PreSurgMapp: a MATLAB Toolbox for Presurgical Mapping of Eloquent Functional Areas Based on Task-Related and Resting-State Functional MRI

The main goal of brain tumor surgery is to maximize tumor resection while minimizing the risk of irreversible postoperative functional sequelae. Eloquent functional areas should be delineated preoperatively, particularly for patients with tumors near eloquent areas. Functional magnetic resonance imaging (fMRI) is a noninvasive technique that demonstrates great promise for presurgical planning. However, specialized data processing toolkits for presurgical planning remain lacking. Based on several functions in open-source software such as Statistical Parametric Mapping (SPM), Resting-State fMRI Data Analysis Toolkit (REST), Data Processing Assistant for Resting-State fMRI (DPARSF) and Multiple Independent Component Analysis (MICA), here, we introduce an open-source MATLAB toolbox named PreSurgMapp. This toolbox can reveal eloquent areas using comprehensive methods and various complementary fMRI modalities. For example, PreSurgMapp supports both model-based (general linear model, GLM, and seed correlation) and data-driven (independent component analysis, ICA) methods and processes both task-based and resting-state fMRI data. PreSurgMapp is designed for highly automatic and individualized functional mapping with a user-friendly graphical user interface (GUI) for time-saving pipeline processing. For example, sensorimotor and language-related components can be automatically identified without human input interference using an effective, accurate component identification algorithm using discriminability index. All the results generated can be further evaluated and compared by neuro-radiologists or neurosurgeons. This software has substantial value for clinical neuro-radiology and neuro-oncology, including application to patients with low- and high-grade brain tumors and those with epilepsy foci in the dominant language hemisphere who are planning to undergo a temporal lobectomy.     

Effects of Maternal Marginal Iodine Deficiency on Dendritic Morphology in the Hippocampal CA1 Pyramidal Neurons in Rat Offspring

Although the salt iodization programmes are taken to control iodine deficiency (ID), some regions are still suffering from marginal ID. During pregnancy, marginal ID frequently leads to subtle insufficiency of thyroid hormones, characterized as low serum T₄ levels. Therefore, the present research was to explore the effects of maternal marginal ID exposure on dendritic arbor growth in the hippocampal CA1 region and the underlying mechanisms. We established Wistar rat models with ID diet during pregnancy and lactation. The overall daily iodine intakes of the rats were estimated as 7.0, 5.0 and 1.5 μg/day in the control, marginal ID and severe ID groups, respectively. To study the morphological alterations of pyramidal neurons, Golgi–Cox procedure was conducted in the hippocampus. Sholl analyses demonstrated a slight decrease in the total length and branching numbers of basal dendrites on postnatal day (PN) 7, PN14 and PN21 in marginal ID group relative to the controls. However, there was no overt morphological change observed in apical dendrites. Immunofluorescence and Western blot analysis indicated that phosphorylation of MAP2, stathmin and JNK1 was down-regulated in marginal ID group. We speculate that the pups treated with maternal marginal ID subjected to subtle changes in dendritic growth of CA1 pyramidal neurons, which may be associated with the dysregulation of MAP2 and stathmin in a JNK1-dependent manner.     

Scutellarin as a Potential Therapeutic Agent for Microglia-Mediated Neuroinflammation in Cerebral Ischemia

The cerebral ischemia is one of the most common diseases in the central nervous system that causes progressive disability or even death. In this connection, the inflammatory response mediated by the activated microglia is believed to play a central role in this pathogenesis. In the event of brain injury, activated microglia can clear the cellular debris and invading pathogens, release neurotrophic factors, etc., but in chronic activation microglia may cause neuronal death through the release of excessive inflammatory mediators. Therefore, suppression of microglial over-reaction and microglia-mediated neuroinflammation is deemed to be a therapeutic strategy of choice for cerebral ischemic damage. In the search for potential herbal extracts that are endowed with the property in suppressing the microglial activation and amelioration of neuroinflammation, attention has recently been drawn to scutellarin, a Chinese herbal extract. Here, we review the roles of activated microglia and the effects of scutellarin on activated microglia in pathological conditions especially in ischemic stroke. We have further extended the investigation with special reference to the effects of scutellarin on Notch signaling, one of the several signaling pathways known to be involved in microglial activation. Furthermore, in light of our recent experimental evidence that activated microglia can regulate astrogliosis, an interglial “cross-talk” that was amplified by scutellarin, it is suggested that in designing of a more effective therapeutic strategy for clinical management of cerebral ischemia both glial types should be considered collectively.     

