A MOF-derived flower-shaped CeCo-oxide as a multifunctional material for high-performance lithium-ion batteries and supercapacitors.

Precursor method is a well-known technology for preparing certain functional materials. In this work, a novel 3d-4f bimetallic organic framework, denoted as 45MCeCo (45 M representing 4,5-imidazole dicarboxylic acid), was successfully synthesized via a hydrothermal technique. The compound thus obtained has the molecular formula of C10H11CeCoN4O12. By meticulously controlling the amounts of the experimental materials, it was feasible to prepare flower-like crystals possessing identical single crystal structures and significantly larger specific surface areas. As a precursor for electrode materials, this structure underwent calcination at different temperatures to prepare Co3O4/CeO2 composites with in situ composite heterostructures. Post-electrochemical tests revealed that CeO2 remains unreactive across all potentials, thereby contributing to the stabilization of the electrode material structure. In contrast, Co3O4 participated in redox reactions to provide a specific capacity to the sample. In addition, when comparing the performance of the electrode material under different calcination conditions, it became evident that the material exhibited optimal electrochemical performance when subjected to a temperature of 700 °C for 2 h.

Synthesis and clinical application of new drugs approved by FDA in 2023.

In 2023, the U.S. Food and Drug Administration (FDA) granted approval to a total of 55 new drugs, comprising 29 new chemical entities (NCEs) and 25 new biological entities (NBEs). These drugs primarily focus on oncology, the central nervous system, anti-infection, hematology, cardiovascular, ophthalmology, immunomodulatory and other therapeutic areas. Out of the 55 drugs, 33 (60 %) underwent an accelerated review process and received approval, while 25 (45 %) were specifically approved for the treatment of rare diseases. The purpose of this review is to provide an overview of the clinical uses and production techniques of 29 newly FDA-approved NCEs in 2023. Our intention is to offer a comprehensive understanding of the synthetic approaches employed in the creation of these drug molecules, with the aim of inspiring the development of novel, efficient, and applicable synthetic methodologies.

[Effect of different suspension moxibustion methods on syndrome characteristics of rats with rheumatoid arthritis of heat bi syndrome based on "moxibustion can be used for heat syndrome"].

OBJECTIVE: To observe the effects of different suspension moxibustion methods on the syndrome characteristics and inflammatory factors of rats with rheumatoid arthritis (RA) of heat bi syndrome and to prove the concept of "moxibustion can be used for heat syndrome". METHODS: Among seventy Wistar rats, 12 rats were randomly selected as a normal group, and the remaining rats were induced by collagen combined with wind, dampness, and heat environmental stimulation to establish the RA model of heat bi syndrome. Forty-eight rats with successful model establishment were further randomly divided into a model group and three moxibustion groups (mild moxibustion group, rotating moxibustion group and sparrow-pecking moxibustion group), with 12 rats in each group. The acupoints "Quchi" (LI 11), "Dazhui" (GV 14) and ashi point were used in all moxibustion groups, with mild moxibustion, rotating moxibustion, and sparrow-pecking moxibustion intervention given respectively, each acupoint was treated with moxibustion for 10 min a day, and 6 days were considered one course of treatment, with a total of three courses. After the intervention, the arthritis index (AI), the Evans blue (EB) extravasated volume in the soft tissue of the right hind paw, and the levels of tumor necrosis factor (TNF)-α and interleukin (IL)-10 in the serum were measured by ELISA in each group. The volume of the bilateral hind paw was measured; the infrared thermal imaging was collected to analyze the temperature of the plantar area of the bilateral foot pads, and the reaction time of plantar heat pain was calculated before and after modeling, as well as after the 1st, 2nd and 3rd courses of interrention. The ankle dorsiflexion angle of the right hind foot was also measured before and after modeling, as well as after the intervention. RESULTS: After modeling, compared with the normal group, the rats in the model group had more high-temperature areas in the bilateral hind limbs, abnormal AI score, abnormal bilateral hind paw volume, abnormal temperature of the plantar area of the bilateral foot pads, abnormal foot pain response time, abnormal right hind ankle dorsiflexion angle, abnormal right hind paw soft tissue EB extravasation, and abnormal serum TNF-α and IL-10 levels (P<0.01, P<0.05). After the intervention, compared with the model group, the rats in each moxibustion group had decreased or disappeared high-temperature areas in the bilateral hind limbs, EB extravasated volume in the soft tissue of the right hind paw was reduced (P<0.05), and the right ankle dorsiflexion angle was increased (P<0.05), serum level of TNF-α was reduced, and level of IL-10 increased (P<0.05); the AI scores in the mild moxibustion group and the sparrow-pecking moxibustion group was decreased (P<0.01, P<0.05). After the 1st, 2nd and 3rd courses of intervention, compared with the model group, the bilateral hind paw volume of rats in each moxibustion group was decreased (P<0.05, P<0.01), and plantar heat pain reaction time was increased (P<0.05). After the 2nd course and the 3rd course of intervention, the temperature of the right hind paw pad area was decreased in each moribustion group (P<0.05); after the 3rd courses of intervention, the temperature of the left hind paw pad area was decreased in the mild moxibustion group (P<0.05). CONCLUSION: Suspension moxibustion could adjust the serum levels of TNF-α and IL-10 to improve the syndrome characteristics of RA rats of heat bi syndrome, such as joint redness, swelling, heat, pain and activity restriction. The effect of mild moxibustion is the most prominent. The findings could provide scientific basis for "moxibustion can be used for heat syndrome".

