In vivo electrophysiological experiments were conducted to evaluate the effects of intraventricular and cortical administration of orexins on electrically evoked epileptiform discharges (EEDs) in the hippocampal CA1 field. Bipolar electrodes were stereotaxically implanted into the CA1 region of anesthetized rats, and epileptiform activity was induced by high‑frequency electrical stimulation (HFES). Orexin‑A and orexin‑B (10 μg/10 μl) were administered into the lateral ventricle or applied to the frontal cortex. Intracerebroventricular administration of orexin‑A significantly reduced the duration of EEDs within 20 minutes and abolished the progressive, HFES‑related prolongation of epileptiform discharges observed in control animals. In contrast, cortical administration of orexin‑A selectively reduced the incidence of high‑amplitude (7-10 mV) population spikes during EEDs without affecting the duration of epileptiform activity. Neither cortical nor intraventricular administration of orexin‑B produced significant changes in evoked epileptiform activity in the CA1 field, suggesting a possible involvement of OX1 receptor signaling in mediating the effects of orexin‑A. The differential effects observed after cortical versus intraventricular administration of orexin‑A appear to reflect site‑specific mechanisms of action. The effects of intraventricular administration of orexin‑A were predominantly induced via direct activation of hippocampal orexinergic receptors, whereas cortical application of orexin‑A induced its effects via modulation of cortico‑hippocampal mechanisms.
Proton pump inhibitors are widely used, but their long‑term effects on the central nervous system are not well understood. In this study, we investigated whether chronic pantoprazole use alters sensorimotor function, oxidative stress, inflammatory response, and apoptosis in the motor cortex and cerebellum. Twenty‑one female Wistar rats were randomized to control (C), gavage control (GC), or pantoprazole (P; 20 mg/kg/day for 12 weeks) groups. Sensorimotor coordination (rotarod), water‑maze swim velocity, and open‑field locomotion were assessed as behavioral parameters. The cortical and cerebellar tissues were analyzed by Enzyme‑Linked Immunosorbent Assay (ELISA) for apoptosis, inflammation, and oxidative stress. Pantoprazole impaired sensorimotor coordination compared to both control groups. However, its effects on swim velocity and locomotor activity were primarily significant when compared to the naive control group, suggesting that gavage‑related stress may have contributed to these behavioral outcomes. Bcl‑2‑associated X protein (BAX) and Bcl‑2 associated agonist of cell death (BAD) protein levels and the BAX/Bcl‑2 ratio increased with pantoprazole, particularly in the motor cortex, indicating enhanced pro‑apoptotic activity. While tumor necrosis factor levels did not change, interleukin (IL)‑6 and IL‑1β levels were significantly higher in the cerebellum, suggesting neuroinflammatory activation associated with both pantoprazole and gavage‑induced stress. Furthermore, oxidative stress analyses revealed elevated malondialdehyde and oxidative stress index levels, as well as increased total antioxidant status, in specific regions, suggesting an imbalance between oxidative and antioxidant responses. Chronic pantoprazole administration resulted in modest motor deficits and region‑specific molecular alterations, including a pro‑apoptotic shift in the motor cortex. In addition, an inflammatory/compensatory antioxidant response in the cerebellum was observed due to both gavage‑induced stress and pantoprazole administration. These findings highlight the need for further studies on dose‑response, reversibility, and synaptic consequences, and suggest the importance of considering the risks of prolonged proton pump inhibitors exposure.
Multiple sclerosis (MS) is a chronic inflammatory disorder of the central nervous system (CNS) affecting millions worldwide, leading to significant disability. Current treatments focus on symptom management and reducing disease exacerbations. Noninvasive brain stimulation techniques such as transcranial direct current stimulation (tDCS) have emerged as potential therapies due to their ability to modulate cortical excitability and neuroplasticity. This review explores the therapeutic potential of tDCS in MS patients by summarizing human and animal studies investigating its effects. Literature was systematically reviewed from inception to October 2024 using PubMed and Google Scholar databases. Key findings include tDCS's ability to alleviate symptoms such as pain, fatigue, cognitive impairment, and motor dysfunction in MS patients. Mechanistically, tDCS is proposed to influence neurotransmitter modulation, inflammatory pathways, and neuronal networks, promoting neuroprotection and functional recovery. Moreover, preclinical studies in MS animal models suggest that tDCS may reduce inflammation, promote remyelination, and enhance neuronal survival. These insights underscore tDCS as a promising adjunctive therapy for MS, potentially improving quality of life and mitigating disease progression. Further research is warranted to elucidate optimal stimulation parameters, long‑term effects, and broader applicability in clinical settings.
