Nervous System Function Research Articles

Nervous system functioning disorders in patients with mandible fractures

Relevance. Fractures of the mandibular fracture are a stressor on the body and lead to changes in the functioning of the autonomic nervous system. At the same time, patients with mandibular fractures often experience local changes in the nervous system associated with the anatomical and physiological features of the location of the third branch of the trigeminal nerve and its damage. These changes affect the course of the post-traumatic period and may increase the likelihood of complications of mandibular fractures.Purpose: to determine the significance of disturbances in the functioning of the nervous system during the post-traumatic period of fractures of the mandibular fracture.Materials and methods. When examining 130 patients with fractures of the mandibular fracture, the state of the autonomic nervous system and local neurological changes were studied.Results. In patients with mandibular fractures, dysfunction of the autonomic (autonomic) nervous system and local neurological changes were revealed.The severity of these changes is reflected in the development of complications of fractures. When studying the autonomic nervous system in patients with mandibular fractures, there was an increase in the activity of the sympathetic nervous system, which increased the likelihood of developing complications of mandibular fractures. A high incidence of injury to the inferior alveolar nerve was also found. The most pronounced deviations in autonomic balance indicators – pathological increased excitability of the autonomic nervous system – were diagnosed in patients with complicated fractures of the mandibular fractures. In most patients with complicated mandibular fractures, damage to the trigeminal nerve was detected, confirming the role of neurotrophic disorders in the development of complications.Conclusion. With fractures of the mandible, there is an increase in the activity of the sympathetic nervous system, which increases the likelihood of complications. The most pronounced deviations in autonomic balance indicators were diagnosed in patients with complicated fractures of the mandible. In addition, in patients with mandibular fractures, a high incidence of damage to the inferior alveolar nerve was revealed; in complicated fractures, neuropathy is severe, which confirms the role of neurotrophic disorders in the development of complications. Thus, methods for preventing purulent-inflammatory complications in jaw fractures should include correction of neurological disorders.

Alternative use of the cough drug - N-acetylcysteine in psychiatry: a review of recent clinical trials

Introduction and purpose N-acetylcysteine (NAC) is one of the more popular drugs, widely available in pharmacies, used to treat wet cough. NAC's diverse mechanism of action has drawn the attention of researchers for its great potential in the treatment of many conditions. Indeed, it has been noted that administration of NAC allows indirect modulation of the central nervous system, which may be important in the treatment of psychiatric diseases. The following review focuses on recent reports of NAC's potentially beneficial effects on psychiatric conditions such as depression, schizophrenia, obsessive-compulsive disorder, and addiction. Description of the state of knowledge Based on studies conducted on animals (rats), a positive effect of NAC has been proven, observing a reduction in the severity of depressive symptoms. Based on the above data, more and more human studies are being conducted, where the effect of NAC on the symptoms of various mental conditions is being investigated. In recent years, the antioxidant, anti-inflammatory and neurotransmitter function modulating effects of NAC on the brain have been proven, with significant potential in the treatment of mental illness. Conclusions The potential impact of NAC on the treatment of mental illness is a rapidly developing topic in recent years. On the basis of available scientific data, partial reduction of symptoms of mental illnesses through the use of NAC has been confirmed. It is a very promising drug, which in this indication requires additional studies to unequivocally confirm its beneficial effects on the functioning of the central nervous system.

