Nerve Impulses Research Articles

The genetic landscape of autism spectrum disorder in an ancestrally diverse cohort

Autism spectrum disorder (ASD) comprises neurodevelopmental disorders with wide variability in genetic causes and phenotypes, making it challenging to pinpoint causal genes. We performed whole exome sequencing on a modest, ancestrally diverse cohort of 195 families, including 754 individuals (222 with ASD), and identified 38,834 novel private variants. In 68 individuals with ASD (~30%), we identified 92 potentially pathogenic variants in 73 known genes, including BCORL1, CDKL5, CHAMP1, KAT6A, MECP2, and SETD1B. Additionally, we identified 158 potentially pathogenic variants in 120 candidate genes, including DLG3, GABRQ, KALRN, KCTD16, and SLC8A3. We also found 34 copy number variants in 31 individuals overlapping known ASD loci. Our work expands the catalog of ASD genetics by identifying hundreds of variants across diverse ancestral backgrounds, highlighting convergence on nervous system development and signal transduction. These findings provide insights into the genetic underpinnings of ASD and inform molecular diagnosis and potential therapeutic targets.

"Electrolyte Imbalance in Chronic Kidney Disease: Management Strategies and Approaches to Enhance Quality Of Life

Chronic Kidney Disease (CKD) is a progressive condition characterized by a gradual loss of kidney function, significantly impairing the body's ability to maintain electrolyte and fluid balance. Electrolytes, including sodium, potassium, calcium, phosphorus, and magnesium, play a crucial role in homeostasis, influencing nerve signaling, muscle function, and acid-base equilibrium. In CKD, the diminished renal function disrupts this delicate balance, leading to prevalent and clinically significant electrolyte imbalances. These imbalances contribute to a range of complications, such as cardiovascular disorders, bone disease, and neuromuscular dysfunction, severely impacting patients' overall quality of life (QoL). Management strategies for electrolyte disturbances in CKD include dietary modifications, pharmacological interventions, and advanced therapies like dialysis and kidney transplantation. These approaches aim to stabilize electrolyte levels, prevent complications, and enhance patients' QoL. This review explores the pathophysiology, clinical manifestations, and diagnostic approaches to electrolyte imbalances in CKD, emphasizing evidence-based management strategies and emerging innovations. Addressing these challenges holistically is crucial for improving clinical outcomes and supporting the well-being of individuals living with CKD.

Evaluating the Efficacy of Targeted Muscle Reinnervation (TMR) in Extremities Amputations of Pedis Squamous Cell Carcinoma: A Comprehensive Systematic Review, Meta-Analysis, and Meta-regression of Functional and Pain Outcomes

Introduction Targeted Muscle Reinnervation (TMR) is an innovative surgical procedure initially designed for upper-limb amputations, which has shown growing potential for improving functional outcomes in below-knee amputees. TMR involves redirecting severed nerves from the amputated limb to nearby residual muscles, allowing these muscles to act as amplifiers for nerve signals, thereby improving prosthetic control. Recent advancements in TMR for below-knee amputations have highlighted its ability to reduce post-amputation complications, such as neuroma pain and phantom limb pain, while offering enhanced control over prosthetic limbs, thus improving mobility and quality of life. Methods Following PRISMA guidelines, a systematic review was conducted, sourcing studies up to May 2024 from PubMed, Cochrane Library, Scopus, Springer, and Epistemonikos. The analysis included randomized controlled trials (RCTs) and clinical trials. A meta-analysis was performed to assess phantom limb pain reduction, while study quality was evaluated using RoB 2.0, ROBINS-I, and ROBINS-E. Meta-regression examined the influence of variables such as age and sex on pain outcomes. Results Seven studies, including 363 patients, were analyzed. The meta-analysis showed that TMR significantly reduced phantom limb pain (MD: -1.74; 95% CI: -2.46 to -1.02; P<0.00001; I2=0%). However, the pooled risk ratio for phantom pain incidence (RR: 1.58; 95% CI: 0.61 to 4.11; P=0.35; I2=93%) indicated variable outcomes. Conclusion TMR significantly reduces phantom limb pain and improves prosthetic control, particularly for patients with SCC of the foot, ultimately enhancing their quality of life.

Functional Assessment of Rat Sciatic Nerve Regeneration Using a Nerve Conduit Based on Ion Exchange Membrane.

