Cerebellar Granule Cells Research Articles

Gravity-driven flow of liquid bridges between vertical fibres

Liquid bridges are formed when a flowing liquid interacts with multiple parallel fibres, as relevant to heat and mass transfer applications that utilize flow down fibre arrays. We perform a comprehensive experimental study of flowing liquid bridges between two vertical fibres whose spacing is controlled dynamically in our experimental apparatus. The bridge patterns exhibit a regular periodic spacing typical of absolute instability for low flow rates, but become spatially inhomogeneous above a critical flow rate where the base flow is convectively unstable. The shapes of individual bridges and their associated dynamics are measured, as they depend upon the liquid properties, and fibre geometry/spacing. The bridge length scales similarly to static bridges between parallel fibres. The bridge dynamics exhibits a dependence on viscosity and scale with the impedance. A simple energy balance is used to derive a scaling relationship for the bridge velocity that captures the general trend of our experimental data. Finally, we demonstrate that these scalings similarly apply when the fibres are dynamically separated or brought together.

An increase in reactive oxygen species underlies neonatal cerebellum repair.

The neonatal mouse cerebellum shows remarkable regenerative potential upon injury at birth, wherein a subset of Nestin-expressing progenitors (NEPs) undergoes adaptive reprogramming to replenish granule cell progenitors that die. Here, we investigate how the microenvironment of the injured cerebellum changes upon injury and contributes to the regenerative potential of normally gliogenic-NEPs and their adaptive reprogramming. Single cell transcriptomic and bulk chromatin accessibility analyses of the NEPs from injured neonatal cerebella compared to controls show a temporary increase in cellular processes involved in responding to reactive oxygen species (ROS), a known damage-associated molecular pattern. Analysis of ROS levels in cerebellar tissue confirm a transient increased one day after injury at postanal day 1, overlapping with the peak cell death in the cerebellum. In a transgenic mouse line that ubiquitously overexpresses human mitochondrial catalase (mCAT), ROS is reduced 1 day after injury to the granule cell progenitors, and we demonstrate that several steps in the regenerative process of NEPs are curtailed leading to reduced cerebellar growth. We also provide evidence that microglia are involved in one step of adaptive reprogramming by regulating NEP replenishment of the granule cell precursors. Collectively, our results highlight that changes in the tissue microenvironment regulate multiple steps in adaptative reprogramming of NEPs upon death of cerebellar granule cell progenitors at birth, highlighting the instructive roles of microenvironmental signals during regeneration of the neonatal brain.

Optical networking that exploits massive wavelength/spectrum and spatial parallelisms

As DWDM transmission offers enhanced wavelength/spectrum parallelism, the capacity of optical networks has been substantially increased. Due to the theoretical capacity limit of C-band transmission over single-mode fibers, research into new frequency bands and parallel fibers has become very active. However, the hardware scale of current optical cross-connect nodes will explode with greater wavelength/spectrum and spatial parallelism. Three optical node/network architectures are presented in this paper that take advantage of one or both of these parallelism technologies. These architectures will provide a baseline for cost-effective and bandwidth-abundant future optical networks based on massive parallelism.

A Flexible Pressure Sensor With Parallel Fiber Structure for Wireless Capsule Detection

A Flexible Pressure Sensor With Parallel Fiber Structure for Wireless Capsule Detection

Experimental Study of Fiber-Optic Temperature Sensor Based on Dual FSIs

To improve the sensitivity measurement of temperature sensors, a fiber optic temperature sensor structure based on the harmonic Vernier effect with two parallel fiber Sagnac interferometers (FSIs) is designed, and theoretical analysis and experimental testing are conducted. The FSI consisting of two polarization maintaining fibers (PMFs) with lengths of 13.62 m and 15.05 m respectively is used to achieve the basic Vernier effect. Then by changing the length of one PMF to approximately i times that of the others, the FSI composed of two PMFs of 7.1 m and 15.05 m is used to achieve the first-order harmonic Vernier effect. Afterward, temperature sensing tests are conducted to observe the wavelength drift during temperature changes and ultimately achieve high sensitivity. The experimental results show that the temperature sensitivity of the sensor based on the first-order harmonic Vernier effect is −28.89 nm/°C, which is 17.09 times that of a single FSI structure (−1.69 nm/°C) and 1.84 times that of the sensitivity generated by the structure based on the basic Vernier effect (−15.69 nm/°C). The experimental results are consistent with the theoretical analysis. The structure proposed in this paper achieves drift measurement of 0.1 °C variation based on 1 °C drift, making the fiber optic temperature sensor applicable to related fields that require high precision temperature. The proposed temperature sensor has the simple structure, low production cost, high sensitivity, and broad application prospects.

