Electrophysiological and morphological heterogeneity of slow firing neurons in medial septal/diagonal band complex as revealed by cluster analysis

Slow firing septal neurons modulate hippocampal and neocortical functions. Electrophysiologically, it is unclear whether slow firing neurons belong to a homogeneous neuronal population. To address this issue, whole-cell patch recordings and neuronal reconstructions were performed on rat brain slices containing the medial septum/diagonal band complex (MS/DB). Slow firing neurons were identified by their low firing rate at threshold (<5 Hz) and lack of time-dependent inward rectification (Ih). Unsupervised cluster analysis was used to investigate whether slow firing neurons could be further classified into different subtypes. The parameters used for the cluster analysis included latency for first spike, slow after-hyperpolarizing potential, maximal frequency and action potential (AP) decay slope. Neurons were grouped into three major subtypes. The majority of neurons (55%) were grouped as cluster I. Cluster II (17% of neurons) exhibited longer latency for generation of the first action potential (246.5+/-20.1 ms). Cluster III (28% of neurons) exhibited higher maximal firing frequency (25.3+/-1.7 Hz) when compared with cluster I (12.3+/-0.9 Hz) and cluster II (11.8+/-1.1 Hz) neurons. Additionally, cluster III neurons exhibited faster action potentials at suprathreshold. Interestingly, cluster II neurons were frequently located in the medial septum whereas neurons in cluster I and III appeared scattered throughout all MS/DB regions. Sholl's analysis revealed a more complex dendritic arborization in cluster III neurons. Cluster I and II neurons exhibited characteristics of "true" slow firing neurons whereas cluster III neurons exhibited higher frequency firing patterns. Several neurons were labeled with a cholinergic marker, Cy3-conjugated 192 IgG (p75NTR), and cholinergic neurons were found to be distributed among the three clusters. Our findings indicate that slow firing medial septal neurons are heterogeneous and that soma location is an important determinant of their electrophysiological properties. Thus, slow firing neurons from different septal regions have distinct functional properties, most likely related to their diverse connectivity.     

Modulators in concert for cognition: modulator interactions in the prefrontal cortex

Research on the regulation and function of ascending noradrenergic, dopaminergic, serotonergic, and cholinergic systems has focused on the organization and function of individual systems. In contrast, evidence describing co-activation and interactions between multiple neuromodulatory systems has remained scarce. However, commonalities in the anatomical organization of these systems and overlapping evidence concerning the post-synaptic effects of neuromodulators strongly suggest that these systems are recruited in concert; they influence each other and simultaneously modulate their target circuits. Therefore, evidence on the regulatory and functional interactions between these systems is considered essential for revealing the role of neuromodulators. This postulate extends to contemporary neurobiological hypotheses of major neuropsychiatric disorders. These hypotheses have focused largely on aberrations in the integrity or regulation of individual ascending modulatory systems, with little regard for the likely possibility that dysregulation in multiple ascending neuromodulatory systems and their interactions contribute essentially to the symptoms of these disorders. This review will paradigmatically focus on neuromodulator interactions in the PFC and be further constrained by an additional focus on their role in cognitive functions. Recent evidence indicates that individual neuromodulators, in addition to their general state-setting or gating functions, encode specific cognitive operations, further substantiating the importance of research concerning the parallel recruitment of neuromodulator systems and interactions between these systems.     

Palatal fusion - where do the midline cells go? A review on cleft palate, a major human birth defect

Formation of the palate, the organ that separates the oral cavity from the nasal cavity, is a developmental process characteristic to embryos of higher vertebrates. Failure in this process results in palatal cleft. During the final steps of palatogenesis, two palatal shelves outgrowing from the sides of the embryonic oronasal cavity elevate above the tongue, meet in the midline, and rapidly fuse together. Over the decades, multiple mechanisms have been proposed to explain how the superficial mucous membranes disappear from the contact line, thus allowing for normal midline mesenchymal confluence. A substantial body of experimental evidence exists for cell death, cell migration, epithelial-to-mesenchymal transdifferentiation (EMT), replacement through new tissue intercalation, and other mechanisms. However, the most recent use of gene recombination techniques in cell fate tracking disfavors the EMT concept, and suggests that apoptosis is the major fate of the midline cells during physiological palatal fusion. This article summarizes the benefits and drawbacks of histochemical and molecular tools used to determine the fates of cells within the palatal midline. Mechanisms of normal disintegration of the midline epithelial seam are reviewed together with pathologic processes that prevent this disintegration, thus causing cleft palate.     

Postural control anomalies in children with Tourette syndrome

The goal of the present study was to determine whether postural control is affected in Gilles-de-la-Tourette syndrome (TS). Center of pressure (COP) displacements were recorded in children with TS and unaffected siblings in three conditions using a force platform: (1) Eyes-Open, (2) Eyes-Closed, (3) One-Leg standing with eyes open. The COP range and velocity were higher in children with TS than in unaffected siblings in all conditions. These differences could not be attributed to age, present tic severity, comorbidities (hyperactivity and compulsions) or medication. The data suggest that sub-clinical postural control anomalies are present in TS. Disclosure: The authors have reported no conflicts of interest.     