[Gly14]-Humanin Protects Against Amyloid β Peptide-Induced Impairment of Spatial Learning and Memory in Rats

Alzheimer disease（AD）, a progressive neurodegenerative disorder, is characterized by cognitive decline and the accumulation of senile plaques in the brain.Amyloid b protein（Aβ） in the plaques is thought to be responsible for the memory loss in AD patients. [Gly14]-humanin（HNG）, a derivative of humanin（HN）, has much stronger neuroprotective effects than natural HN in vitro.However, clarification of the Aβ active center and the neuroprotective mechanism of HN still need in vivo evidence. The present study first compared the in vivo biological effects of three Aβ fragments（1–42, 31–35, and 35–31） on spatial memory in rats, and investigated the neuroprotective effects and molecular mechanisms of HNG. The results showed that intrahippocampal injection of Aβ_1–42and Aβ_31–35almost equally impaired spatial learning and memory, but the reversed sequence Aβ_35–31 did not have any effect; a high dose of Aβ_31–35（20 nmol） produced a more detrimental response than a low dose（2 nmol）; Aβ_31–35 injection also disrupted gene and protein expression in the hippocampus, with up-regulation of caspase3 and down-regulation of STAT3; pretreatment with HNG not only protected spatial memory but also rescued STAT3 from Aβ-induced disruption; and the neuroprotective effects of HNG were effectively counteracted by genistein, a specific tyrosine kinase inhibitor. These results clearly show that sequence 31–35 in Aβ is the shortest active center responsible for the neurotoxicity of Aβ from molecule to behavior; and HNG protects spatial learning and memory in rats against Aβ-induced insults; and probably involves the activation of tyrosine kinases and subsequent beneficial modulation of STAT3 and caspase3.     

GABAergic Interneurons are Required for Generation of Slow CA1 Oscillation in Rat Hippocampus

Neuronal oscillations are fundamental to hippocampal function. It has been shown that GABAergic interneurons make an important contribution to hippocampal oscillations, but the underlying mechanism is not well understood. Here, using whole-cell recording in the complete hippocampal formation isolated from rats at postnatal days 14–18, we showed that GABA_Areceptormediated activity enhanced the generation of slow CA1 oscillations. In vitro, slow oscillations(0.5–1.5 Hz) were generated in CA1 neurons, and they consisted primarily of excitatory rather than inhibitory membrane-potential changes. These oscillations were greatly reduced by blocking GABA_Areceptor-mediated activity with bicuculline and were enhanced by increasing such activity with midazolam, suggesting that interneurons are required for oscillation generation. Consistently, CA1 fast-spiking interneurons were found to generate action potentials usually preceding those in CA1 pyramidal cells. These findings indicate a GABA_Areceptor-based mechanism for the generation of the slow CA1 oscillation in the hippocampus.     

Subject-Specific Channel Selection Using Time Information for Motor Imagery Brain–Computer Interfaces

Keeping a minimal number of channels is essential for designing a portable brain–computer interface system for daily usage. Most existing methods choose key channels based on spatial information without optimization of time segment for classification. This paper proposes a novel subject-specific channel selection method based on a criterion called F score to realize the parameterization of both time segment and channel positions. The F score is a novel simplified measure derived from Fisher’s discriminant analysis for evaluating the discriminative power of a group of features. The experimental results on a standard dataset (BCI competition III dataset IVa) show that our method can efficiently reduce the number of channels (from 118 channels to 9 in average) without a decrease in mean classification accuracy. Compared to two state-of-the-art methods in channel selection, our method leads to comparable or even better classification results with less selected channels.     

Intra-regional and inter-regional abnormalities and cognitive control deficits in young adult smokers

Tobacco use during later adolescence and young adulthood may cause serious neurophysiological changes; rationally, it is extremely important to study the relationship between brain dysfunction and behavioral performances in young adult smokers. Previous resting state studies investigated the neural mechanisms in smokers. Unfortunately, few studies focused on spontaneous activity differences between young adult smokers and nonsmokers from both intra-regional and inter-regional levels, less is known about the association between resting state abnormalities and behavioral deficits. Therefore, we used fractional amplitude of low frequency fluctuation (fALFF) and resting state functional connectivity (RSFC) to investigate the resting state spontaneous activity differences between young adult smokers and nonsmokers. A correlation analysis was carried out to assess the relationship between neuroimaging findings and clinical information (pack-years, cigarette dependence, age of onset and craving score) as well as cognitive control deficits measured by the Stroop task. Consistent with previous addiction findings, our results revealed the resting state abnormalities within frontostriatal circuits, i.e., enhanced spontaneous activity of the caudate and reduced functional strength between the caudate and anterior cingulate cortex (ACC) in young adult smokers. Moreover, the fALFF values of the caudate were correlated with craving and RSFC strength between the caudate and ACC was associated with the cognitive control impairments in young adult smokers. Our findings could lead to a better understanding of intrinsic functional architecture of baseline brain activity in young smokers by providing regional and brain circuit spontaneous neuronal activity properties as well as their association with cognitive control impairments.