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Recent progress in optically pumped magnetometers (OPMs) and high-temperature superconducting quantum interference devices (SQUIDs) has facilitated the development of an on-scalp magnetoencephalography (MEG) system that offers high signal intensity and flexibility at a lower cost. While the on-scalp sensor array has high flexibility, it brings new challenges to accurate sensor-to-brain coregistration, which is essential for MEG source localization.
A novel automatic filtering algorithm based on plane segmentation was proposed to locate on-scalp MEG sensors in 3D images reconstructed from optical scanning. Global image registration was employed for the automatic alignment of anatomical images and sensor positions.
Seventy-one sensor dummies on the scalp were located and registered to brain anatomical images. The deviations of the sensor location and orientation from the averaged result of 10 measurements were less than 1 mm and 0.6°, respectively. The entire process could be completed in less than 4 min.
Compared with existing methods that involve various manual procedures, such as moving digitizers to fiducials and repeatedly pulling out sensors, our proposed coregistration method is more efficient and accurate.
An automatic method for the coregistration of anatomical structure and on-scalp sensors that will have a large impact on the practical use of on-scalp MEG is developed.
An automatic method for the coregistration of anatomical structure and on-scalp sensors that will have a large impact on the practical use of on-scalp MEG is developed.Hypertension is a major cause of cardiovascular morbidity and mortality, despite the availability of antihypertensive drugs with different targets and mechanisms of action. Here, we provide evidence that pharmacological inhibition of TMEM16A (ANO1), a calcium-activated chloride channel expressed in vascular smooth muscle cells, blocks calcium-activated chloride currents and contraction in vascular smooth muscle in vitro and decreases blood pressure in spontaneously hypertensive rats. The acylaminocycloalkylthiophene TMinh-23 fully inhibited calcium-activated TMEM16A chloride current with nanomolar potency in Fischer rat thyroid cells expressing TMEM16A, and in primary cultures of rat vascular smooth muscle cells. TMinh-23 reduced vasoconstriction caused by the thromboxane mimetic U46619 in mesenteric resistance arteries of wild-type and spontaneously hypertensive rats, with a greater inhibition in spontaneously hypertensive rats. Epigenetic Reader Domain inhibitor Blood pressure measurements by tail-cuff and telemetry showed up to a 45-mmHg reduction in systolic blood pressure lasting for four-six hours in spontaneously hypertensive rats after a single dose of TMinh-23. A minimal effect on blood pressure was seen in wild-type rats or mice treated with TMinh-23. Five-day twice daily treatment of spontaneously hypertensive rats with TMinh-23 produced sustained reductions of 20-25 mmHg in daily mean systolic and diastolic blood pressure. TMinh-23 action was reversible, with blood pressure returning to baseline in spontaneously hypertensive rats by three days after treatment discontinuation. Thus, our studies provide validation for TMEM16A as a target for antihypertensive therapy and demonstrate the efficacy of TMinh-23 as an antihypertensive with a novel mechanism of action.Increased perineuronal net (PNN) deposition has been observed in association with corticosteroid administration and stress in rodent models of depression. PNNs are a specialized form of extracellular matrix (ECM) that may enhance GABA-mediated inhibitory neurotransmission to potentially restrict the excitation and plasticity of pyramidal glutamatergic neurons. In contrast, antidepressant administration increases levels of the PNN-degrading enzyme matrix metalloproteinase-9 (MMP-9), which enhances glutamatergic plasticity and neurotransmission. In the present study, we compare pro-MMP-9 levels and measures of stress in females from two mouse strains, C57BL/6 J and BALB/cJ, in the presence or absence of tail grasping versus tunnel-associated cage transfers. Prior work suggests that C57BL/6 J mice show relatively enhanced neuroplasticity and stress resilience, while BALB/c mice demonstrate enhanced susceptibility to adverse effects of stress. Herein we observe that as compared to the C57BL/6 J strain, BALB/c mice demonstrate a higher level of baseline anxiety as determined by elevated plus maze (EPM) testing. Moreover, as determined by open field testing, anxiety is differentially reduced in BALB/c mice by a choice-driven tunnel-entry cage transfer technique. Additionally, as compared to tail-handled C57BL/6 J mice, tail-handled BALB/c mice have reduced brain levels of pro-MMP-9 and increased levels of its endogenous inhibitor, tissue inhibitor of metalloproteinase-1 (TIMP-1); however, tunnel-associated cage transfer increases pro-MMP-9 levels in BALB/c mice. BALB/c mice also show increases in Western blot immunoreactive bands for brevican, a constituent of PNNs. Together, these data support the possibility that MMP-9, an effector of PNN remodeling, contributes to the phenotype of strain and handling-associated differences in behavior.The symptoms of human depression often include cognitive deficits. However, cognition is not frequently included in the behavioral assessments conducted in preclinical models of depression. For example, it is well known that repeated corticosterone (CORT) injections in rodents produce depression-like behavior as measured by the forced swim test, sucrose preference test, and tail suspension test, but the cognitive impairments produced by repeated CORT have not been thoroughly examined. The purpose of this experiment was to assess the effect of repeated CORT injections on several versions of object recognition memory and modulation of the acoustic startle response by relatively low intensity prepulses, along with the more traditional assessment of depression-like behavior using the forced swim test. Rats received 21 days of CORT (40 mg/kg) or vehicle injections followed by a battery of behavioral tests. Importantly, during behavioral testing CORT treatment did not occur (CORT withdrawal). Corticosterone decreased body weight, increased immobility in the forced swim test, lowered startle amplitudes, and facilitated responding to trials with a short interval (30 ms) between the prepulse and pulse.
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