Accumulating evidence continues to emphasize the role of microRNAs as significant contributors to depression-like behavior and memory disorders. The current study aimed to investigate the mechanism by which miR-96 influences depression-like behavior and memory deficit in mice. A depression-like behavior and memory disorder mouse model was initially established by means of intraperitoneal injection with lipopolysaccharide. Memory deficits in the mice were evaluated using the Novel Object Recognition Test and Morris water maze experiments, whereas the Sucrose Preference Experiment and forced swimming experiments were performed to identify depression-like behavior in mice. The levels of tumor necrosis factor-α, malondialdehyde, superoxide dismutase, glutathione, and the monoamine transmitters 5-hydroxytryptamine and dopamine were subsequently detected in the serum. Reverse transcription-quantitative polymerase chain reaction and Western blot analysis evaluated the expression of miR-96 and SV2C expression in the es the expression of SV2C, which consequently leads to depression-like behavior and memory impairment in mice. Our findings highlight the potential of miR-96-targeted therapeutics.

Auditory steady-state response (ASSR) is a gamma oscillation evoked by periodic auditory stimuli, which is commonly used in clinical electroencephalographic examination to evaluate the neurological functions. Though it has been suggested that auditory cortex is the origin of ASSR, how the laminar architecture of the neocortex contributes to the ASSR recorded from the brain surface remains unclear.

We used a 16-channel silicon probe to record the local field potential and the single-unit spike activity in the different layers of the auditory cortex of unanesthetized mice. Click-trains with a repetition rate at 40-Hz were present as sound stimuli to evoke ASSR.

We found that the LFPs of all cortical layers showed a stable ASSR synchronizing to the 40-Hz click stimuli, while the ASSR was strongest in the granular (thalamorecipient) layer. Furthermore, time-frequency analyses also revealed the strongest coherence between the signals recorded from the granular layer and pial surface.

Our results reveal that the 40-Hz ASSR primarily shows the evoked gamma oscillation of thalamorecipient layers in the neocortex, and that the ASSR may be a biomarker to detect the cognitive deficits associated with impaired thalamo-cortical connection.