The problem with modern nerve conduits is inability to transmit nerve impulses to the distal part of the damaged nerve. Cationic conductivity is a necessary characteristic of the nerve conduit ensuring effective regeneration of the peripheral nerves. We performed a functional assessment of the regeneration of rat sciatic nerve using a nerve conduit based on an ion-exchange membrane. A sciatic nerve defect was experimentally simulated in Wistar rats with further implantation of the LF-4SK membrane. On days 60 and 90 after surgery, the sciatic functional index and the ratio of the shin girth of the operated limb to the intact limb were calculated; on day 90, an electrophysiological assessment of nerve recovery was carried out. The results of the study showed that the conduit based on the LF-4SK membrane optimizes the functional recovery of the sciatic nerve defect.

Two scientific perspectives on nerve signal propagation: how incompatible approaches jointly promote progress in explanatory understanding

We present a case study of two scientific perspectives on the phenomenon of nerve signal propagation, a bio-electric and a thermodynamic perspective, and compare this case with two accounts of scientific perspectivism: those of Michela Massimi and Juha Saatsi, respectively. We demonstrate that the interaction between the bio-electric perspective and the thermodynamic perspective can be captured in Saatsi’s terms of progress in explanatory understanding. Using insights from our case study, we argue that both the epistemic and pragmatic dimensions of scientific understanding are important for increasing explanatory understanding of phenomena. The epistemic dimension of understanding is important for increasing the number of actually answered what-if-things-had-been-different questions about a phenomenon, the pragmatic dimension for pointing out the potentially answerable what-if questions that have been overlooked or purposefully neglected thus far. Exposing the limitations of the acquired understanding within a particular perspective can be achieved by criticizing the assumptions that have been adopted to make models of the perspective intelligible, but that are considered problematic from a rival perspective.

Adiabatic evolution of solitons embedded in lipid membranes

Abstract The Heimburg-Jackson model, or thermodynamic soliton theory of nervous impulses, has a well-established record as an alternative model for studying the dynamics of nerve impulses and lipid membranes. Within this framework, nerve impulses can be represented as nonlinear excitations of low amplitude depicted by the damped nonlinear Schrödinger equation and their adiabatic evolution can be analyzed using direct perturbative methods. Based on the foregoing, we carry out the current study using the quasi-stationary approach to obtain the adiabatic evolution of solitons embedded in lipid membranes under the influence of a viscous elastic fluid. This analysis encompasses liquid-to-gel transition of the lipid bilayers, for whose dark and bright solitons arise, respectively.

Electrochemistry and Biochemistry of Nerve Impulse Generation and Its Propagation

Electrochemistry and Biochemistry of Nerve Impulse Generation and Its Propagation

Microglial and Macrophage Plasticity and Regional Cerebral Blood Flow in the Prenatal Brain and Gut Under Vagus Nerve Stimulation.

An intricate relationship exists between the vagus nerve and systemic immune cell regulation, specifically during fetal development. Little is known about the connection between the vagus nerve and the brain's regional circulatory control. In this chapter, we present a methodology for studying the impact of vagus nerve signaling on these connections in the developing fetus using the sheep model for human fetal physiology. First, we present the protocol to study the connection between the vagus nerve physiology and the regional cerebral blood flow (rCBF). Next, we detail the protocol for measuring how vagal signaling alters microglial cell plasticity in gut and brain. In previous work, our team showed that vagotomy results in amplified redistribution of rCBF toward subcortical structures in the fetal brain. Conversely, efferent VNS reduces rCBF to cortical structures while afferent VNS diminishes the rise of rCBF to subcortical structures (independent of cortical rCBF) when compared to controls in the fetal brain. Additionally, our team showed that Iba-1 expression, a marker for microglial cellular signaling activation, rises in a dose-dependent relationship with systemic inflammatory activation in the setting of vagotomy. The findings support existing preclinical and clinical evidence in adult human physiology that vagotomy is neuroprotective for neurodegenerative diseases such as Parkinson's likely via a glial cell-mediated mechanism. Vagus nerve stimulation (VNS) has also been shown to alter rCBF patterns in adults with treatment-resistant depression, underscoring the importance of further investigation of the relationship between the vagus nerve and rCBF as early as in utero. Together, the body of evidence emphasizes that the vagal pathway is an important player in the programming of microglial cell phenotypes within the developing brain. Further study is needed to better understand the significance of these relationships for the development and treatment of early susceptibility to neuroinflammatory and neurodegenerative disorders in later life. Therefore, we present a methodology for assessing rCBF and morphometric features of microglial and macrophage cell activation to allow future teams to expand on the existing body of work and further examine these relationships at a cellular and systems' levels.