Sensory Reinforced Corticostriatal Plasticity.

BACKGROUND: Regional changes in corticostriatal transmission induced by phasic dopaminergic signals are an essential feature of the neural network responsible for instrumental reinforcement during discovery of an action. However, the timing of signals that are thought to contribute to the induction of corticostriatal plasticity is difficult to reconcile within the framework of behavioural reinforcement learning, because the reinforcer is normally delayed relative to the selection and execution of causally-related actions. OBJECTIVE: While recent studies have started to address the relevance of delayed reinforcement signals and their impact on corticostriatal processing, our objective was to establish a model in which a sensory reinforcer triggers appropriately delayed reinforcement signals relayed to the striatum via intact neuronal pathways and to investigate the effects on corticostriatal plasticity. METHODS: We measured corticostriatal plasticity with electrophysiological recordings using a light flash as a natural sensory reinforcer, and pharmacological manipulations were applied in an in vivo anesthetized rat model preparation. RESULTS: We demonstrate that the spiking of striatal neurons evoked by single-pulse stimulation of the motor cortex can be potentiated by a natural sensory reinforcer, operating through intact afferent pathways, with signal timing approximating that required for behavioural reinforcement. The pharmacological blockade of dopamine receptors attenuated the observed potentiation of corticostriatal neurotransmission. CONCLUSION: This novel in vivo model of corticostriatal plasticity offers a behaviourally relevant framework to address the physiological, anatomical, cellular, and molecular bases of instrumental reinforcement learning.

A novel detection method for neuronal death indicates abnormalities in intracellular membranous components in neuronal cells that underwent delayed death.

Acute neuronal degeneration is always preceded under the light and electron microscopes by a stage called microvacuolation, which is characterized by a finely vacuolar alteration in the cytoplasm of the neurons destined to death. In this study, we reported a method for detecting neuronal death using two membrane-bound dyes, rhodamine R6 and DiOC6(3), which may be associated with the so-called microvacuolation. This new method produced a spatiotemporally similar staining pattern to Fluoro-Jade B in kainic acid-damaged brains in mice. Further experiments showed that increased staining of rhodamine R6 and DiOC6(3) was observed only in degenerated neurons, but not in glia, erythrocytes, or meninges. Different from Fluoro-Jade-related dyes, rhodamine R6 and DiOC6(3) staining is highly sensitive to solvent extraction and detergent exposure. Staining with Nile red for phospholipids and filipin III for non-esterified cholesterol supports that the increased staining of rhodamine R6 and DiOC6(3) might be associated with increased levels of phospholipids and free cholesterol in the perinuclear cytoplasm of damaged neurons. In addition to kainic acid-injected neuronal death, rhodamine R6 and DiOC6(3) were similarly useful for detecting neuronal death in ischemic models either in vivo or in vitro. As far as we know, the staining with rhodamine R6 or DiOC6(3) is one of a few histochemical methods for detecting neuronal death whose target molecules have been well defined and therefore may be useful for explaining experimental results as well as exploring the mechanisms of neuronal death.