Parkinson's disease (PD) is a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons. The G2019S mutation in the leucine‑rich repeat kinase 2 (LRRK2) gene is the most common genetic cause of familial and sporadic PD. In dopaminergic neurons, increased kinase activity caused by LRRK2‑G2019S mutation impairs synaptic vesicle recycling and dopamine storage, increasing cytosolic dopamine, which is prone to oxidation and generates reactive oxygen species. Simultaneously, the mutation alters iron metabolism through Rab misregulation, increasing iron uptake and lysosomal dysfunction, further amplifying oxidative stress and creating a pro‑ferroptotic environment. At the same time, dysregulated calcium signaling, driven by the enhanced activity of L‑type calcium channels and impaired mitochondrial calcium buffering via the mitochondrial calcium uniporter, enhances mitochondrial dysfunction. This minireview integrates current evidence linking LRRK2‑G2019S to these pathological pathways, highlighting this mutation's role in dopamine, iron, and calcium imbalance. Understanding this molecular interplay may provide novel insights into PD pathogenesis and guide the development of targeted neuroprotective therapies.
Scopolamine, a muscarinic acetylcholine receptor antagonist, disturbs learning and memory processes. Clozapine, an atypical antipsychotic, has beneficial predictive validity for confirming principles to help new treatment approaches. It could improve the cognitive deficit. Furthermore, clozapine has affinity for the cholinergic and GABAergic receptors. This investigation examined the effects of clozapine and/or GABAA receptor drugs on scopolamine‑induced memory impairment in male mice. Step‑down passive avoidance and open‑field tests were utilized for assessing memory acquisition and locomotor activity, respectively. The results exhibited that pre‑training administration of muscimol but not bicuculline induced amnesia without affecting locomotor activity. Moreover, pre‑training administration of clozapine did not significantly modify memory acquisition, but co‑administration of scopolamine and clozapine improved the amnesia produced with scopolamine. Also, co‑administration of muscimol along with clozapine potentiated memory impairment induced by scopolamine, whereas co‑injection of bicuculline along with clozapine reversed memory impairment produced by scopolamine. These treatments did not significantly change locomotor activity. Based on the findings, it is concluded that the GABAergic system modulates memory acquisition, and clozapine interacts with both muscarinic and GABAergic systems to bidirectionally regulate scopolamine‑induced amnesia. These results suggest the potential involvement of GABAergic mechanisms in the memory‑impairing effects of scopolamine and highlight the therapeutic potential of clozapine in mitigating cholinergic dysfunction‑related memory deficits.
Microglia accumulate in malignant gliomas and play a pivotal role in tumor progression. Using single‑cell RNA sequencing studies researchers have probed gene expression in the myeloid cells in experimental gliomas at relatively late stages of the tumor development. Therefore, the early changes in gene expression in microglia in response to glioma are not fully characterized. We have previously reported distinct profiles of gene expression in the rat primary microglia cultures treated for 6 hours with either rat C6 glioma‑conditioned medium (GCM) or lipopolysaccharide. In the current study, using RNA‑seq, we characterized the transcriptional response of rat primary microglia to GCM in vitro at different time‑points: 6 h, 24 h, and 48 h, as compared to the control treated for 6 h with its own medium. We observed that during the GCM treatment gene expression changes in a biphasic, swing‑like pattern. This includes the genes involved in innate immune response, which are mostly down‑regulated at 6 h by the GCM treatment, as compared to the time‑matched control, and subsequently up‑regulated at 48 h, as compared to the earlier time‑points of the GCM treatment. Conversely, the genes involved in the cell cycle are up‑regulated at 6 h and down‑regulated at 48 h, which coincides with the induction of Tgfb1. Notable exceptions to this biphasic pattern include key genes activating immune response, such as Tlr9 and Myd88, which are down‑regulated early and persistently, while genes inhibiting immune activation, such as Trem1, and genes involved in a metabolic switch, such as Pfkl, are persistently up‑regulated. Most notably, the up‑regulated genes include Ptgs1 (alias Cox1) and Tbxas1, which encode the enzymes catalyzing the synthesis of thromboxane A2, a known inducer of T cell suppression. Further studies are needed to test the functional consequences of their up‑regulation.