Plasticity of basal ganglia neurocircuitries following perinatal asphyxia: effect of nicotinamide

The potential neuroprotection of nicotinamide on the consequences of perinatal asphyxia was investigated with triple organotypic cultures. Perinatal asphyxia was induced in vivo by immersing foetuses-containing uterine horns removed from ready-to-deliver rats into a water bath for 20 min. Sibling caesarean-delivered pups were used as controls. Three days later tissue from substantia nigra, neostriatum and neocortex was dissected and placed on a coverslip. After a month, the cultures were processed for immunocytochemistry and phenotyped with markers against the NMDA receptor subunit NR1, tyrosine hydroxylase (TH), or neuronal nitric oxide synthase (nNOS). Some cultures were analysed for cell viability. Nicotinamide (0.8 mmol/kg, i.p.) or saline was administered to asphyxia-exposed and caesarean-delivered control pups 24, 48 and 72 h after birth. Perinatal asphyxia produced a decrease of cell viability in substantia nigra, but not in neostriatum or neocortex. Immunocytochemistry confirmed the vulnerability of the substantia nigra, demonstrating that there was a significant decrease in the number of NR1 and TH-positive (+) cells/mm², as well as a decrease in the length of TH⁺ processes, suggesting neurite atrophy. In control cultures, many nNOS⁺ cells were seen, with different features, regional distribution and cell body sizes. Following perinatal asphyxia, there was an increase in the number of nNOS⁺ cells/mm² in substantia nigra, versus a decrease in neostriatum including reduced neurite length, and no apparent changes in neocortex. The main effect of nicotinamide was seen in the neostriatum, preventing the asphyxia-induced decrease in the number of nNOS⁺ cells and neurite length. Nicotinamide also prevented the effect of perinatal asphyxia on TH-positive neurite length. The present results support the idea that nicotinamide can prevent the effects produced by a sustained energy-failure condition, as occurring during perinatal asphyxia. The contribution of VK and PM has been equally relevant.     

左室心尖与心底旋转变化规律的超声研究

目的检测心尖旋转发生变化时心底旋转的变化规律。方法14只杂种犬作为研究对象,用加热的方法破坏心尖部心肌使心尖旋转幅度变小,用超声组织多普勒检测施加条件前、后心尖及心底旋转幅度的变化,并以收缩期旋转的峰值作为比较的参数。用配备了PhilipQLAB高级软件的个人电脑计算心尖及心底旋转幅度。结果心尖部心肌被破坏后心尖旋转幅度明显降低,由8.48°±4.02°降为3.14°±1.35°（P〈0.001）;左室扭转因心尖旋转的明显减低而减低（左室扭转=左室心尖旋转-左室心底旋转）;心底旋转幅度也有一定程度的减低,由2.41°±0.68°减低为1.11°±0.90°（P〈0.001）。结论心尖旋转幅度明显减低时,心底旋转幅度也减低。虽然心底旋转减低并未使左室扭转保持不变,但其部分代偿了左室扭转的降低,这显示了除收缩期左室被破坏心肌以外的其它部位心肌代偿收缩增强的同时左室扭转也有代偿的过程。左室扭转是左室收缩的组成部分,一定程度上反映左室的收缩情况。     

Cutaneous basal cell carcinoma with endobronchial metastasis

Although basal cell carcinoma is a very common malignancy, metastasis from this tumour is extremely rare. For this reason, many plastic surgeons, dermatologists and physicians dealing with skin malignancies consider this as a locally invasive malignancy. We present a rare case of metastatic basal cell carcinoma manifested as a bronchial tumour. This case highlights the fact that despite basal cell carcinoma’s local invasive potential, the possibility of distant metastasis still exists and clinicians should therefore be cautious about interpreting extracutaneous symptoms. Chest physicians should always consider the possibility of this rare tumour in the lungs in patients with a history of large basal cell carcinomas in the head and neck region.     

改良软通道微创穿刺引流治疗基底节血肿的临床体会

目的：探讨改良软通道微创穿刺引流治疗基底节血肿的临床效果。方法选择2011年2月~2014年2月本院收治的基底节血肿患者52例,采用改良软通道微创穿刺引流技术进行治疗,手术后7 d采用格拉斯哥昏迷量表（GCS）评估患者的意识水平,手术后14 d采用斯堪的纳维亚卒中量表（SSS）对神经功能进行评分。结果52例患者中,完全恢复26例,生活基本自理22例,中转开颅4例,无一例死亡。术后7 d GCS评分与治疗前比较,差异无统计学意义（P〉0.05）,术后14 d GCS评分与治疗前比较,差异有统计学意义（P〈0.05）。术后14 d及28 d SSS评分与治疗前比较,差异有统计学意义（P〈0.05,P〈0.01）。结论改良软通道微创穿刺引流治疗基底节血肿有效,操作相对简单,适宜在临床推广。     

神经内镜与显微镜手术治疗早期基底节区高血压性脑出血的临床疗效对比

目的分析神经内镜手术与显微镜手术对早期基底节区高血压性脑出血（HICH）的疗效。 方法回顾性分析张家口市第一医院神经外科自2016年3月至2021年3月手术治疗的188例早期基底节区HICH患者的临床资料,根据手术方式分为神经内镜组（95例）与显微镜组（93例）。对比分析2组患者术中失血量、手术时间、术后血肿清除率、术后并发症（颅内感染）发生率,以及术后6个月改良Rankin量表（mRs）评分情况。 结果神经内镜组与显微镜组比较,手术时间明显缩短[（96.6±10.7）min vs（171.3±26.4）min],术中出血量显著减少[（32.8±6.2）mL vs（112.8.0±17.0）mL]、血肿清除率提高（95.9%±4.2% vs 87.4%±6.5%）,差异均有统计学意义（P<0.05）。2组并发症发生率比较,差异无统计学意义（P>0.05）。根据术后6个月mRs评分,神经内镜组的预后良好率（26.3%,25/95）高于显微镜组（15.1%,14/93）,差异具有统计学意义（P<0.05）。 结论神经内镜治疗早期基底节区HICH较显微镜手术快速安全、视野清晰,且患者的预后更好。