Regulatory roles of dopamine D2 receptor in milk protein production and apoptosis in mammary epithelial cells

Dopamine D2 receptors (D2Rs) play crucial roles in regulating diverse physiological functions of the central nervous system and peripheral organs. D2Rs are also expressed in mammary glands. However, which cell types express D2Rs and whether they are involved in milk production remains unclear. The present findings revealed that D2Rs are expressed in the apical regions of the lateral membranes of mammary epithelial cells (MECs) in lactating mice. We also investigated the effects of the D2R agonist bromocriptine and/or antagonist domperidone on intracellular cAMP levels, milk protein production, and apoptosis in a lactation culture model of MECs that produce major milk components like lactating MECs in vivo. We found that bromocriptine decreased intracellular cAMP levels, whereas domperidone dose-dependently neutralized this effect. Bromocriptine also inhibited casein and lactoferrin production and suppressed activities of STAT5 and glucocorticoid receptors (GRs). Domperidone neutralized the inhibition of casein production as well as STAT5 and GR inactivation induced by bromocriptine. Furthermore, D2R activation by bromocriptine induced apoptosis and inactivated ERK, a signaling molecule responsible for promoting cell proliferation and survival. Domperidone attenuated ERK inactivation and apoptosis induced by bromocriptine. These findings suggest that D2Rs play regulatory roles in milk protein production and apoptosis in MECs.

Unavoidability and Functionality of Nervous System and Behavioral Randomness

Unavoidability and Functionality of Nervous System and Behavioral Randomness

Design, Synthesis, and Insecticidal Activity of Pyridino[1,2-a]pyrimidines Containing Indole Moeites at the 1-Position.

Research on mesoionic structures in pesticide design has gained significant attention in recent years. However, the 1-position of pyridino[1,2-a]pyrimidine is usually designed with 2-chlorothiazole, 2-chloropyridine, or cyano moieties commonly found in neonicotinoid insecticides. In order to enrich the available pharmacophore library, here, we disclose a series of new pyridino[1,2-a]pyrimidine mesoionics bearing indole-containing substituents at the 1-position. Most of these target compounds are confirmed to have good insecticidal activity against aphids through bioevaluation. In addition, a three-dimensional structure-activity relationship model is established to allow access to optimal compound F45 with an LC50 value of 2.97 mg/L. This value is comparable to the property achieved by the positive control triflumezopyrim (LC50 = 2.94 mg/L). Proteomics and molecular docking analysis suggest that compound F45 has the potential to modulate the functioning of the aphid nervous system through its interaction with neuronal nicotinic acetylcholine receptors. This study expands the existing pharmacophore library for the future development of new mesoionic insecticides based on 1-position modifications of the pyridino[1,2-a]pyrimidine scaffold.

O-GlcNAcylation in ischemic diseases.

Protein glycosylation is an extensively studied field, with the most studied forms being oxygen or nitrogen-linked N-acetylglucosamine (O-GlcNAc or N-GlcNAc) glycosylation. Particular residues on proteins are targeted by O-GlcNAcylation, which is among the most intricate post-translational modifications. Significantly contributing to an organism's proteome, it influences numerous factors affecting protein stability, function, and subcellular localization. It also modifies the cellular function of target proteins that have crucial responsibilities in controlling pathways related to the central nervous system, cardiovascular homeostasis, and other organ functions. Under conditions of acute stress, changes in the levels of O-GlcNAcylation of these proteins may have a defensive function. Nevertheless, deviant O-GlcNAcylation nullifies this safeguard and stimulates the advancement of several ailments, the prognosis of which relies on the cellular milieu. Hence, this review provides a concise overview of the function and comprehension of O-GlcNAcylation in ischemia diseases, aiming to facilitate the discovery of new therapeutic targets for efficient treatment, particularly in patients with diabetes.

Effects of Acupuncture on Autonomic Nervous System Parameters and Salivary Cortisol Level Among Mental Stress University Students: A Pilot Randomized Controlled Trial