Antagonistic action of Siah2 and Pard3/JamC to promote germinal zone exit of differentiated cerebellar granule neurons by modulating Ntn1 signaling via Dcc.

Exiting a germinal zone (GZ) initiates a cascade of events that promote neuronal maturation and circuit assembly. Developing neurons and their progenitors must interpret various niche signals-such as morphogens, guidance molecules, extracellular matrix components, and adhesive cues-to navigate this region. How differentiating neurons integrate and adapt to multiple cell-extrinsic niche cues with their cell-intrinsic machinery in exiting a GZ is unknown. We establish cooperation between cell polarity-regulated adhesion and Netrin-1 (Ntn-1) signaling comprises a coincidence detection circuit repelling maturing neurons from their GZ. In this circuit, the Partitioning defective 3 (Pard3) polarity protein and Junctional adhesion molecule-C (JamC) adhesion protein promote, while the Seven in absentia 2 (Siah2) ubiquitin ligase inhibits, Deleted in colorectal cancer (Dcc) receptor surface recruitment to gate differentiation linked repulsion to GZ Ntn-1. These results demonstrate cell polarity as a central integrator of adhesive- and guidance cues cooperating to spur GZ exit.

Development of a sensor to detect methylmercury toxicity

Methylmercury (MeHg) is a well-known neurotoxicant that induces various cellular functions depending on cellular- and developmental-specific vulnerabilities. MeHg has a high affinity for selenol and thiol groups, thus impairing the antioxidant system. Such affinity characteristics of MeHg led us to develop sensor vectors to assess MeHg toxicity. In this study, MeHg-mediated defects in selenocysteine (Sec) incorporation were demonstrated using thioredoxin reductase 1 cDNA fused with the hemagglutinin tag sequence at the C-terminus. Taking advantage of such MeHg-mediated defects in Sec incorporation, a cDNA encoding luciferase with a Sec substituted for cysteine-491 was constructed. This construct showed MeHg-induced decreases in signaling in a dose-dependent manner. To directly detect truncated luciferase under MeHg exposure, we further constructed a new sensor vector fused with a target for proteasomal degradation. However, this construct was inadequate because of the low rate of Sec insertion, even in the absence of MeHg. Finally, a Krab transcriptional suppressor fused with Sec was constructed and assessed to demonstrate MeHg-dependent increases in signal intensity. We confirmed that the vector responded specifically and in a dose-dependent manner to MeHg in cultured cerebellar granule cells. This vector is expected to allow monitoring of MeHg-specific toxicity via spatial and temporal imaging.

Heterogeneity in Slow Synaptic Transmission Diversifies Purkinje Cell Timing.

The cerebellum plays an important role in diverse brain functions, ranging from motor learning to cognition. Recent studies have suggested that molecular and cellular heterogeneity within cerebellar lobules contributes to functional differences across the cerebellum. However, the specific relationship between molecular and cellular heterogeneity and diverse functional outputs of different regions of the cerebellum remains unclear. Here, we describe a previously unappreciated form of synaptic heterogeneity at parallel fiber synapses to Purkinje cells in the mouse cerebellum (both sexes). In contrast to uniform fast synaptic transmission, we found that the properties of slow synaptic transmission varied by up to threefold across different lobules of the mouse cerebellum, resulting in surprising heterogeneity. Depending on the location of a Purkinje cell, the time of peak of slow synaptic currents varied by hundreds of milliseconds. The duration and decay time of these currents also spanned hundreds of milliseconds, based on lobule. We found that, as a consequence of the heterogeneous synaptic dynamics, the same brief input stimulus was transformed into prolonged firing patterns over a range of timescales that depended on Purkinje cell location.