Time-dependent changes in genome-wide gene expression and post-transcriptional regulation across the post-death process in silkworm.

Despite death marking the end of life, several gene expression and miRNA-mediated post-transcriptional regulation events may persist or be initiated. The silkworm (Bombyx mori) is a valuable model for exploring life processes, including death. In this study, we combined transcriptomics and miRNAomics analyses of young, old, and post-mortem silkworms across the entire process after death to unravel the dynamics of gene expression and miRNA-mediated post-transcriptional regulation. In total, 171 genes exhibited sustained differential expression in post-mortem silkworms compared to the pre-death state, which are primarily involved in nerve signalling, transport, and immune response. Post-mortem time-specific genes were associated with cell cycle regulation, thermogenesis, immunity, and zinc ion homeostasis. We found that the down-regulated expression of 36 genes related to transcription, epigenetic modification, and homeostasis resulted in a significant shift in global gene expression patterns at 2h post-death. We also identified 5 mRNA-miRNA pairs (i.e. bmo-miR-2795-mhca, 2784-achi, 2762-oa1, 277-5p-creb, and 1000-tcb1) associated with stress hormone regulation, transcription activity, and signal transduction. The roles of these pairs were validated through in vivo experiments using miRNA mimics in silkworms. The findings provide valuable insights into the intricate mechanisms underlying the transcriptional and miRNA-mediated post-transcriptional regulation events in animals after death.

Development of a near infrared region based non-invasive therapy device for diabetic peripheral neuropathy

Diabetic Peripheral Neuropathy (DPN) is a nerve damage that is treated with painkillers and steroids which have the drawback of interference with other medications and the dangers of side effects. Novelty of the proposed work is to develop a Near Infrared Region (NIR) based non-invasive therapy device called ‘DPNrelief-1.0V’developed with a 890 nm wavelength diodes. DPNrelief-1.0V delivers a total dosage of 6.174 J/cm2 with heat absorption by tissue of 61.74 Joules at 30 minutes. The device was tested by carrying out a pilot study with 8 patients where 4 were treatment group and control group. The DPNrelief-1.0V is validated by Nerve Conduction Study (NCS) test. The degenerated nerves pre-therapy showed less amplitude, Conduction Velocity (CV) and latency which was improved post-therapy by 100% in amplitude of nerve signal, 100% in CV and a decrease of 36.2% in latency. Independent t-test was conducted to find the difference between control and treatment, wherein a p value < 0.05 was obtained depicting significant difference between two groups. Furthermore, the performance of the device is validated by one-way test repeated measures Analysis of Variance (ANOVA), wherein a p value of < 0.05 was obtained depicting a difference in nerve condition pre-and post-therapy. The performance of DPNrelief-1.0V has outperformed Anodyne therapy device with lesser dosage, treatment time and portability and in curing the symptoms of DPN. DPNrelief-1.0V finds its potential in the field of medicine for treating DPN.

Targeting Glucose Metabolism: A Novel Therapeutic Approach for Parkinson's Disease.

Glucose metabolism is essential for the maintenance and function of the central nervous system. Although the brain constitutes only 2% of the body weight, it consumes approximately 20% of the body's total energy, predominantly derived from glucose. This high energy demand of the brain underscores its reliance on glucose to fuel various functions, including neuronal activity, synaptic transmission, and the maintenance of ion gradients necessary for nerve impulse transmission. Increasing evidence shows that many neurodegenerative diseases, including Parkinson's disease (PD), are associated with abnormalities in glucose metabolism. PD is characterized by the progressive loss of dopaminergic neurons in the substantia nigra, accompanied by the accumulation of α-synuclein protein aggregates. These pathological features are exacerbated by mitochondrial dysfunction, oxidative stress, and neuroinflammation, all of which are influenced by glucose metabolism disruptions. Emerging evidence suggests that targeting glucose metabolism could offer therapeutic benefits for PD. Several antidiabetic drugs have shown promise in animal models and clinical trials for mitigating the symptoms and progression of PD. This review explores the current understanding of the association between PD and glucose metabolism, emphasizing the potential of antidiabetic medications as a novel therapeutic approach. By improving glucose uptake and utilization, enhancing mitochondrial function, and reducing neuroinflammation, these drugs could address key pathophysiological mechanisms in PD, offering hope for more effective management of this debilitating disease.