Stress is a common and often unavoidable aspect of daily life that can negatively impact the autonomic nervous system, which controls the functions of internal organs and glands. Chronic stress has been associated with an imbalance in autonomic nervous system function, leading to a range of health conditions. Acupuncture is a medical treatment modality that has been applied to health care in different dimensions including physical, mental, and spiritual. This study aimed to investigate the effect of acupuncture on blood pressure, heart rate, and salivary cortisol level in mild stress university students, a population particularly vulnerable to stress. Twenty-eight university students were recruited and divided into two groups, a real acupuncture group and a sham acupuncture group. Heart rate, blood pressure, and salivary cortisol level were evaluated before and after a 30-minute acupuncture session on the ST36 acupoint. The results showed that the real acupuncture group had a significant decrease in blood pressure and heart rate, whereas the sham acupuncture group showed no change. Both groups had a slightly decrease in salivary cortisol level with no statistically significant. There was a statistically significant difference in the decrease of systolic blood pressure and heart rate after acupuncture between the two groups, but there was no significant difference between the groups in salivary cortisol level after acupuncture. The findings suggest that the acupuncture can be a valuable treatment for restoring balance to the symptoms of the autonomic nervous system in university students experiencing stress. A larger sample size, a non-intervention control, as well as different sources and times of cortisol collection, could contribute to the validation of the findings in this study.

The Role of GLP-1 Affects Fate of Astrocytes Following Ischemic Stroke in Mice

Stroke is one of the leading causes of physical and intellectual disability and mortality in adults of most of the developed countries. The most of studies in ischemic stroke focus on neuronal pathological mechanisms and neuronal death trying to rescue neurons via stopping the detrimental pathological processes or enhancing neuronal viability. Although astrocytes are the most abundant cells and in mammal central nervous system (CNS), they were ignored for period of time but are return to spotlight in recent years. Astrocyte play multiple roles in maintain normal function of central nervous system and respond to all kinds of CNS injury and disease. Responses of astrocytes to CNS damage lead to both detrimental and beneficial consequences. Previous studies have reported that astrocyte inflammatory responses to ischemic stroke may devastate the ischemic lesion, but other astrocytic responses lead to anti-excitotoxicity, secreting neurotrophic factors, neurogenesis, synaptogenesis, axonal remodeling, and angiogenesis promoting neuroprotective effects. Glucagon-like peptide-1 (GLP-1) have been intensively studied on beneficial effects of neurons, but not many studies work on effects of GLP-1 to astrocytes. Our early study has found that activation of GLP-1 receptors prevented ischemia-induced brain cell death and observed newly neuronal progenitor cells were from astrocyte-lineage in penumbral area of 3-day post-ischemic mouse brains by immunohistochemistry (IHC). RT-PCR, immunoblotting, and immunofluorescent results also clearly indicated the astrocytes expressed GLP-1 receptors. Furthermore, Western blotting results showed administration of GLP-1 analogue, exendin-4 (EX-4), suppressed expression of pro-inflammatory proteins in oxygen-glucose deprivation (OGD) treated mouse primary astrocytes. Interestingly, we also observed that infarct site obtained sever DNA damage and less GFAP positive astrocytes, on contrary, the penumbral area had more GFAP positive astrocytes and less DNA damage in IHC images of stroke brains. The results implied that A1 and A2 astrocytes play certain roles in ischemic brains and recovery. The goal of this study is to determine the mechanisms of GLP-1 involving in astrocytic fate decision and approach on minimizing detrimental effects and amplifying the beneficial effects, which possibly develop innovative therapies for ischemic stroke. The study is supported by 108-2320-B-182A-005-MY3 and 112-2320-B-182A-003- from Taiwan National Science and Technology Council. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Exploring the properties and potential of the neural extracellular matrix for next-generation regenerative therapies.