Orientation effect of chopped steel fiber on tribological performance of very low metallic brake pads: An interface study

The orientation effect of chopped tiny steel fibres (length < 3 mm; diameter < 200 µm) in brake pads parallel (NAPA) to the sliding direction is studied using two different methods. Inverting the specimen during testing yields fibre perpendicular (NAPE) to the sliding direction, which is compared to commercial random-oriented fibre pads (NARA). The orientation coefficient value of near unity is achieved only in NAPA. NAPA and NAPE have a lower density than NARA by 13.2% due to less than 54.55% of steel fibres in the formulation. More and larger plateaus stabilized friction in NARA, utilising the elongation properties of parallel steel fibres, than in NAPE, which produced only tiny plateaus. However, the wear resistance decreases when the sliding path or direction changes from parallel to perpendicular. The measurement of thickness loss is misleading during wear because of the swelling effect, and hence energy requirements are considered. The energy required to wear 1 cc of specimen in the NAPE is 23.78% greater than that in the NAPA, and hence wear resistance is better. Adhesion followed by delamination at elevated temperatures are the dominant wear mechanisms in NAPA, whereas abrasion is dominant in NAPE. Thus, semi-metallic performance can be obtained in a very low metallic pad by orienting these fibres.

Behavioral regression in shank3Δex4-22 mice during early adulthood corresponds to cerebellar granule cell glutamatergic synaptic changes.

Shank3, a gene encoding a synaptic scaffolding protein, is implicated in autism spectrum disorder (ASD) and is disrupted in Phelan-McDermid syndrome (PMS). Despite evidence of regression or worsening of ASD-like symptoms in individuals with PMS, the underlying mechanisms remain unclear. Although shank3 is highly expressed in the cerebellar cortical granule cells, its role in cerebellar function and contribution to behavioral deficits in ASD models are unknown. This study investigates behavioral changes and cerebellar synaptic alterations in shank3 Δex4-22 mice at two developmental stages. Shank3 Δex4-22 wildtype, heterozygous, and homozygous knockout mice lacking exons 4-22 (all functional isoforms) were subjected to a behavioral battery in both juvenile (5-7 weeks old) and adult (3-5 months old) mouse cohorts of both sexes. Immunostaining was used to show the expression of SHANK3 in the cerebellar cortex. Spontaneous excitatory postsynaptic currents (sEPSCs) from cerebellar granule cells (CGCs) were recorded by whole-cell patch-clamp electrophysiology. Deletion of shank3 ex4-22 caused deficits in motor function, heightened anxiety, and repetitive behaviors. These genotype-dependent behavioral alterations were more prominent in adult mice than in juveniles. Reduced social preference was only identified in adult shank3 Δex4-22 knockout mice and self-grooming was uniquely elevated only in males across both age groups. Immunofluorescence staining indicates the presence of SHANK3 predominantly in the dendrite-containing rosette-like structures in CGCs, colocalizing with presynaptic markers of glutamatergic mossy fiber. Electrophysiological findings identify a parallel relationship between the age-related exacerbation of behavioral impairments and the enhancement of sEPSC amplitude in CGCs. Other behavioral tests of muscle strength (grip strength test), memory (Barnes/water maze), and communication (ultrasonic vocalization), were not performed. Further study is necessary to elucidate how SHANK3 modulates synaptic function at the mossy fiber-granule cell synapse in the cerebellum. Our findings reveal an age-related exacerbation of behavioral impairments in shank3 Δex4-22 mutant mice. These results suggest that SHANK3 may play a role in maintaining glutamatergic receptors and synapses in CGCs, as well as the potential involvement of the cerebellum in ASD.

Genome binding properties of Zic transcription factors underlie their changing functions during neuronal maturation

BackgroundThe Zic family of transcription factors (TFs) promote both proliferation and maturation of cerebellar granule neurons (CGNs), raising the question of how a single, constitutively expressed TF family can support distinct developmental processes. Here we use an integrative experimental and bioinformatic approach to discover the regulatory relationship between Zic TF binding and changing programs of gene transcription during postnatal CGN differentiation.ResultsWe first established a bioinformatic pipeline to integrate Zic ChIP-seq data from the developing mouse cerebellum with other genomic datasets from the same tissue. In newborn CGNs, Zic TF binding predominates at active enhancers that are co-bound by developmentally regulated TFs including Atoh1, whereas in mature CGNs, Zic TF binding consolidates toward promoters where it co-localizes with activity-regulated TFs. We then performed CUT&RUN-seq in differentiating CGNs to define both the time course of developmental shifts in Zic TF binding and their relationship to gene expression. Mapping Zic TF binding sites to genes using chromatin looping, we identified the set of Zic target genes that have altered expression in RNA-seq from Zic1 or Zic2 knockdown CGNs.ConclusionsOur data show that Zic TFs are required for both induction and repression of distinct, developmentally regulated target genes through a mechanism that is largely independent of changes in Zic TF binding. We suggest that the differential collaboration of Zic TFs with other TF families underlies the shift in their biological functions across CGN development.