Our results reveal that the 40-Hz ASSR primarily shows the evoked gamma oscillation of thalamorecipient layers in the neocortex, and that the ASSR may be a biomarker to detect the cognitive deficits associated with impaired thalamo-cortical connection.We previously reported that rhesus monkeys recover spontaneous use of the more impaired (contralesional) hand following neurosurgical lesions to the arm/hand representations of primary motor cortex (M1) and lateral premotor cortex (LPMC) (F2 lesion) when tested for reduced use (RU) in a fine motor task allowing use of either hand. Recovery occurred without constraint of the less impaired hand and with occasional forced use of the more impaired hand, which was the preferred hand for use in fine motor tasks before the lesion. Here, we compared recovery of five F2 lesion cases in the same RU test to recovery after unilateral lesions of M1, LPMC, S1 and anterior portion of parietal cortex (F2P2 lesion – four cases). Average and highest %use of the contralesional hand in the RU task in F2 cases were twice that in F2P2 cases (p less then 0.05). Recovery in the RU task was closely associated with volume and percentage of lesion to caudal (new) M1 (M1c) in both F2 and F2P2 lesion cases. One F2P2 case, with the largest M1c lesion and a large rostral somatosensory cortex (S1r) lesion developed severe contralesional hand non-use despite exhibiting some recovery of fine motor function initially. We conclude that the degree of reduced use of the contralesional hand is primarily related to the volume of M1c injury and that severe non-use requires extensive injury to M1c and S1r. Thus, assessing peri-Rolandic injury extent in stroke patients may have prognostic value for predicting susceptibility to RU and non-use in rehabilitation.Guidance errors and unrefined neural map configurations appear linked to certain neurodevelopmental conditions, including autism spectrum disorders. Deficits in specific multisensory tasks that require midbrain processing are highly predictive of cognitive and behavioral phenotypes associated with such syndromes. The lateral cortex of the inferior colliculus (LCIC) is a shell region of the mesencephalon that integrates converging information from multiple levels and modalities. Mature LCIC sensory maps are discretely-organized, mimicking its compartmental micro-organization. Intermittent modular domains receive patchy somatosensory connections, while inputs of auditory origin terminate in the encompassing extramodular matrix.Eph-ephrin signaling mechanisms instruct comparable topographic arrangements in a variety of other systems. this website Whether Eph-ephrin interactions also govern the assembly of LCIC multimodal maps remains unaddressed. Previously, we identified EphA4 and ephrin-B2 as key mediators, with overlapping expression patterns that align with emerging LCIC modules. Here, we implicate another member of this guidance family, ephrin-B3, and quantify its transient expression with respect to neurochemically-defined LCIC compartments. Multiple-labeling studies in GAD67-GFP knock-in mice reveal extramodular ephrin-B3 expression, complementary to that of EphA4 and ephrin-B2. This distinctive pattern sharpens over the early postnatal period (birth to P8), prior to ephrin-B3 downregulation once multimodal LCIC inputs are largely segregated (P12). Channel-specific sampling of LCIC ROIs show ephrin-B3 signal periodicities that are out-of-phase with glutamic acid decarboxylase (GAD;modular marker) signal fluctuations, and match calretinin (CR) waveforms (matrix marker). Taken together, the guidance mosaic registry with emerging LCIC compartments and its interfacing afferent streams suggest a prominent role for Eph-ephrins in ordering behaviorally significant multisensory midbrain networks.Background Schizophrenia affects around 1% of the global population. Functional connectivity extracted from resting-state functional magnetic resonance imaging (rs-fMRI) has previously been used to study schizophrenia and has great potential to provide novel insights into the disorder. Some studies have shown abnormal functional connectivity in the default mode network (DMN) of individuals with schizophrenia, and more recent studies have shown abnormal dynamic functional connectivity (dFC) in individuals with schizophrenia. However, DMN dFC and the link between abnormal DMN dFC and symptom severity have not been well-characterized. Method Resting-state fMRI data from subjects with schizophrenia (SZ) and healthy controls (HC) across two datasets were analyzed independently. We captured seven maximally independent subnodes in the DMN by applying group independent component analysis and estimated dFC between subnode time courses using a sliding window approach. A clustering method separated the dFCs into five retween SZ symptom severity and the dynamics of DMN functional connectivity. We validated our results across two datasets. These results support the potential of dFC for use as a biomarker of schizophrenia and shed new light upon the relationship between schizophrenia and DMN dynamics.Objective We aimed to examine the effects of repetitive peripheral nerve magnetic stimulation (rPNMS) on the excitability of the contralateral motor cortex and motor function of the upper limb in healthy subjects. Methods Forty-six healthy subjects were randomly assigned to either a repetitive peripheral nerve magnetic stimulation group (n = 23) or a sham group (n = 23). The repetitive peripheral nerve magnetic stimulation group received stimulation using magnetic pulses at 20 Hz, which were applied on the median nerve of the non-dominant hand, whereas the sham group underwent the same protocol without the stimulation output. The primary outcome was contralateral transcranial magnetic stimulation (TMS)-induced corticomotor excitability for the abductor pollicis brevis of the stimulated hand in terms of resting motor threshold (rMT), the slope of recruitment curve, and peak amplitude of motor evoked potential (MEP), which were measured at baseline and immediately after each session. The secondary outcomes were motor hand function including dexterity and grip strength of the non-dominant hand assessed at baseline, immediately after stimulation, and 24 h post-stimulation. Results Compared with the sham stimulation, repetitive peripheral nerve magnetic stimulation increased the peak motor evoked potential amplitude immediately after the intervention. The repetitive peripheral nerve magnetic stimulation also increased the slope of the recruitment curve immediately after intervention and enhanced hand dexterity after 24 h. However, the between-group difference for the changes was not significant. The significant changes in hand dexterity and peak amplitude of motor evoked potential after repetitive peripheral nerve magnetic stimulation were associated with their baseline value. Conclusions Repetitive peripheral nerve magnetic stimulation may modulate the corticomotor excitability together with a possible lasting improvement in hand dexterity, indicating that it might be helpful for clinical rehabilitation.Primary dissociated neuronal cultures have become a standard model for studying central nervous system (CNS) development. Such cultures are predominantly prepared from the hippocampus or cortex of rodents (mice and rats), while other mammals are less used. Here, we describe the establishment and extensive characterization of the primary dissociated neuronal cultures derived from the cortex of the gray South American short-tailed opossums, Monodelphis domestica. Opossums are unique in their ability to fully regenerate their CNS after an injury during their early postnatal development. Thus, we used cortex of postnatal day (P) 3-5 opossum to establish long-surviving and nearly pure neuronal cultures, as well as mixed cultures composed of radial glia cells (RGCs) in which their neurogenic and gliogenic potential was confirmed. Both types of cultures can survive for more than 1 month in vitro. We also prepared neuronal cultures from the P16-18 opossum cortex, which were composed of astrocytes and microglia, in addition to neurons. The long-surviving opossum primary dissociated neuronal cultures represent a novel mammalian in vitro platform particularly useful to study CNS development and regeneration.Although the increased expression of members of the chondroitin sulfate proteoglycan family, such as neuron-glial antigen 2 (NG2), have been well documented after an injury to the spinal cord, a complete picture as to the cellular origins and function of this NG2 expression has yet to be made. Using a spinal cord injury (SCI) mouse model, we describe that some infiltrated bone marrow-derived macrophages (BMDMΦ) are early contributors to NG2/CSPG4 expression and secretion after SCI. We demonstrate for the first time that a lesion-related form of cellular debris generated from damaged myelin sheaths can increase NG2/CSPG4 expression in BMDMΦ, which then exhibit enhanced proliferation and decreased phagocytic capacity. These results suggest that BMDMΦ may play a much more nuanced role in secondary spinal cord injury than previously thought, including acting as early contributors to the NG2 component of the glial scar.