The extracellular matrix (ECM) is a dynamic and complex network of proteins and molecules that surrounds cells and tissues in the nervous system and orchestrates a myriad of biological functions. This review carefully examines the diverse interactions between cells and the ECM, as well as the transformative chemical and physical changes that the ECM undergoes during neural development, aging, and disease. These transformations play a pivotal role in shaping tissue morphogenesis and neural activity, thereby influencing the functionality of the central nervous system (CNS). In our comprehensive review, we describe the diverse behaviors of the CNS ECM in different physiological and pathological scenarios and explore the unique properties that make ECM-based strategies attractive for CNS repair and regeneration. Addressing the challenges of scalability, variability, and integration with host tissues, we review how advanced natural, synthetic, and combinatorial matrix approaches enhance biocompatibility, mechanical properties, and functional recovery. Overall, this review highlights the potential of decellularized ECM as a powerful tool for CNS modeling and regenerative purposes and sets the stage for future research in this exciting field. This article is categorized under: Implantable Materials and Surgical Technologies > Nanotechnology in Tissue Repair and Replacement Therapeutic Approaches and Drug Discovery > Nanomedicine for Neurological Disease Implantable Materials and Surgical Technologies > Nanomaterials and Implants.

Glial Cell Development and Function in the Zebrafish Central Nervous System.

Over the past decades the zebrafish has emerged as an excellent model organism with which to study the biology of all glial cell types in nervous system development, plasticity, and regeneration. In this review, which builds on the earlier work by Lyons and Talbot in 2015, we will summarize how the relative ease to manipulate the zebrafish genome and its suitability for intravital imaging have helped understand principles of glial cell biology with a focus on oligodendrocytes, microglia, and astrocytes. We will highlight recent findings on the diverse properties and functions of these glial cell types in the central nervous system and discuss open questions and future directions of the field.

The source of TAFA4 and its role in CNS immune cell recruitment during neuroinflammation

Abstract TAFA4, also known as Fam19a4, has been reported to be secreted by C-low-threshold mechanoreceptors (C-LTMRs) and alleviate mechanical pain hypersensitivity. However, its immunological function in the central nervous system (CNS) remains incompletely understood. Our study aims to elucidate the wider source of TAFA4 in the CNS and its role in CNS inflammation. We generated lines of TAFA4-knockout (KO)-reporter mice, wherein the TAFA4 gene is deleted and replaced with a membrane-bound green fluorescent protein (GFP) and secretable nano-luciferase. We discovered that TAFA4 expression extended beyond C-LTMRs, encompassing neurons in the habenula-fasciculus retroflexus, hypothalamus, and olfactory bulb. Notably, the kinetics of TAFA4 expression followed a decreased trend during EAE-induced inflammation by nano-luciferase assay. Furthermore, we showed that mice with TAFA4 deficiency exhibited diminished immune cell infiltration and reduced demyelination in the spinal cord after EAE induction. These results underscore the involvement of TAFA4 in pro-inflammatory responses during EAE pathogenesis. Additionally, we showed that TAFA4 acted with chemoattractant properties towards M1 macrophages and neutrophils but not T cells by trans-well analysis. In summary, our study revealed the diverse sources of TAFA4 within the CNS and unveiled its inflammatory role during EAE inflammation. We propose that TAFA4 is potentially involved in CNS immune cell recruitment and inflammation.

The Synergistic Trio of Metabolic Master Regulators Sustaining a Vicious Circle of Pathological Processes in Post-Traumatic Stress Disorder

Post-traumatic stress disorder (PTSD) is a maladaptive responseto the exposure of an extraordinary-intensity stressor. The animaland human body responds to any external challenges at the systemic, organismaland cellular levels. In stress-sensitive individuals, the collaborationof stress-implementing and stress-limiting systems is compromised,causing the transformation of behavior, cognitive abilities andother functions of the central nervous system. It is commonly acceptednow that changes in the abundance and repertoire of the intestinalmicrobiota play an important role in the pathogenesis of PTSD. Inthis regard, the methods of improving the microflora are high onthe agenda. Analyzing the literature data, we came to the conclusionthat metabolic, somatic and mental health largely depends on thecoordinated functioning of the key interdependent metabolic components:hepatobiliary system, intestinal microbiota and, as we believe,the state of mast cells. Close scrutiny of the interplay of these componentswill help identify new therapeutic targets and the most effectivemethods to treat PTSD.