The rearrangement of actin cytoskeleton in mossy fiber synapses in a model of experimental febrile seizures.

Background: Experimental complex febrile seizures induce a persistent hippocampal hyperexcitability and an enhanced seizure susceptibility in adulthood. The rearrangement of filamentous actin (F-actin) enhances the excitability of hippocampus and contributes to epileptogenesis in epileptic models. However, the remodeling of F-actin after prolonged febrile seizures is to be determined. Methods: Prolonged experimental febrile seizures were induced by hyperthermia on P10 and P14 rat pups. Changes of actin cytoskeleton in hippocampal subregions were examined at P60 and the neuronal cells and pre- /postsynaptic components were labeled. Results: F-actin was increased significantly in the stratum lucidum of CA3 region in both HT + 10D and HT + 14D groups and further comparison between the two groups showed no significant difference. The abundance of ZNT3, the presynaptic marker of mossy fiber (MF)-CA3 synapses, increased significantly whereas the postsynaptic marker PSD95 did not change significantly. Overlapping area of F-actin and ZNT3 showed a significant increase in both HT+ groups. The results of cell counts showed no significant increase or decrease in the number of neurons in each area of hippocampus. Conclusion: F-actin was significantly up-regulated in the stratum lucidum of CA3, corresponding to the increase of the presynaptic marker of MF-CA3 synapses after prolonged febrile seizures, which may enhance the excitatory output from the dentate gyrus to CA3 and contribute to the hippocampal hyperexcitability.

Overexpression of Sedum SpHMA2, SpHMA3 and SpNramp6 in Brassica napus increases multiple heavy metals accumulation for phytoextraction.

Phytoextraction is an environmentally friendly phytoremediation technology that can reduce the total amount of heavy metals (HMs) in the soil. Hyperaccumulators or hyperaccumulating transgenic plants with biomass are important biomaterials for phytoextraction. In this study, we show that three different HM transporters from the hyperaccumulator Sedum pumbizincicola, SpHMA2, SpHMA3, and SpNramp6, possess Cd transport. These three transporters are located at the plasma membrane, tonoplast, and plasma membrane, respectively. Their transcripts could be strongly stimulated by multiple HMs treatments. To create potential biomaterials for phytoextraction, we overexpressed the three single genes and two combining genes, SpHMA2&SpHMA3 and SpHMA2&SpNramp6, in rapes having high biomass and environmental adaptability, and found that the aerial parts of the SpHMA2-OE3 and SpHMA2&SpNramp6-OE4 lines accumulated more Cd from single Cd-contaminated soil because SpNramp6 transports Cd from root cells to the xylem and SpHMA2 from the stems to the leaves. However, the accumulation of each HM in the aerial parts of all selected transgenic rapes was strengthened in multiple HMs-contaminated soils, probably due to the synergistic transport. The HMs residuals in the soil after the transgenic plant phytoremediation were also greatly reduced. These results provide effective solutions for phytoextraction in both Cd and multiple HMs-contaminated soils.

TREM-1 governs NLRP3 inflammasome activation of macrophages by firing up glycolysis in acute lung injury.

The triggering receptor expressed on myeloid cells-1 (TREM-1) is a pro-inflammatory immune receptor potentiating acute lung injury (ALI). However, the mechanism of TREM-1-triggered inflammation response remains poorly understood. Here, we showed that TREM-1 blocking attenuated NOD-, LRR- and pyrin domain-containing 3 (NLRP3) inflammasome activation and glycolysis in LPS-induced ALI mice. Then, we observed that TREM-1 activation enhanced glucose consumption, induced glycolysis, and inhibited oxidative phosphorylation in macrophages. Specifically, inhibition of glycolysis with 2-deoxyglucose diminished NLRP3 inflammasome activation of macrophages triggered by TREM-1. Hypoxia-inducible factor-1α (HIF-1α) is a critical transcriptional regulator of glycolysis. We further found that TREM-1 activation facilitated HIF-1α accumulation and translocation to the nucleus via the phosphoinositide 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) pathway. Inhibiting mTOR or HIF-1α also suppressed TREM-1-induced metabolic reprogramming and NLRP3/caspase-1 activation. Overall, the mTOR/HIF-1α/glycolysis pathway is a novel mechanism underlying TREM-1-governed NLRP3 inflammasome activation. Therapeutic targeting of the mTOR/HIF-1α/glycolysis pathway in TREM-1-activated macrophages could be beneficial for treating or preventing inflammatory diseases, such as ALI.