Chronic pain conditions are often linked with depression, a common chronic mental health disorder that severely impairs quality of life. This association is particularly present in chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS). CP/CPPS is a prevalent urological disorder characterized by pelvic pain accompanied by neuropsychiatric comorbidities such as depression, for which underlying pathophysiological mechanisms remain unclear. Recently, anti‑inflammatory and neuroprotective effects of carbon monoxide‑releasing molecules (CORMs) have been demonstrated. The aim of this study was to investigate whether CO releaser, CORM‑A1 could have beneficial effects on depressive‑like behavior in an animal model of CP/CPPS. Adult male Wistar albino rats were divided into four groups (Sham‑PBS, Sham‑CORM, CP/CPPS‑PBS and CP/CPPS‑CORM), receiving intraprostatic injections of saline or λ‑carrageenan, followed by daily treatments with PBS or CORM‑A1 for seven days. Pain thresholds were measured by von Frey esthesiometer, while depression‑like behaviors were assessed by the forced swimming test (FST). CP/CPPS rats exhibited mechanical hyperalgesia which has been significantly diminished by CORM‑A1 administration. CORM‑A1 treatment caused a significant decrease in floating time and a significant increase in swimming time in CP/CPPS rats compared to those treated with vehicle (CP/CPPS‑PBS group). Correlation analysis showed a significant link between pain threshold and FST floating time as indicator of depressive‑like behaviors. These findings suggest that CORM‑A1 beneficially modulates pain perception and depressive‑like behaviors in CP/CPPS rats.
Large conductance cation channels (LCC‑channels), located in the nuclear membrane, are potential mediators of potassium (K+) countercurrent during calcium ion (Ca2+) release from intracellular stores. This study examined the effects of epinephrine, norepinephrine, isoprenaline, and propranolol on the electrophysiological properties of these channels to evaluate their potential as blocking agents in future studies of LCC‑channel involvement in Ca2+ release. The patch‑clamp method, using voltage‑clamp mode and a nucleus‑attached configuration, was employed to record currents passing through LCC‑channels in Purkinje cell nuclei. The effectiveness of Ca2+ blocking was estimated by analyzing changes in current amplitude and the probability of the channels being in an open state. All tested adrenergic receptor modulators decreased current amplitude through LCC‑channels at negative membrane potentials to varying extents, while no changes in amplitude were found for positive applied potentials for any compound. Epinephrine, norepinephrine, and propranolol demonstrated blocking capabilities comparable to nicotinic acetylcholine receptor (nAChR) modulators under similar conditions. Notably, only norepinephrine significantly inhibited the open‑state probability of LCC‑channels, whereas isoprenaline increased this parameter and induced rapid flickering. Furthermore, isoprenaline produced a greater reduction in current amplitude through LCC‑channels than the other compounds.
Seizures in epilepsy result from excessive neuronal electrical discharges. Imbalances in potassium homeostasis can increase neuronal excitability and trigger epileptic seizures. Drugs that enhance potassium currents are expected to suppress seizures. Pinacidil, an ATP‑sensitive potassium channel opener, has shown anticonvulsant effects in acute seizure models in rodents. However, its effects following chronic systemic administration in pentylenetetrazole (PTZ)-kindled rats remain unknown. The aim of this study was to investigate the impact of long‑term pinacidil treatment in the PTZ‑kindling model of epilepsy. Male Wistar Hannover rats were treated intraperitoneally with pinacidil 30 min before each PTZ injection, administered intraperitoneally every other day for 27 days (14 injections). Behavioral responses were recorded for 30 min immediately after each PTZ injection. Twenty‑four hours after the last PTZ injection, animals underwent the rotarod test and were then euthanized for toxicological analysis of renal and hepatic biochemical markers in serum. Chronic pinacidil treatment prevented the development of PTZ‑induced kindling. Biochemical data showed that chronic pinacidil did not provoke changes in serum creatinine and urea levels or in aspartate aminotransferase and alanine aminotransferase levels. These findings suggest that long‑term administration of pinacidil impairs the progression of PTZ‑induced kindling without causing nephrotoxic or hepatotoxic effects.