Hydrogen peroxide disrupts the regulatory pathway of saliva secretion in two salivary acinar rat cell lines.

Secretion of saliva is controlled by autonomic nerve signals via regulation of Ca2+-dependent ion transport across acinar cell membranes. Oxidative stress may affect this process, leading to a decrease in saliva production. This study investigates elements of the Ca2+ regulatory pathway and their vulnerability to hydrogen peroxide-induced oxidative stress. Rat parotid and submandibular salivary gland acinar cell lines were exposed to different hydrogen peroxide concentrations to simulate oxidative stress. Cell viability and intracellular reactive oxygen species were measured, mRNA levels were assessed via RT-qPCR, and protein expression was studied using western blot and immunofluorescence microscopy. Elevated concentrations of hydrogen peroxide reduced cell viability and increased intracellular levels of reactive oxygen species and led to a decrease in cholinergic receptor muscarinic 3 and adrenoreceptor alpha 1A mRNA and protein levels in both cell lines. In parotid gland cells, both mRNA and protein levels of stromal interaction molecule 1 and Orai1 decreased with increasing concentrations of hydrogen peroxide. In contrast, in submandibular gland cells stromal interaction molecule 1 and Orai1 displayed differential mRNA and protein expression levels. Our study revealed that hydrogen peroxide exposure alters rat parotid and submandibular acinar cells, increasing reactive oxygen species and reducing autonomic receptor expression. Differential mRNA and protein expression of stromal interaction molecule 1 and Orai1 highlight complex oxidative stress effects on Ca2⁺ signaling. Most likely these effects will be deleterious to salivary secretion, but some effects may be protective.

STEM-12. A NEURONAL STEM-LIKE PHENOTYPE IN GRADE 4 IDH-MUTANT ASTROCYTOMA WITH CDKN2A/B LOSS IS ASSOCIATED WITH CUX2 DEFICIENCY

Abstract Diffuse gliomas represent the most common type of primary adult malignant brain tumor historically diagnosed and graded from histologic criteria alone. Gliomas harboring isocitrate dehydrogenase (IDH) 1 or 2 mutations are associated with lower grade tumors and portend a favorable prognosis relative to IDH-wildtype glioma. However, the loss of CDKN2A/B in IDH-mutant astrocytoma confers an aggressive high grade phenotype and is the strongest implicated molecular alteration associated poor clinical survival, thus is now sufficient to define a grade 4 tumor regardless of histologic grade. However, there remains no effective therapies targeted at molecular subgroups in aggressive gliomas to date. Here, we sought to elucidate the biologic pathways and functional outcomes associated with the acquisition of high-grade behavior under loss of CDKN2A/B in IDH-mutant astrocytoma to inform future therapeutic strategies. We analyzed a cohort of patient IDH-mutant astrocytomas with RNA sequencing data and found the increased expression of regulators of embryonic nervous system development and signaling concurrent with CDKN2A/B loss. Using grade 4 IDH-mutant astrocytoma patient-derived (PDX) and cell-lines harboring CDKN2A/B homozygous deletion, we stably re-expressed p14ARF, p15INK4B, and p16INK4A using a Tet-inducible system. IDH-mutant cell lines with re-expression of p14, p15, or p16 displayed differential transcription factor activation, impaired neurosphere capability, decreased colony formation, and lower neurosphere proliferation. Intriguingly, RNA-seq data revealed CUX2, a transcription factor known to control neuronal precursor behavior, as the likely candidate regulating the differential expression profile across CDKN2A/B status. We observed increased CUX2 expression in cell lines stably re-expressing p14, p15, and p16. We validated the CUX2 signature across publicly available datasets of IDH-mutant astrocytoma where CUX2 expression negatively correlated with loss of CDKN2A/B in patient tumors. Together our work suggests CUX2 deficiency in IDH-mutant astrocytoma with CDKN2A/B deletion enables an increased neuronal stem-like phenotype in these grade 4 tumors.

A data compression algorithm with the improved SRLE for high-throughput neural signal acquisition device.