The Integration of Top-down and Bottom-up Inputs to the Striatal Cholinergic Interneurons.

BACKGROUND: Cholinergic interneurons (ChIs) are important for learning and memory. They exhibit a multiphasic excitation-pause-rebound response to reward or sensory cues indicating a reward, believed to gate dopamine-dependent learning. Although ChIs receive extensive top-down inputs from the cortex and bottom-up inputs from the thalamus and midbrain, it is unclear which inputs are involved in the development of ChI multiphasic activity. METHODS: We used a single-unit recording of putative ChIs (pChIs) in response to cortical and visual stimulation to investigate how top-down and bottom-up inputs regulate the firing pattern of ChIs. RESULTS: We demonstrated that cortical stimulation strongly regulates pChIs, with the maximum firing rate occurring at the peak of the inverted local field potential (iLFP), reflecting maximum cortical stimulation. Pauses in pChIs occurred during the descending phase of iLFP, indicating withdrawal of excitatory cortical input. Visual stimulation induced long pauses in pChIs, but it is unlikely that bottom- up inputs alone induce pauses in behaving animals. Also, the firing pattern of ChIs triggered by visual stimulation did not correlate with the iLFP as it did after cortical stimulation. Top-down and bottom-up inputs independently regulate the firing pattern of ChIs with similar efficacy but notably produce a well-defined pause in ChI firing. CONCLUSION: This study provides in vivo evidence that the multiphasic ChI response may require both top-down and bottom-up inputs. The findings suggest that the firing pattern of ChIs correlated to the iLFP might be a useful tool for estimating the degree of contribution of top-down and bottom-up inputs in regulating the firing activity of ChIs.

Mitochondrial citrate accumulation drives alveolar epithelial cell necroptosis in lipopolysaccharide-induced acute lung injury.

Necroptosis is the major cause of death in alveolar epithelial cells (AECs) during acute lung injury (ALI). Here, we report a previously unrecognized mechanism for necroptosis. We found an accumulation of mitochondrial citrate (citratemt) in lipopolysaccharide (LPS)-treated AECs because of the downregulation of Idh3α and citrate carrier (CIC, also known as Slc25a1). shRNA- or inhibitor-mediated inhibition of Idh3α and Slc25a1 induced citratemt accumulation and necroptosis in vitro. Mice with AEC-specific Idh3α and Slc25a1 deficiency exhibited exacerbated lung injury and AEC necroptosis. Interestingly, the overexpression of Idh3α and Slc25a1 decreased citratemt levels and rescued AECs from necroptosis. Mechanistically, citratemt accumulation induced mitochondrial fission and excessive mitophagy in AECs. Furthermore, citratemt directly interacted with FUN14 domain-containing protein 1 (FUNDC1) and promoted the interaction of FUNDC1 with dynamin-related protein 1 (DRP1), leading to excessive mitophagy-mediated necroptosis and thereby initiating and promoting ALI. Importantly, necroptosis induced by citratemt accumulation was inhibited in FUNDC1-knockout AECs. We show that citratemt accumulation is a novel target for protection against ALI involving necroptosis.

The EEG Features of Four Cases of Subacute Sclerosing Panencephalitis in North China : SSPE EEG Features.

Objective. To analyze the EEG features of four subacute sclerosing panencephalitis cases in North China. Methods. We retrospectively analyzed the EEG features in four patients with subacute sclerosing panencephalitis and 12 patients in control group from North China. Results. The periodic long-interval diffuse discharges were found in all of the four cases with subacute sclerosing panencephalitis. The morphology and component of periodic complexes were varied in different patients and different wakefulness states. Some EEG parameter settings help to identify periodic long-interval diffuse discharges including the slowed sweep speed, decreased sensitivity and reduced number of montages. In each patient with subacute sclerosing panencephalitis, the periodic long-interval diffuse discharges associated with two types of brief episodes (1:1) during awake period were found and none of the patients in the control group had this EEG pattern. The score system based on the periodic discharges and brief episodes also shows that all the patients with SSPE reached score 5 while none of the patients in the control group has a score greater than 3, which suggests that this EEG pattern may have diagnostic value. Conclusions. In subacute sclerosing panencephalitis, the morphology and component of periodic long-interval diffuse discharges were varied in different patients and different wakefulness states. Specific EEG parameter settings help to identify periodic long-interval diffuse discharges. Periodic long-interval diffuse discharges associated with two types of brief episodes (1:1) during awake period may strongly suggest the diagnosis of subacute sclerosing panencephalitis.