Neuropathic pain is a condition that results from nerve injury. There is a relationship between neuropathic pain and mood disorders. Citicoline, when used as a dietary supplement, exhibits neuroprotective, antidepressant, and anxiolytic properties. Moreover, bupropion is an atypical antidepressant with unique pharmacologic properties. We sought to investigate the effects of citicoline and bupropion as well as their possible interaction on the control of anxiety‑ and depression‑like behaviors in nerve‑ligated mice. Unilateral sciatic nerve ligation was performed on the right hind limb. Anxiety‑ and depression‑like behaviors were measured using the elevated plus‑maze and the tail suspension test, respectively. The results showed that sciatic nerve ligation decreased the percentage of time spent in the open arms of the elevated plus‑maze and increased the immobility time in the tail suspension test, displaying anxiogenic‑ and depressant‑like responses in the nerve‑ligated mice. Intraperitoneal administration of citicoline increased the percentage of time spent in the open arms and diminished the immobility time of the tail suspension test compared to the saline group, showing anxiolytic and antidepressant‑like responses. Additionally, the injection of bupropion induced antianxiety‑ and antidepressant‑like responses increasing the percentage of time spent in the open arms and reducing immobility time in nerve‑ligated mice. Co‑injection of bupropion and citicoline potentiated the antidepressant property of bupropion in nerve‑ligated mice. Additionally, we determined an additive effect between bupropion and citicoline on the generation of anxiolytic and antidepressant‑like behaviors in the nerve‑ligated mice. Based on these results, we concluded that there is a crosstalk between bupropion and citicoline in the control of anxiety‑ and depression‑like behaviors in the nerve‑ligated mice.
Aversive experiences lead to the formation of long‑lasting memories. Despite the need to better understand how enduring fear memories can be attenuated, the underlying brain circuits remain largely unknown. In this study, employing a combination of genetic manipulations, neuronal circuit mapping, and chemogenetics in mice, we identify a new projection from the thalamic nucleus reuniens (RE) to the medial septum (MS), and show that this circuit is involved in the extinction of remote (30‑day old), but not recent (1‑day old), fear memories. We also demonstrate that the activity of this circuit, as well as consolidation of remote extinction memory, require autophosphorylation of αCaMKII, a key signaling molecule in the excitatory synapses. Our findings provide the first functional description of the RE→MS circuit and highlight the significance of the thalamo‑septal regions in memory organization as a function of memory age, a phenomenon known as systems consolidation.
Interhemispheric communication is a fundamental feature of the mammalian brain, supporting the bilateral integration of sensory, motor, cognitive, and emotional processes. While the corpus callosum has long been recognized as the principal commissural pathway, recent advances have illuminated a far more complex molecular and circuit‑level architecture. This review synthesizes evidence from neuroanatomy, electrophysiology, molecular neuroscience, and neuroimaging to outline how interhemispheric signaling is organized and dynamically regulated. Fast excitatory and inhibitory neurotransmission provides the scaffold for callosal transfer, while neuromodulatory systems, including dopaminergic, cholinergic, serotonergic, and noradrenergic pathways, introduce a chemical layer of regulation that tunes excitability, synchrony, and hemispheric dominance. Developmental processes involving axon guidance molecules and neurotrophins shape the establishment of commissural networks, whereas activity‑dependent plasticity refines functional architecture of these networks across the lifespan. Importantly, interhemispheric interactions are not static but fluctuate dynamically according to behavioral demands, as demonstrated by recent models of dynamic laterality. Disruption of these lateralized processes is implicated in a broad spectrum of conditions, including stroke, dyslexia, autism spectrum disorder, schizophrenia, and mood disorders. By bridging cellular, molecular, and systems‑level insights, this review highlights interhemispheric communication as a key organizing principle of brain function and a promising target for therapeutic interventions aimed at restoring interhemispheric balance.