Ablation of TrkB from Enkephalinergic Precursor-Derived Cerebellar Granule Cells Generates Ataxia.

In ataxia disorders, motor incoordination (ataxia) is primarily linked to the dysfunction and degeneration of cerebellar Purkinje cells (PCs). In spinocerebellar ataxia 6 (SCA6), for example, decreased BDNF-TrkB signalling appears to contribute to PC dysfunction and ataxia. However, abnormal BDNF-TrkB signalling in granule cells (GCs) may contribute to PC dysfunction and incoordination in ataxia disorders, as TrkB receptors are also present in GCs that provide extensive input to PCs. This study investigated whether dysfunctional BDNF-TrkB signalling restricted to a specific subset of cerebellar GCs can generate ataxia in mice. To address this question, our research focused on TrkbPenk-KO mice, in which the TrkB receptor was removed from enkephalinergic precursor-derived cerebellar GCs. We found that deleting Ntrk2, encoding the TrkB receptor, eventually interfered with PC function, leading to ataxia symptoms in the TrkbPenk-KO mice without affecting their cerebellar morphology or levels of selected synaptic markers. These findings suggest that dysfunctional BDNF-TrkB signalling in a subset of cerebellar GCs alone is sufficient to trigger ataxia symptoms and may contribute to motor incoordination in disorders like SCA6.

The artifact of cerebellar granule cell layer conglutination in veterinary medicine: a brief historical perspective and review.

Cerebellar granule cell layer conglutination is a tissue artifact associated with postmortem autolysis that causes cerebellar granule cell changes once thought to be caused by degeneration and necrosis. Granule cell layer conglutination has been reported mainly in humans and cattle and rarely in other animal species, but its frequency remains vastly unknown in veterinary medicine, mostly because this postmortem change is typically not recorded in autopsy reports. Pathology trainees should be aware of autolytic tissue changes that may mimic pathologic changes in the CNS, particularly when those changes are highly selective for a specific cell population within the cerebellar cortex. Here we provide a brief historical perspective on the evolution of cerebellar granule cell layer conglutination from "enzootic cerebellar necrosis," a presumed necrotic lesion affecting granule neurons in humans and cattle, to a tissue change associated with postmortem autolysis and increased tissue acidity in the cerebellum. We also provide an update on the animal species in which cerebellar granule cell layer conglutination has been observed during our diagnostic pathology routine.

Single-nucleus multiome analysis of human cerebellum in Alzheimer's disease-related dementia.

Although human cerebellum is known to be neuropathologically impaired in Alzheimer's disease (AD) and AD-related dementias (ADRD), the cell type-specific transcriptional and epigenomic changes that contribute to this pathology are not well understood. Here, we report single-nucleus multiome (snRNA-seq and snATAC-seq) analysis of 103,861 nuclei isolated from cerebellum from 9 human cases of AD/ADRD and 8 controls, and with frontal cortex of 6 AD donors for additional comparison. Using peak-to-gene linkage analysis, we identified 431,834 significant linkages between gene expression and cell subtype-specific chromatin accessibility regions enriched for candidate cis-regulatory elements (cCREs). These cCREs were associated with AD/ADRD-specific transcriptomic changes and disease-related gene regulatory networks, especially for RAR Related Orphan Receptor A (RORA) and E74 Like ETS Transcription Factor 1 (ELF1) in cerebellar Purkinje cells and granule cells, respectively. Trajectory analysis of granule cell populations further identified disease-relevant transcription factors, such as RORA, and their regulatory targets. Finally, we prioritized two likely causal genes, including Seizure Related 6 Homolog Like 2 (SEZ6L2) in Purkinje cells and KAT8 Regulatory NSL Complex Subunit 1 (KANSL1) in granule cells, through integrative analysis of cCREs derived from snATAC-seq, genome-wide AD/ADRD loci, and Hi-C looping data. This first cell subtype-specific regulatory landscape in the human cerebellum identified here offer novel genomic and epigenomic insights into the neuropathology and pathobiology of AD/ADRD and other neurological disorders if broadly applied.