Evaluation of Pelvic Floor Dysfunction by Pelvic Floor Ultrasonography after Total Hysterectomy for Cervical Cancer.

Objective: To study the value of pelvic floor ultrasonography in evaluating pelvic floor dysfunction (PFD) after total hysterectomy for cervical cancer. Methods: All the enrolled patients were given 4D pelvic floor ultrasound examination before and after surgery. The results of ultrasonic examination and the parameters of four-dimensional ultrasonic examination before and after surgery were analyzed, and the quality of life of the patients before and after surgery was evaluated. Results: Postoperatively, the posterior angle of bladder and urethra, the rotation angle of urethra, the decreased value of bladder neck, and the distance between bladder neck and pubic symphysis were (122.60 ± 9.53)°, (136.47 ± 14.67)°, (58.90 ± 18.19)°, (18.14 ± 7.32) mm, and (2.76 ± 0.46) cm, significantly greater than the preoperative (89.90 ± 9.59)°, (107.30 ± 9.96)°, (27.59 ± 10.96)°, (13.27 ± 5.69) mm, and (2.24 ± 0.21) cm (P < 0.05). Postoperative detrusor muscle thickness, bladder neck movement, residual urine volume, and bladder rotation angle (4.48 ± 0.82) mm, (0.64 ± 0.17) cm, (12.82 ± 2.69) ml, (12.11 ± 2.43)° were significantly higher than those of preoperative (3.70 ± 0.64) mm, (0.43 ± 0.18) cm, (4.83 ± 1.07) ml, (4.30 - 1.19)° (P < 0.05). The scores of emotional function, psychological function, social function, and physiological function were (2.35 ± 0.75) points, (2.45 ± 0.66) points, (2.30 ± 0.77) points, and (2.19 ± 0.71) points, significantly higher than those of (1.01 ± 0.50) points, (1.25 ± 0.54) points, and (1.00 ± 0.57) points before surgery, (1.05 ± 0.46) (P < 0.05). Conclusions: The application of pelvic floor ultrasonography to detect pelvic floor dysfunction after total hysterectomy can clearly display the anatomical structure of the pelvic floor, which is conducive to disease prevention and treatment. Four-dimensional pelvic floor ultrasound can clearly show the postoperative pelvic floor function, which is worthy of clinical promotion and reference.

Coincidence of cholinergic pauses, dopaminergic activation and depolarisation of spiny projection neurons drives synaptic plasticity in the striatum.

Dopamine-dependent long-term plasticity is believed to be a cellular mechanism underlying reinforcement learning. In response to reward and reward-predicting cues, phasic dopamine activity potentiates the efficacy of corticostriatal synapses on spiny projection neurons (SPNs). Since phasic dopamine activity also encodes other behavioural variables, it is unclear how postsynaptic neurons identify which dopamine event is to induce long-term plasticity. Additionally, it is unknown how phasic dopamine released from arborised axons can potentiate targeted striatal synapses through volume transmission. To examine these questions we manipulated striatal cholinergic interneurons (ChIs) and dopamine neurons independently in two distinct in vivo paradigms. We report that long-term potentiation (LTP) at corticostriatal synapses with SPNs is dependent on the coincidence of pauses in ChIs and phasic dopamine activation, critically accompanied by SPN depolarisation. Thus, the ChI pause defines the time window for phasic dopamine to induce plasticity, while depolarisation of SPNs constrains the synapses eligible for plasticity.

Heavy metal transporters: Functional mechanisms, regulation, and application in phytoremediation.

