Sensory Neurons Research Articles

"Effect Of Electroacupuncture On Sensory Peripheral Nerve Function In Diabetic Peripheral Neuropathy: A Randomized Controlled Trial Protocol."

Background: Diabetes, a chronic metabolic disorder, affects millions globally, with Type 2 diabetes being the most prevalent. Diabetic Peripheral Neuropathy (DPN) is a common complication, characterized by symptoms such as pain, tingling, and numbness due to peripheral nerve damage. The global burden of diabetes has been rising, particularly in low- and middle-income countries. In India, the number of diabetes cases is projected to reach over 134 million by 2045. Traditional treatments for DPN often have limited efficacy and adverse longterm effects, highlighting the need for alternative therapies. Objective: This study aims to investigate the efficacy of electroacupuncture in improving sensory nerve functions in patients with DPN. Specific acupuncture points will be targeted to assess their impact on vibration perception, hot and cold perception, touch sensitivity, and skin temperature. Methods: A randomized controlled trial will be conducted with 80 participants divided equally into an interventional group and a control group. The interventional group will receive electroacupuncture at specific points (ST44, ST36, ST43, K2, K3, BL60, SP9, and GB41) three times a week for 8 weeks. The control group will continue their usual routine and receive the treatment post-study. Primary outcomes will be measured using the NEURO TOUCH instrument to assess sensory thresholds and skin temperature. Secondary outcomes will include pain assessment using the Visual Analog Scale (VAS). Data will be analyzed using SPSS version 16. Results: The study will evaluate the degree of sensory improvement in peripheral nerves and the effectiveness of electroacupuncture in reducing neuropathic pain. This research seeks to bridge the gap in understanding the mechanisms and efficacy of electroacupuncture in DPN treatment. Conclusion: This study will provide significant insights into the potential benefits of electroacupuncture for DPN, offering an alternative approach to improve the management of this debilitating condition. The findings could inform future clinical practices and guidelines for DPN treatment

Sural sparing reversible sensorimotor abnormalities in hypokalemia: A close mimic of GBS

Nerve conduction studies (NCS) in hypokalemic paralysis usually show decreased compound muscle action potential (CMAP) which improves with correction of hypokalemia and normalizes in between the attacks. Inactivity of Na+ K+ ATPase pump due to hypokalemia results in decreased excitability of muscle fibers resulting in reduced CMAP on NCS. Sensory symptoms, as well as abnormalities in sensory NCS is a rare phenomenon. Here we describe a 40-year-old male who presented with acute onset rapidly progressive ascending quadriparesis with type 2 respiratory failure due to hypokalemia following hepatorenal dysfunction. NCS done before hypokalemia correction, suggested sural sparing with generalized reduced CMAPs, nonrecordable median and ulnar nerves sensory nerve action potential (SNAP) and abnormal F waves. After hypokalemia correction there was improvement in CMAPs as well as SNAPs. Thus, hypokalemia can present as an axonal sensorimotor involvement with sural sparing on NCS study similar to Guillain-Barré syndrome subtype.

The importance of medial plantar nerve conduction study in detectıon of polyneuropathy in inflammatory bowel disease

Background & Objective: Peripheral neuropathy is the most frequent neurologic complication of inflammatory bowel disease (IBD). We aimed to evaluate the clinical utility of medial plantar nerve conduction study (NCS) in the detection of distal sensory polyneuropathy in IBD patients. Methods: The study was performed with 21 Crohn’s disease (Group 1) patients, 24 Ulcerative Colitis (Group 2) patients without clinical peripheral neuropathy and 28 healthy participants (Group 3). Each patient group underwent electrophysiological conduction studies. The findings were analyzed statistically. Results: Abnormal medial plantar nerve conduction was present on both sides in 11 (24.4 %) patients with IBD; 5 (11.1 %) patients had low sural nerve amplitude, and 5 (11.1 %) had low superficial peroneal nerve amplitude bilaterally. There were significant differences between the IBD groups (Group 1 and 2) and Group 3 in the mean sensory nerve action potential amplitude of the right medial plantar nerve (p<0.024), and in the mean sensory nerve action potential amplitude of the left medial plantar nerve (p<0.025). The polyneuropathy pattern was mostly of the sensory axonal type in patients with IBD. Conclusions: These electrophysiologic findings indicate that peripheral neuropathy is more prevalent in IBD. In IBD patients the amplitudes of the medial plantar nerve were abnormal more than in the sural and superficial peroneal nerves.

"Effect Of Electroacupuncture On Sensory Peripheral Nerve Function In Diabetic Peripheral Neuropathy: A Randomized Controlled Trial Protocol."