Mild-to-moderate COVID-19 may affect nervous system function in convalescents

Mild-to-moderate COVID-19 may affect nervous system function in convalescents

Disrupted Phosphorylated Phosphoinositide 3-kinase in the NTS of Type 2 Diabetic Rats

The hallmark of type 2 diabetes mellitus (T2DM) is systemic insulin resistance, where insulin signaling is impaired, blood glucose is chronically elevated, and various pathophysiological processes ensue. Much is known about the cardiovascular and metabolic consequences of T2DM. However, the impact of T2DM on autonomic nervous system function remains to be fully elucidated. Increasing evidence suggests that in both human and animal models of T2DM, the exercise pressor reflex (EPR) is abnormally augmented, characterized by heightened cardiovascular and sympathetic responses to physical activity. The underlying mechanisms are still not completely understood. Our recent studies suggest that T2DM induces alterations in peripheral somatosensory nerve activity that could explain the augmented EPR function. However, it is possible that neurons within the cardiovascular control areas of the brainstem, such as the nucleus tractus solitarius (NTS), could also be impaired by this disease. In the central nervous system, insulin has been shown to hyperpolarize neurons through activation of the phosphoinositide 3-kinase (PI3K) pathway, resulting in reduced neuronal excitability. Therefore, we hypothesized that decreased insulin transport into the brain in T2DM rats, results in increased cellular excitability as evidenced by decreased activity of the PI3K pathway in the NTS. Purpose: The aim of this study was to examine alterations in brain insulin levels and the PI3K pathway in T2DM rats as compared to control rats. Methods: Control rats were fed a low fat control diet (13% fat, 67.8% carbohydrate, and 19.2% protein) for 12-16 wks, while T2DM were generated by two low dose bolus injections of i.p. streptozotocin (35mg/kg, week 1; 25mg/kg week 2) and then fed a high fat diet (42% fat, 42.8% carbohydrate, and 15.2% protein) for 12-16wks. Cerebrospinal fluid (CSF) were collected from control and T2DM rats after an overnight fast. NTS micro-punches were performed, and then total and phosphorylated PI3K protein expressions were examined by the western blot technique. Results: CSF insulin was significantly decreased in T2DM rats as compared to control rats (0.41 ± 0.19 vs 0.11 ± 0.05 (ng/mL), Control (n=14) vs T2DM (n=4), p<0.01). Total PI3K expression in the NTS did not differ between control and T2DM (1.0 ± 0.2 vs 1.1 ± 0.2 (au), Control (n=9) vs T2DM (n=9), P=0.172). However, phosphorylated PI3K expression in the NTS of T2DM was significantly decreased as compared with control animals (1.0 ± 0.2 vs 0.8 ± 0.1 (au), Control (n=9) vs T2DM (n=9), p<0.05). Conclusion: These results suggest that 1) in consistent with earlier studies, insulin transport into the brain is impaired in high fat diet/streptozotocin-induced T2DM animals, and 2) decreased phospho-PI3K signaling in the NTS of diabetic animals is associated with lower brain insulin. Taken together, these alterations may increase neuronal excitability in the NTS, thereby contributing, at least in part, to the exaggerated EPR response to exercise in this disease. Supported by NIH HL-151632 and NIH HL-151632-01S1. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Circadian changes of autonomic function in patients with zoster-associated pain: A heart rate variability analysis.