Multi-channel acquisition systems of brain neural signals can provide a powerful tool with a wide range of information for the clinical application of brain computer interfaces. High-throughput implantable systems are limited by size and power consumption, posing challenges to system design. To acquire more comprehensive neural signals and wirelessly transmit high-throughput brain neural signals, a FPGA-based acquisition system for multi-channel brain nerve signals has been developed. And the Bluetooth transmission with low-power technology are utilized. To wirelessly transmit large amount of data with limited Bluetooth bandwidth and improve the accuracy of neural signal decoding, an improved sharing run length encoding (SRLE) is proposed to compress the spike data of brain neural signal to improve the transmission efficiency of the system. The functional prototype has been developed, which consists of multi-channel data acquisition chips, FPGA main control module with the improved SRLE, a wireless data transmitter, a wireless data receiver and an upper computer. And the developed functional prototype was tested for spike detection of brain neural signal by animal experiments. From the animal experiments, it shows that the system can successfully collect and transmit brain nerve signals. And the improved SRLE algorithm has an excellent compression effect with the average compression rate of 5.94%, compared to the double run-length encoding, the FDR encoding, and the traditional run-length encoding. The developed system, incorporating the improved SRLE algorithm, is capable of wirelessly capturing spike signals with 1024 channels, thereby realizing the implantable systems of High-throughput brain neural signals.

Nerve Signal Transferring Mechanism and Mathematical Modeling of Artificial Biological System Design

Nerve Signal Transferring Mechanism and Mathematical Modeling of Artificial Biological System Design

Effect of Chronic Consumption of Fluoridated Water on Sciatic Nerve Conduction Velocity in Male Wistar Rats.

The long-term effect of fluoridated water consumption during development on the velocity of nerve impulse conduction in the sciatic nerve of rats was assessed. Thirty male Wistar rats, 21 days old, were randomly assigned to five groups. Three groups were given fluoridated water ad libitum (as the only source) at different concentrations (10, 100, and 150 ppm), designated as groups F10, F100, and F150, respectively. The study included a control group (C) that received fluoridated water at the maximum level established by the World Health Organization (1.5 ppm of fluorides) and another group that received deionized water (DW). The animals were treated until they reached 90 days of age. Electrophysiological recordings were performed on the rats' sciatic nerves to determine nerve conduction velocity, and blood plasma was extracted for fluoride concentration analysis. The study found that the F150 group had a lower nerve impulse conduction velocity in the sciatic nerve compared to the C group (P = 0.0015). Additionally, there was a negative correlation between the concentration of fluorides in plasma and the nerve conduction velocity (r = -0.5132, P = 0.0037). These findings indicate that chronic consumption of high concentrations of fluoride leads to a decrease in nerve conduction velocity. This, in conjunction with potential alterations in the central nervous system, may explain the deficits in learning and memory tests that have been documented in numerous studies evaluating individuals exposed to fluoride consumption. These results provide valuable information for understanding the effects and action mechanisms of fluoride in exposed individuals.

Identifying the Role of Oligodendrocyte Genes in the Diagnosis of Alzheimer's Disease through Machine Learning and Bioinformatics Analysis.

Due to the heterogeneity of Alzheimer's disease (AD), the underlying pathogenic mechanisms have not been fully elucidated. Oligodendrocyte (OL) damage and myelin degeneration are prevalent features of AD pathology. When oligodendrocytes are subjected to amyloid-beta (Aβ) toxicity, this damage compromises the structural integrity of myelin and results in a reduction of myelin-associated proteins. Consequently, the impairment of myelin integrity leads to a slowdown or cessation of nerve signal transmission, ultimately contributing to cognitive dysfunction and the progression of AD. Consequently, elucidating the relationship between oligodendrocytes and AD from the perspective of oligodendrocytes is instrumental in advancing our understanding of the pathogenesis of AD. Here, an attempt is made in this study to identify oligodendrocyte-related biomarkers of AD. AD datasets were obtained from the Gene Expression Omnibus database and used for consensus clustering to identify subclasses. Hub genes were identified through differentially expressed genes (DEGs) analysis and oligodendrocyte gene set enrichment. Immune infiltration analysis was conducted using the CIBERSORT method. Signature genes were identified using machine learning algorithms and logistic regression. A diagnostic nomogram for predicting AD was developed and validated using external datasets and an AD model. A small molecular compound was identified using the eXtreme Sum algorithm. 46 genes were found to be significantly correlated with AD progression by examining the overlap between DEGs and oligodendrocyte genes. Two subclasses of AD, Cluster A, and Cluster B, were identified, and 9 signature genes were identified using a machine learning algorithm to construct a nomogram. Enrichment analysis showed that 9 genes are involved in apoptosis and neuronal development. Immune infiltration analysis found differences in immune cell presence between AD patients and controls. External datasets and RT-qPCR verification showed variation in signature genes between AD patients and controls. Five small molecular compounds were predicted. It was found that 9 oligodendrocyte genes can be used to create a diagnostic tool for AD, which could help in developing new treatments.