The present study aims to elucidate the role of the Sigma‑1 receptor in the pathogenesis of neuropathic pain and evaluate its potential therapeutic implications. To systematically assess the effects of the Sigma‑1 receptor, neuropathic pain was induced in rats using the chronic constriction injury (CCI) model. Subjects were subsequently divided into three groups: Sham, CCI, and CCI+BD1047 (where BD1047 is a Sigma‑1 receptor antagonist). Following intrathecal administration of the respective agents, thermal withdrawal latency (TWL) and mechanical withdrawal threshold (MWT) were measured. Additionally, Western blotting was utilized to examine Sigma‑1 receptor, phosphorylated protein kinase Cα (p‑PKCα), and P2X3 receptor expression in the dorsal root ganglia (DRG). Immunofluorescence techniques were employed to examine p‑PKCα and P2X3 receptor expression. The results indicate a direct correlation between Sigma‑1 receptor activity and pain perception, evidenced by changes in TWL and MWT. In the CCI group, both TWL and MWT were significantly reduced compared to the Sham group. Furthermore, protein levels of the Sigma‑1 receptor, p‑PKCα, and P2X3 receptor in the DRG were elevated, and immunofluorescence expression of p‑PKCα and the P2X3 receptor also increased. Conversely, in the CCI+BD1047 group, TWL and MWT were significantly enhanced. Additionally, protein levels of the Sigma‑1 receptor, p‑PKCα, and P2X3 receptor in the DRG decreased, along with reduced immunofluorescence expression of p‑PKCα and P2X3 receptor. The findings indicate that neuropathic pain is intricately associated with the Sigma‑1 receptor, p‑PKCα, and P2X3 receptor in the dorsal root ganglia. Notably, the Sigma‑1 receptor regulates the expression of p‑PKCα and P2X3 receptor, presenting a novel therapeutic target for neuropathic pain management.
Diabetes is the most common cause of vision deterioration and subsequent vision loss in people worldwide. Long-term hyperglycemia causes structural, neurovascular and metabolic changes in the eye, leading to a progressive loss of light sensitive retinal cells, degeneration of retinal layers and neuroinflammation of optic nerve fibers and, if not treated, leading to the development of diabetic retinopathy and optic nerve damage. Growing evidence indicates that the pathological changes observed in the retina and optic nerve affected by prolonged hyperglycemia might results from several interconnected molecular events and biochemical signaling cascades such as excessive protein glycation, increased oxidative stress and local inflammation triggered by the receptor for advanced glycation end‑products (RAGE) along with the upregulation of molecules involved in angiogenesis and cytoskeleton modification including vascular endothelial growth factor (VEGF) and RhoA/Diaph1/profilin1 system. In this review, we focus on the latest advances in uncovering major factors involved in the pathogenesis of diabetic retinopathy and discuss novel, non‑invasive treatment options aimed at the cause rather than symptoms of the disease.
The role of prefrontal somatostatin interneurons in emotion recognition is well characterized. Here, for the first time, we investigated the role of these neurons during remote transfer of emotional information in the safe environment of the home cage. To do that mice with fluorescently labelled somatostatin interneurons were housed in pairs for three weeks, one labelled an Observer, and the other a Demonstrator. In the test session, the Demonstrator was subjected to aversive stimuli outside of the home cage, while the Observer remained there undisturbed. Upon the return of the Demonstrator to the home cage, we recorded the interactions of the two animals. The behavior of both partners, assessed and classified with machine learning algorithms, was clearly affected by the emotional state of the Demonstrator. To assess the role of prefrontal somatostatin interneurons in this process we chemogenetically manipulated their activity in the Observers and found that activation of these cells abolishes the enhanced social investigation of a stressed Demonstrator. This is associated with disinhibition of the prefrontal cortex. The manipulation also affects the neuronal activation patterns in Demonstrators, which seems to reflect the change in the behavior of the Observers.
Astrocytes express a set of neurotransmitter receptors (glioreceptors) that enable them to regulate synaptic transmission and neuroplasticity, and to function as integral partners in synaptic signaling and the modification of neural circuits. This review presents the current understanding of how glioreceptors on astrocytes (astro‑gliorecptors) mediate bidirectional communication between neurons and glia across major neurotransmitter systems. The review focuses on receptors for glutamate, GABA, acetylcholine, monoamines, neuropeptides, opioids, and purines. Through these receptors, astrocytes can modulate synaptic strength, LTP and LTD expression, network dynamics, and state‑dependent modulation of arousal and reward circuits. Despite potentially having lower receptor density than neurons, astrocytes can amplify their functional impact through unique structural properties, such as extensive process arborisation, contact with thousands of synapses, and the formation of electrically coupled syncytia that propagate calcium waves across neural networks. Metabolic integration via glycogen regulation, lactate production, and gliotransmitter release modulates neuronal excitability and synaptic strength. Therefore, astrocytes can be viewed as integrators of neuronal activity patterns and gatekeepers of experience‑dependent plasticity, essential for maintaining synaptic homeostasis and enabling adaptive behavioral responses. Astro‑glioreceptors dysfunctions contribute to neurological and psychiatric disorders, including Alzheimer's disease, Parkinson's disease, epilepsy, and depression. Therefore, targeting specific glioreceptor subtypes represents a promising therapeutic strategy for modulating neural circuits while minimizing neuronal side effects.