To investigate the circadian changes of the autonomic function in patients with zoster-associated pain (ZAP). A total of 37 patients with ZAP from April 2022 to October 2022 were enrolled as the observation group, and 37 normal volunteers at the same time were selected as the control group. All participants were required to wear a 24-h Holter, which was used to compare the heart rate variability (HRV) between the two groups. HRV analysis involved time- and frequency-domain parameters. There was no statistically significant difference in general information between two groups. Patients with ZAP had an increased mean heart rate and decreased the standard deviation of normal-to-normal (SDNN) R-R interval, the root mean square of the differences (RMSSD) in successive RR interval, low frequency (LF), and high frequency (HF) compared with control groups in all periods (p<.05). The ratio of LF/HF between two groups had no significant difference (p=.245). SDNN had no significant difference between day and night in the control group (p>.05), whereas SDNN of ZAP patients in night period was reduced than that in day period (p<.001). The level of RMSSD during the day was lower than those at night in the control group (p<.05), whereas no significant difference of RMSSD between two periods was observed in patients with ZAP (p>.05). The results of this study indicated that ZAP contributes to the decline of autonomic nervous system (ANS) function, especially parasympathetic components. The patients with ZAP lost parasympathetic advantage and had a worse ANS during the night.

Subacute Use of Aqueous Extract of Water Melon (Citrullus lanatus) Seeds Mitigates against Pyramidal Neuronal Toxicity of Lead Acetate in Adult Wistar Rats

Introduction: Lead exposure remains a significant public health burden across the globe, impacting millions of individuals and posing a major threat to nervous system development and function As a reported bio-toxic environmental and industrial pollutant, Lead (Pb) do accumulates in almost all body tissues to cause health complications with the cerebellar region of the central nervous system reported to be more susceptible to cellular distortions. As a flowering plant species of the Cucurbitaceae family, watermelon (Citrullus lanatus) is associated with numerous medicinal properties. Aim: This study aim to investigate the possible neuroprotective potential of aqueous extract of citrulus lanatus seed on lead acetates-induced neurotoxicity in the Cerebral cortex of adult Wistar rats. Place of Study: Department of Anatomy, Faculty of Basic Medical Sciences Olabisi Onabanjo University, Ogun State, Nigeria. Methods: Twenty (20) healthy adult female wistar rats weighing 150±50g were randomly assigned into 4 groups (n=5). The Control group received 2mls/kg of distilled water, Treatment group (T1) was administered 7.5 mg/kg of lead acetate, Treatment group (T2) was administered 200 mg/kg of aqueous extract of citrullus lanatus and Treatment group (T3) was administered 7.5 mg/kg of lead acetate and 200 mg/kg of aqueous extract of citrullus lanatus concomitantly orally for fourteen (14) days. H&amp;E and Cresyl violet histological stains and Biochemical assays for SOD, CAT activities and MDA concentration was determined. Data obtained from the study were analyzed using one-way ANOVA and subjected to Turkeys post hoc test from the multiple comparison. Results: Revealed no statistically significant differences (p&gt;0.05) in body weight and brain weight changes across groups relatives to the control group while SOD and Catalase activities were increased significantly in the Treatment groups compared to control group. Histological findings in control group and T2 showed normal histoarchitectural appearance of cerebral cortex Pyramidal neurons while the lead exposed group (T1) revealed features of neurodegenerative changes evident by nuclear shrinkage with pyknosis and karryorrhexis. while T3 revealed near normal presentations. Conclusion: In summary, Citrullus lanatus mitigates against pyramidal neuronal cells distortions following lead acetate induced toxicity in Wistar Rats and also further affirms its antioxidative potential.

Hypoglycemia as a complication of diabetes mellitus treatment acute eff ect on central nervous system function

Hypoglycemia as a complication of diabetes mellitus treatment acute eff ect on central nervous system function

Effects of Biofeedback Training on HRV, Mood State and Shooting Performance of Shooters

This study examines how biofeedback training affects athletes' HRV, emotional states, and shooting performance. Findings reveal substantial improvements in HRV indices (p &lt; 0.05) and reductions in negative emotions such as tension and anger (p &lt; 0.05). There were increases in vitality and positivity, although changes in fatigue and self-emotional state were not statistically significant (p &gt; 0.05). Shooting performance showed significant enhancement following the training (p &lt; 0.01). These results indicate that biofeedback training positively influences autonomic nervous system function, emotional stability, and shooting performance. By enhancing HRV, improving mood states, biofeedback training markedly improves shooting performance.