A nanofibrous polycaprolactone/collagen neural guidance channel filled with sciatic allogeneic schwann cells and platelet-rich plasma for sciatic nerve repair.

Sciatic nerve damage, a common condition affecting approximately 2.8% of the US population, can lead to significant disability due to impaired nerve signal transmission, resulting in loss of sensation and motor function in the lower extremities. In this study, a neural guidance channel was developed by rolling a nanofibrous scaffold produced via electrospinning. The scaffold's microstructure, biocompatibility, biodegradation rate, porosity, mechanical properties, and hemocompatibility were evaluated. Platelet-rich plasma (PRP) activated with 30,000 allogeneic Schwann cells (SCs) was injected into the lumen of the channels following implantation into a rat model of sciatic nerve injury. Recovery of motor function, sensory function, and muscle re-innervation was assessed using the sciatic function index (SFI), hot plate latency time, and gastrocnemius muscle wet weight loss. Results showed mean hot plate latency times of Autograft: 7.03, PCL/collagen scaffolds loaded with PRP and SCs (PCLCOLPRPSCs): 8.34, polymer-only scaffolds (PCLCOL): 10.66, and untreated animals (Negative Control): 12.00. The mean SFI values at week eight were Autograft: -49.30, PCLCOLPRPSCs: -64.29, PCLCOL: -75.62, and Negative Control: -77.14. The PCLCOLPRPSCs group showed a more negative SFI compared to the Autograft group but performed better than both the PCLCOL and Negative Control groups. These findings suggest that the developed strategy enhanced sensory and functional recovery compared to the negative control and polymer-only scaffold groups.

The Ayurvedic management of Spastic Paralysis w.s.r. Pakshaghata: A Case Report

In Ayurveda, Vata Dosha is considered to play a significant role in neurological health due to its association with movement and communication within the body. Vata governs the nervous system and is linked to the movement of nerve impulses and the coordination of bodily functions. When Vata is imbalanced, it can contribute to various neurological issues, including Nervous system disorders, Mental Health Issues, Cognitive Function, and Movement Disorders. Vata Dosha is associated with the movement and function of the nervous system, and imbalances can contribute to spastic paralysis (Pakshaghata). The pathology of paralysis related to Vata dosha is understood through its effects on the body’s neurological and muscular systems. Vata Dosha influences paralysis by nerve Impairment, muscle dysfunction, circulatory Issues and joint and tissue degradation which may be associated with paralysis. In this study, an attempt has been made to describe the scientific effects of Panchakarma procedures and Shamana Aushadha in this case.

Simulations of nerve signal propagation in axons

PurposeIn the literature, soliton solutions of the Heimburg–Jackson model have been proposed by Drab et al. (2022), but for the considered models, i.e. Eq.(1) and Eq.(2), the existence of solitons, the dispersion analysis and the pseudospectral method have been studied (Engelbrecht et al., 2006, 2018, 2020; Tamm et al., 2017, 2022; Peets et al., 2013). Therefore, the gap should be filled by this work.Design/methodology/approachWhen nonlinear terms, dissipative terms and forcing terms are ignored, the system (Eq.(2)) reduces to a single, sixth-order partial differential equation (Tamm et al., 2022). In this work, our aim is to propose analytical solutions in the explicit form via ansatz-based method. Therefore, the parameter effects in wave profile will be proposed clearly in figures.FindingsWhile progress has been made in signal propagation in nerves, thanks to many experimental studies and theoretical predictions over the last two centuries, the results obtained in this study may answer new questions that arise.Originality/valueIn the literature, the existence of solitons, dispersion analysis and pseudospectral method have been investigated for the Heimburg-Jackson model (Engelbrecht et al., 2006, 2018, 2020; Tamm et al., 2017, 2022; Peets et al., 2013), and this study fills the gap in soliton solutions. Additionally, when nonlinear terms, dissipative term and forcing terms are ignored, the system (Eq.(2)) reduced to a single equation that is sixth-order partial differential equation (Tamm et al., 2022). In this work, our aim is to propose analytical solutions in the explicit form via ansatz-based method. Therefore, the parameter effects in wave profile will be proposed clearly in figures.