Heavy metal pollution in soil is a global problem with serious impacts on human health and ecological security. Phytoextraction in phytoremediation, in which plants uptake and transport heavy metals (HMs) to the tissues of aerial parts, is the most environmentally friendly method to reduce the total amount of HMs in soil and has wide application prospects. However, the molecular mechanism of phytoextraction is still under investigation. The uptake, translocation, and retention of HMs in plants are mainly mediated by a variety of transporter proteins. A better understanding of the accumulation strategy of HMs via transporters in plants is a prerequisite for the improvement of phytoextraction. In this review, the biochemical structure and functions of HM transporter families in plants are systematically summarized, with emphasis on their roles in phytoremediation. The accumulation mechanism and regulatory pathways related to hormones, regulators, and reactive oxygen species (ROS) of HMs concerning these transporters are described in detail. Scientific efforts and practices for phytoremediation carried out in recent years suggest that creation of hyperaccumulators by transgenic or gene editing techniques targeted to these transporters and their regulators is the ultimate powerful path for the phytoremediation of HM contaminated soils.

Association Between HDL-C and Bone Mineral Density: An Cross-Sectional Analysis.

BACKGROUND: Dyslipidemia has been found to contribute to increased risk of osteoporosis and its association with bone mineral density (BMD) remains controversial. We determined whether blood lipid levels are linked with change of BMD. METHODS: In a large sample from the MIDUS II study, we sought to evaluate the relationship between blood lipid levels and BMD. Multivariate linear regression models and smooth curve analysis were constructed by controlling a great range of confounding factors. RESULTS: The median age of them was 52.5 years, and the number of males was 176 (40%). Univariate analysis showed that blood high-density lipoprotein-cholesterol (HDL-C) level was negatively related to lunar total femur (r = -0.266, P < 0.001), lunar radius ultradistal (UD) (r = -0.297, P < 0.001), lunar radius 1/3 (r = -0.307, P = 0.001) and femoral neck (r = -0.172, P = 0.001). In multivariate linear analysis, except for blood triglyceride, total cholesterol and low-density lipoprotein cholesterol (LDL-C), we found that blood HDL-C level was still negatively related to lunar total femur [B = -0.002, B 95% CI (-0.002, -0.001), P < 0.001], lunar radius UD [B = -0.001, 95% CI (-0.001, 0), P = 0.002], lunar radius 1/3 [B = -0.001, 95% CI (-0.001, 0), P = 0.003] and femoral neck [B = -0.001, 95% CI (-0.002, 0), P = 0.039] after adjustments of demographic characteristics, lifestyle, disease history were made. Furthermore, we found that age, sex, and body mass index (BMI) had modifying effects on this negative association. CONCLUSION: This study confirmed the negative association between HDL-C and BMD in the observational analysis from (MIDUS) study and provides high-quality evidence that age, sex and BMI had modifying effects on this negative association.

Revisiting dopamine-acetylcholine imbalance in Parkinson's disease: Glutamate co-transmission as an exciting partner in crime.

Striatal dopamine and acetylcholine are thought to be imbalanced in Parkinson's disease. In this issue of Neuron, Cai et al. report that restoration of nigral glutamate co-transmission, acting on dorsolateral striatal cholinergic interneuron mGluR1s, can rescue motor dysfunction in a mouse model of Parkinson's.

Paroxysmal tonic upgaze accompanied by occipital discharge on electroencephalography: a case report and literature review.

BACKGROUND: Paroxysmal tonic upgaze (PTU) is an infantile-onset paroxysmal neurological disorder that is characterized by episodes of sustained conjugate upward eye deviation. The paroxysmal abnormal eye movements need to be differentiated from seizures. We report a case of PTU with occipital discharge on electroencephalography (EEG), which made the diagnosis more complicated. CASE PRESENTATION: A 6-month-old girl presented with paroxysmal upward deviation or left strabismus of the eyes, with a bowed head, lowered jaw, raised eyebrows, closed lips, and slight grin. Each episode lasted for a few seconds, and episodes occurred multiple times per day. EEG showed spike waves in the right occipital region, and the girl was initially misdiagnosed with epilepsy. After further analysis using video EEG, we corrected her diagnosis as PTU and stopped the administration of an antiepileptic drug. CONCLUSION: PTU accompanied by discharge on EEG may lead to a misdiagnosis. Video EEG monitoring, and especially the analysis of EEG traces synchronized with attacks, can provide evidence to distinguish between seizures and non-epileptic events.