Reduced sympathetic activity is associated with the development of pain and muscle atrophy in a female rat model of fibromyalgia

Fibromyalgia (FM) is characterized by chronic widespread musculoskeletal pain accompanied by fatigue and muscle atrophy. Although its etiology is not known, studies have shown that FM patients exhibit altered function of the sympathetic nervous system (SNS), which regulates nociception and muscle plasticity. Nevertheless, the precise SNS-mediated mechanisms governing hyperalgesia and skeletal muscle atrophy in FM remain unclear. Thus, we employed two distinct FM-like pain models, involving intramuscular injections of acidic saline (pH 4.0) or carrageenan in prepubertal female rats, and evaluated the catecholamine content, adrenergic signaling and overall muscle proteolysis. Subsequently, we assessed the contribution of the SNS to the development of hyperalgesia and muscle atrophy in acidic saline-injected rats treated with clenbuterol (a selective β2-adrenergic receptor agonist) and in animals maintained under baseline conditions and subjected to epinephrine depletion through adrenodemedullation (ADM). Seven days after inducing an FM-like model with acidic saline or carrageenan, we observed widespread mechanical hyperalgesia along with loss of strength and/or muscle mass. These changes were associated with reduced catecholamine content, suggesting a common underlying mechanism. Notably, treatment with a β2-agonist alleviated hyperalgesia and prevented muscle atrophy in acidic saline-induced FM-like pain, while epinephrine depletion induced mechanical hyperalgesia and increased muscle proteolysis in animals under baseline conditions. Together, the results suggest that reduced sympathetic activity is involved in the development of pain and muscle atrophy in the murine model of FM analyzed.

Aflatoxin B1 exposure exacerbates chemokine receptor expression in the BTBR T+ Itpr3tf/J Mouse Model, unveiling insights into autism spectrum disorder: A focus on brain and spleen

ObjectiveAutism spectrum disorder (ASD) is a neurodevelopmental condition characterized by significant difficulties in social interaction, communication, and repeated stereotypic behaviour. Aflatoxin B1 (AFB1) is the most potent and well-known mycotoxin in various food sources. Despite its propensity to generate significant biochemical and structural changes in human and animal tissues, the influence of AFB1 on ASD has yet to be thoroughly studied. Mounting evidence indicates that chemokine receptors play a crucial function in the central nervous system and are implicated in developing several neuroinflammatory disorders. Chemokine receptors in individuals with ASD were elevated in the anterior cingulate gyrus astrocytes, cerebellum, and brain. MethodsThe BTBR T+Itpr3tf/J (BTBR) mice are inbred strains that exhibit strong and consistently observed deficits in social interactions, characterized by excessive self-grooming and limited vocalization in social contexts. We examined the impact of AFB1 on CCR3-, CCR7-, CCR9-, CXCR3-, CXCR4-, and CXCR6-expressing I-A/I-E+ cells in the spleen of the BTBR mouse model of autism. We evaluated the mRNA levels of CCR3, CCR7, CCR9, CXCR3, CXCR4, and CXCR6 chemokine receptors in the brain. ResultsThe exposure to AFB1 in BTBR mice resulted in a significant rise in the number of I-A/I-E+CCR3+, I-A/I-E+CCR7+, I-A/I-E+CCR9+, I-A/I-E+CXCR3+, I-A/I-E+CXCR4+, and I-A/I-E+CXCR6+ cells. Furthermore, exposure to AFB1 increased mRNA expression levels of CCR3, CCR7, CCR9, CXCR3, CXCR4, and CXCR6 in the brain. ConclusionsThese findings highlight that AFB1 exposure increases the expression of chemokine receptors in BTBR mice, indicating the necessity for further research into AFB1's role in the development of ASD.