3-Nitrotyrosine shortens axons of non-dopaminergic neurons by inhibiting mitochondrial motility

3-Nitrotyrosine (3-NT), a byproduct of oxidative and nitrosative stress, is implicated in age-related neurodegenerative disorders. Current literature suggests that free 3-NT becomes integrated into the carboxy-terminal domain of α-tubulin via the tyrosination/detyrosination cycle. Independently of this integration, 3-NT has been associated with the cell death of dopaminergic neurons. Given the critical role of tyrosination/detyrosination in governing axonal morphology and function, the substitution of tyrosine with 3-NT in this process may potentially disrupt axonal homeostasis, although this aspect remains underexplored. In this study, we examined the impact of 3-NT on the axons of cerebellar granule neurons, which is used as a model for non-dopaminergic neurons. Our observations revealed axonal shortening, which correlated with the incorporation of 3-NT into α-tubulin. Importantly, this axonal effect was observed prior to the onset of cellular death. Furthermore, 3-NT was found to diminish mitochondrial motility within the axon, leading to a subsequent reduction in mitochondrial membrane potential. The suppression of syntaphilin, a protein responsible for anchoring mitochondria to microtubules, restored the mitochondrial motility and axonal elongation that were inhibited by 3-NT. These findings underscore the inhibitory role of 3-NT in axonal elongation by impeding mitochondrial movement, suggesting its potential involvement in axonal dysfunction within non-dopaminergic neurons.

Toll-like receptor 4 deficiency in Purkinje neurons drives cerebellar ataxia by impairing the BK channel-mediated after-hyperpolarization and cytosolic calcium homeostasis

Toll-like receptor (TLR) 4 contributes to be the induction of neuroinflammation by recognizing pathology-associated ligands and activating microglia. In addition, numerous physiological signaling factors act as agonists or antagonists of TLR4 expressed by non-immune cells. Recently, TLR4 was found to be highly expressed in cerebellar Purkinje neurons (PNs) and involved in the maintenance of motor coordination through non-immune pathways, but the precise mechanisms remain unclear. Here we report that mice with PN specific TLR4 deletion (TLR4PKO mice) exhibited motor impairments consistent with cerebellar ataxia, reduced PN dendritic arborization and spine density, fewer parallel fiber (PF) – PN and climbing fiber (CF) – PN synapses, reduced BK channel expression, and impaired BK-mediated after-hyperpolarization, collectively leading to abnormal PN firing. Moreover, the impaired PN firing in TLR4PKO mice could be rescued with BK channel opener. The PNs of TLR4PKO mice also exhibited abnormal mitochondrial structure, disrupted mitochondrial endoplasmic reticulum tethering, and reduced cytosolic calcium, changes that may underly abnormal PN firing and ultimately drive ataxia. These results identify a previously unknown role for TLR4 in regulating PN firing and maintaining cerebellar function.

DERE-Net: A dual-encoder residual enhanced U-Net for muscle fiber segmentation of H&E images

Accurate segmentation of hematoxylin-eosin (H&E) muscle fiber images is crucial for the diagnosis of weightless muscle atrophy. However, uneven contrast, blurred fiber boundaries and adhesions in H&E images are still challenges for accurate segment complete muscle fiber. Although the existing single-encoder based U-shaped networks can extract local information about the target in H&E images, ignores remote dependencies between muscle fibers and low-level detail features, resulting in poor segmentation accuracy when facing H&E images with complex contrast. Therefore, we propose a dual-encoder residual enhanced U-Net segmentation model (DERE-Net) for effective segment muscle fibers in H&E images. DERE-Net uses Transformer and residual CNN to extract global context information and local features of muscle fibers in parallel, and fuses these two features to enable the model to accurately identify the muscle fibers. The multi-scale semantic information fusion (MSIF) module also utilizes the differences between multi-scale features to recover undetected muscle fiber, thus improving the network’s ability to recognize the object regions. In addition, the attention module is added to the skip connection, making the muscle fiber regions information more prominent and improving the robustness of the model. To demonstrate the DERE-Net effect, the comparative experiments are conducted on our own muscle fiber H&E image dataset, GLAS and MoNuSeg. DERE-Net achieved excellent performance on the muscle fiber H&E dataset (DSC 0.919), GLAS dataset (DSC 0.912), and MoNuSeg dataset (DSC 0.821). These results indicate that DERE-Net can accurately predict muscle fiber regions, providing a new method for accurate diagnosis of muscle atrophy in the future.