Stratification of hippocampal electrophysiological activation evoked by selective electrical stimulation of different angular and linear acceleration sensors in the rat peripheral vestibular system.

It has become well established that vestibular information is important for hippocampal function and spatial memory. However, as yet, relatively little is known about how different kinds of vestibular information are 'represented' in different parts of the hippocampus. This study used selective electrical stimulation of each of the 5 vestibular sensors (the horizontal (HC), anterior (AC) and posterior (PC) semi-circular canals, and the utricle and saccule) in the rat and recorded local field potentials (LFPs) across the hippocampus, using a 16 electrode microarray. We found that stimulation of any vestibular sensor in the left labyrinth evoked triphasic LFPs in both hippocampi, although it was clear that, in general, the amplitudes were greater for the right, contralateral side. This was particularly true for Phase 1 for the HC, AC, utricle and saccule, Phase 2 for the HC, PC, utricle and saccule, and Phase 3 for the AC, PC and saccule. Overall, our results suggest that vestibular input to the hippocampus is bilateral, preferentially contralateral, but highly stratified in that stimulation of the same vestibular sensor results in activation of different specific areas of the hippocampus, with different LFP amplitudes and latencies. This suggests the possibility that different regions of the hippocampus use different kinds of vestibular information for different purposes and that there may be a high degree of redundancy in the representation of vestibular input, perhaps ensuring that the hippocampus is more robust to the partial loss of vestibular information.

The effects of selective electrical stimulation of the rat cochlea on hippocampal field potentials.

The hippocampus is a brain structure well known for its importance to spatial learning and memory. As such it is assumed to use multisensory integration in order to generate mathematical maps of the spatial environment. Auditory inputs to the hippocampus have been described to a limited extent. Although it has been demonstrated that natural auditory stimulation can evoke local field potentials (LFPs) and single neuron responses in the hippocampus, and that noise trauma and tinnitus can cause maladaptive hippocampal plasticity, to the best of our knowledge no one has selectively, electrically stimulated the cochlea and recorded electrophysiological responses in the hippocampus. Here, we used unilateral electrical cochlear stimulation in rats while recording LFPs in the hippocampus bilaterally, with a multi-electrode array. We observed triphasic LFP responses bilaterally from unilateral stimulation, but with larger amplitudes on the contralateral side, especially for Phase 1 and 3 of the LFP, for which the latencies were also longer. The latencies under urethane anaesthesia were consistent with auditory information from the cochlea travelling across approximately 6-7 synapses. These data demonstrate that the cochlea contributes a powerful auditory input to the hippocampus, which is also lateralized, and may have implications for spatial cognition in cochlear implant patients.

Effects of Dexamethasone on Remodeling of the Hippocampal Synaptic Filamentous Actin Cytoskeleton in a Model of Pilocarpine-induced Status Epilepticus.

The filamentous actin (F-actin) cytoskeleton is progressively damaged after status epilepticus (SE), which is related to delayed neuronal death, aberrant recurrent circuits and epileptogenesis. Glucocorticoids regulate dendritic spine remodeling by acting on glucocorticoid receptors and the dynamics of the F-actin cytoskeleton. Our previous study showed that administration of dexamethasone (DEX) in the latent period of the pilocarpine epileptic model reduces damage to the hippocampal filamentous actin cytoskeleton and the loss of hippocampal neurons and aids in maintaining the synaptic structures, but it is not sufficient to stop epileptogenesis. In this work, we focused on the role of glucocorticoids in regulating the hippocampal F-actin cytoskeleton during SE. We examined the abundance of synaptic F-actin, analyzed the hippocampal F-actin/G-actin (F/G) ratio and pCofilin, and evaluated the number of hippocampal neurons and pre/postsynaptic markers in pilocarpine-induced status epilepticus mice with or without administration of dexamethasone (DEX). We found that the latency of Stage 3 seizures increased, the mortality decreased, the damage to the synaptic F-actin cytoskeleton in the hippocampal subfields was significantly attenuated, and a greater number of postsynaptic structures were retained in the hippocampal subfields after treatment with DEX. These results indicate that treatment with dexamethasone stabilizes the synaptic F-actin cytoskeleton and reduces the damage to the brain due to SE. This approach is expected to be beneficial in alleviating delayed neuron damage and the process of epileptogenesis.