Myosin VI (MVI) is a unique unconventional myosin which, unlike other myosins, moves towards the minus end of actin filaments. It is involved in numerous cellular processes such as endocytosis and trafficking, cell migration and adhesion, and gene transcription. It is widely expressed in all tissues, including the brain. Its lack in adult murine brains is associated with gliosis and impairment of neuronal transmission. Here, we demonstrate that the MVI level in the total mouse brain and its regions (cerebral cortex, cerebellum, and hippocampus) increases with the animal's age (from newborn up to 12‑month‑old mice). Its lack leads to enlargement of the brain and its examined areas, and an increase of the level of GFAP, the marker of glia cells, in adult mice. The data indicate an involvement of MVI in the brain maturation and possibly in development of an age‑dependent gliosis.
Angiotensin‑(1‑7) [Ang‑(1‑7)] exerts physiological effects in the brain mediated by its receptor, Mas. Recent studies have successfully demonstrated that Ang‑(1‑7) exerts neuroprotective effects following cerebral ischemia in a rat model. However, prior investigations utilized direct intracerebral cannulation for Ang‑(1‑7) delivery, potentially limiting human application. Hematopoietic stem cells (HSC) have been previously demonstrated to mobilize to the site of cerebral injury in response to stroke. Therefore, we sought to examine the therapeutic potential of HSC transduced via a lentivirus with Ang‑(1‑7) to migrate to the ischemic hemisphere and overexpress Ang‑(1‑7) following stroke. Animals were divided into 3 groups: Stroke + PBS, Stroke + HSC, Stroke + Ang‑(1‑7)‑transduced HSC. Bone marrow from separate animals was harvested and used for injection of the HSC, with or without lentivirus induced Ang‑(1‑7) transduction. A neurological assessment was performed at 72 hours post‑surgery. Ang‑(1‑7) transduced HSC secreted the peptide up to 72 hours post infection, in vitro. Stroked animals injected with the Ang‑(1‑7) infected HSC exhibited reduced behavioral deficits on the Bederson neurological assessment scale. These data suggest that HSC‑mediated delivery of Ang‑(1‑7) to ischemic brain appears to improve post‑stroke outcomes and may offer a novel route of therapeutic agent delivery to the brain.
Peripheral nerve injuries occur due to accidents and in manufacturing every day. Unlike the central nervous system, injured peripheral nerves can self‑regenerate after injury. The study explored changes in gene expression and related biological processes after peripheral nerve injury and regeneration. Male Sprague‑Dawley rats were divided into six groups and underwent sciatic nerve resection followed by recovery for 0, 3, 6, 10, 15, and 20 days; distal sciatic nerve segments were collected for sequencing, real‑time quantitative polymerase chain reaction (RT‑qPCR), and Western blotting. According to DNA microarray analysis, approximately 5,000 genes were differentially expressed, and six biological processes were identified at different time points after nerve transection, with expression mainly observed in the mid and latter stages after injury. Four genes (UDP glycosyltransferase 8 [Ugt8], C‑C motif chemokine ligand 2 [Ccl2], neuregulin 1 [Nrg1], and heme oxygenase‑1 [Hmox1]) with nerve regeneration‑specific function were selected for further verification using RT‑qPCR and Western blot. The results demonstrated that genes such as Ugt8 decreased initially and then peaked at 20 days, whereas Ccl2 and Hmox1 both exhibited two peaks at three and 20 days. Nrg1 showed a gradual increase, peaking around 15 days. The study identified differential gene expression in distal nerve segments during Wallerian degeneration and analyzed the associated dynamic biological changes. The findings provide insights into research on peripheral nerve injury and regeneration, and further studies will involve screening key genes and more detailed investigations.