Nesprin-2 coordinates opposing microtubule motors during nuclear migration in neurons.

Nuclear migration is critical for the proper positioning of neurons in the developing brain. It is known that bidirectional microtubule motors are required for nuclear transport, yet the mechanism of the coordination of opposing motors is still under debate. Using mouse cerebellar granule cells, we demonstrate that Nesprin-2 serves as a nucleus-motor adaptor, coordinating the interplay of kinesin-1 and dynein. Nesprin-2 recruits dynein-dynactin-BicD2 independently of the nearby kinesin-binding LEWD motif. Both motor binding sites are required to rescue nuclear migration defects caused by the loss of function of Nesprin-2. In an intracellular cargo transport assay, the Nesprin-2 fragment encompassing the motor binding sites generates persistent movements toward both microtubule minus and plus ends. Nesprin-2 drives bidirectional cargo movements over a prolonged period along perinuclear microtubules, which advance during the migration of neurons. We propose that Nesprin-2 keeps the nucleus mobile by coordinating opposing motors, enabling continuous nuclear transport along advancing microtubules in migrating cells.

The loss of βΙ spectrin alters synaptic size and composition in the ja/ja mouse.

Deletion or mutation of members of the spectrin gene family contributes to many neurologic and neuropsychiatric disorders. While each spectrinopathy may generate distinct neuropathology, the study of βΙ spectrin's role (Sptb) in the brain has been hampered by the hematologic consequences of its loss. Jaundiced mice (ja/ja) that lack βΙ spectrin suffer a rapidly fatal hemolytic anemia. We have used exchange transfusion of newborn ja/ja mice to blunt their hemolytic pathology, enabling an examination of βΙ spectrin deficiency in the mature mouse brain by ultrastructural and biochemical analysis. βΙ spectrin is widely utilized throughout the brain as the βΙΣ2 isoform; it appears by postnatal day 8, and concentrates in the CA1,3 region of the hippocampus, dentate gyrus, cerebellar granule layer, cortical layer 2, medial habenula, and ventral thalamus. It is present in a subset of dendrites and absent in white matter. Without βΙ spectrin there is a 20% reduction in postsynaptic density size in the granule layer of the cerebellum, a selective loss of ankyrinR in cerebellar granule neurons, and a reduction in the level of the postsynaptic adhesion molecule NCAM. While we find no substitution of another spectrin for βΙ at dendrites or synapses, there is curiously enhanced βΙV spectrin expression in the ja/ja brain. βΙΣ2 spectrin appears to be essential for refining postsynaptic structures through interactions with ankyrinR and NCAM. We speculate that it may play additional roles yet to be discovered.

Mapping the effect of the antisecretory factor on GABAA receptor α1 and α6 subunits in cerebellar granule cells in vitro

The Antisecretory Factor (AF) is a protein that can reduce intestinal hypersecretion and various inflammation disorders in vivo. Discovered in many mammalian tissues and plasma, its mechanism of action remains unknown. Interestingly, its induction has been found to counteract vertigo in patients with Méniere's disease. This suggests an inherent ability to control body balance and posture, an activity that may play a role in cerebellar function. Therefore, it may be worthwhile to investigate whether this activity can inhibit neuronal cells involved in cerebellar circuitries and its potential action on enteric nervous system ganglia, which could explain its antisecretory effect in the intestine.Previously, we studied the role of AF on GABAA receptors in cerebellar granule cells, taking advantage of electrophysiology and evaluating the effects of the administration of AF-16, an AF peptide. Treatment with AF-16 increased GABAA receptor responses, especially those containing the α6 subunit. Here, we performed immunofluorescence experiments by staining α1 and α6 subunits before and after incubation with AF-16, analyzed super-resolved images comparing pre- and post-treatment maps and critically examined these experimental results with our previous electrophysiological data to shed light on the mechanisms of action of AF protein on GABAA receptor subpopulations, specifically the "fast" receptors of αn β2/3 γ2 composition that contain either the α1 or the α6 subunit.The results indicate that the α6 subunit is redistributed, with a decrease in neurites and an increase in soma. Conversely, the α1 subunit shows opposite results, with an increase in neurites and a decrease in soma.