育障碍相关基因的马赛克突变可以引起质量上不同的焦虑样表型。由于焦虑是双相情感障碍的症状谱之一，这些发现支持了神经发育障碍相关基因的马赛克突变作为双相情感障碍遗传结构的一个组成部分的作用。

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引用次数: 0

Synaptic plasticity induced by CA1 synaptic input with bursts superimposed on low-frequency rhythms 低频节奏叠加CA1脉冲突触输入诱导的突触可塑性

IF 2.4 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-08-01 Epub Date: 2025-06-03 DOI: 10.1016/j.neures.2025.104913

Satoshi Fujii , Yoshihiko Yamazaki , Hiroki Fujiwara , Jun-Ichi Goto , Takeo Watanabe , Katsuhiko Mikoshiba

Hippocampal neurons fire synchronously in a population at low frequencies and burst individually at high frequencies, with synaptic plasticity thought to depend on the interplay of these firing patterns. This study investigated synaptic plasticity in the hippocampal CA1 region induced by synaptic input with bursts superimposed on low-frequency rhythms. Low-frequency stimulation (LFS) was varied from 0.5 to 5 Hz, and various numbers of bursts (3–1000) consisting of 2–4 pulses at 100 Hz were superimposed on LFS. The patterned stimuli with 1-Hz LFS effectively induced synaptic plasticity. The direction and magnitude of plasticity depended on the number of bursts. We identified key roles for adenosine A₁ receptors and GABAergic signaling in regulating synaptic plasticity. The blockade of adenosine A₁ receptors increased the magnitude of long-term potentiation induced by specific burst patterns and differentially affected synaptic plasticity induced by 1-Hz LFS. Through its interactions with hippocampal rhythms and inhibitory circuits, adenosine elevated extracellularly during conditioning stimuli regulated the magnitude and direction of synaptic plasticity. This study proposes hypotheses for the role of adenosine in the modulation of synaptic plasticity, which maintains the balance between potentiation and depression in hippocampal circuits.

海马体神经元在群体中以低频率同步放电，在高频率单独爆发，突触的可塑性被认为取决于这些放电模式的相互作用。本研究探讨了低频节奏叠加的突触输入对海马CA1区突触可塑性的影响。低频刺激（LFS）在0.5 ~ 5 Hz范围内变化，在LFS上叠加由2-4次100 Hz脉冲组成的不同次数的脉冲（3-1000次）。1 hz LFS模式刺激能有效诱导突触可塑性。塑性的方向和大小取决于爆发的次数。我们确定了腺苷A1受体和gaba能信号在调节突触可塑性中的关键作用。腺苷A1受体的阻断增加了特定爆发模式诱导的长期增强的强度，并对1 hz LFS诱导的突触可塑性产生了差异影响。通过与海马节律和抑制回路的相互作用，腺苷在条件反射刺激下的细胞外升高调节突触可塑性的大小和方向。本研究提出了腺苷在突触可塑性调节中的作用假设，突触可塑性在海马回路中维持增强和抑制之间的平衡。

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引用次数: 0

The neurobiology of ticklishness 挠痒的神经生物学。

IF 2.4 4区医学 Q3 NEUROSCIENCES

Neuroscience Research

Pub Date : 2025-08-01 Epub Date: 2025-05-16 DOI: 10.1016/j.neures.2025.05.002

Shimpei Ishiyama

Ticklishness is an idiosyncratic form of touch observed in multiple animal species, including humans. Although commonly regarded as trivial, it involves complex neurobiological mechanisms and diverse behavioral phenomena observed across species. Two distinct forms exist: knismesis, a mild tingling sensation elicited by gentle touch, and gargalesis, an intense sensation associated with involuntary laughter. Advocating the importance of clearly distinguishing these two types of ticklishness, this review synthesizes current knowledge on their neuronal underpinnings. Topics include somatosensory processing, self-tickling and sensory attenuation, emotional modulation, sociosexual dimensions, and evolutionary perspectives, among others. Special attention is given to the ambivalent nature of gargalesis, challenging conventional single-dimensional models of emotional valence. Ultimately, studying ticklishness provides a valuable opportunity to investigate playful emotional experiences from a naturalistic perspective, addressing fundamental yet underrepresented questions in contemporary neuroscience. Far from trivial, ticklishness thus provides valuable insights into the neural mechanisms underlying complex, context-dependent emotional and social experiences.

挠痒是在包括人类在内的多种动物中观察到的一种特殊的触摸形式。虽然通常被认为是微不足道的，但它涉及复杂的神经生物学机制和跨物种观察到的多种行为现象。有两种不同的形式：一种是轻触引起的轻微刺痛感，另一种是轻触引起的强烈的笑声。提倡明确区分这两种类型的挠痒的重要性，这篇综述综合了目前关于它们的神经元基础的知识。主题包括体感处理、自挠和感觉衰减、情绪调节、社会性别维度和进化观点等。特别注意的是gargalesis的矛盾性质，挑战传统的情感价的单维模型。最终，研究挠痒提供了一个宝贵的机会，从自然主义的角度来研究好玩的情感体验，解决当代神经科学中基本但未被充分代表的问题。因此，挠痒远非微不足道，它为研究复杂的、情境依赖的情感和社会体验背后的神经机制提供了有价值的见解。

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引用次数: 0