Background: Diabetes, a chronic metabolic disorder, affects millions globally, with Type 2 diabetes being the most prevalent. Diabetic Peripheral Neuropathy (DPN) is a common complication, characterized by symptoms such as pain, tingling, and numbness due to peripheral nerve damage. The global burden of diabetes has been rising, particularly in low- and middle-income countries. In India, the number of diabetes cases is projected to reach over 134 million by 2045. Traditional treatments for DPN often have limited efficacy and adverse longterm effects, highlighting the need for alternative therapies. Objective: This study aims to investigate the efficacy of electroacupuncture in improving sensory nerve functions in patients with DPN. Specific acupuncture points will be targeted to assess their impact on vibration perception, hot and cold perception, touch sensitivity, and skin temperature. Methods: A randomized controlled trial will be conducted with 80 participants divided equally into an interventional group and a control group. The interventional group will receive electroacupuncture at specific points (ST44, ST36, ST43, K2, K3, BL60, SP9, and GB41) three times a week for 8 weeks. The control group will continue their usual routine and receive the treatment post-study. Primary outcomes will be measured using the NEURO TOUCH instrument to assess sensory thresholds and skin temperature. Secondary outcomes will include pain assessment using the Visual Analog Scale (VAS). Data will be analyzed using SPSS version 16. Results: The study will evaluate the degree of sensory improvement in peripheral nerves and the effectiveness of electroacupuncture in reducing neuropathic pain. This research seeks to bridge the gap in understanding the mechanisms and efficacy of electroacupuncture in DPN treatment. Conclusion: This study will provide significant insights into the potential benefits of electroacupuncture for DPN, offering an alternative approach to improve the management of this debilitating condition. The findings could inform future clinical practices and guidelines for DPN treatment.

The Comparison of 940nm and 810nm Diode Laser Effects on the Repair of Inferior Alveolar Sensory Nerve Injury: A Clinical Trial.

Healing of the inferior alveolar nerve injury during dental procedures is one of the biggest concerns of dentists. There are still debates on different treatment modalities. This study aimed to compare the effect of 940nm and 810nm diode lasers on the repair of the inferior alveolar sensory nerve. In this single-blinded randomized clinical trial, 39 patients with inferior alveolar nerve injury were divided into three groups: 1. 810nm laser irradiated, 2. 940nm laser irradiated, and 3. No laser irradiation (control group). All patients were treated in 12 sessions (3 days per week) and evaluated using a complete clinical neurosensory test (CNT), including brushstroke, 2-point discrimination, pinprick nociception, and thermal discrimination before and after treatment. The mean dysesthesia of the patient treated with 810nm diode laser was significantly lower than the control group in all sessions (the 1st (p= 0.003), 3rd (p= 0.008), 7th (p= 0.006), and 12th sessions (p= 0.005)). The 810nm laser resulted in more satisfaction in patients than the control group in almost all sessions (1st (p< 0.001), 7th (p= 0.028), and 12th (p= 0.006)). More patient satisfaction was seen in the 1st and 3rd sessions in the 810nm laser than in the 980nm laser (p< 0.001 and p= 0.003, respectively). 810nm diode laser can be better than 940nm in repairing inferior alveolar sensory nerve damage.

Innovative noninvasive gait-synchronized vibrotactile feedback system : "I can feel myself walking again"

Despite intensive research and development of systems for restoration of sensory information, these have so far only been the subject of study protocols. Anew noninvasive feedback system translates pressure loads on the forefoot and hindfoot into gait-synchronized vibrotactile stimulation of adefined skin area. To increase the authenticity, this treatment can be supplemented by a surgical procedure. Targeted sensory reinnervation (TSR) describes amicrosurgical procedure in which adefined skin area on the amputated stump of the residual limb is first denervated and then reinnervated by aspecific, transposed sensory nerve harvested from the amputated part of the limb. This creates asensory interface at the residual stump. This article presents the clinical and orthopedic technical treatment pathway with this innovative vibrotactile feedback system and explains in detail the surgical procedure of TSR after amputation of the lower limb.

Structural reorganization of medullary dorsal horn astrocytes in a rat model of neuropathic pain.

Multiple studies have shown that astrocytes in the medullary dorsal horn (MDH) play an important role in the development of pathologic pain. However, little is known about the structural reorganization of the peripheral astrocytic processes (PAP), the main functional part of the astrocyte, in MDH in neuropathic state. For this, we investigated the structural relationship between PAP and their adjacent presynaptic axon terminals and postsynaptic dendrites in the superficial laminae of the MDH using electron microscopical immunohistochemistry for ezrin, a marker for PAP, and quantitative analysis in a rat model of neuropathic pain following chronic constriction injury of the infraorbital nerve (CCI-ION). We found that, compared to controls, in rats with CCI-ION, (1) the number, % area, surface density, and volume fraction of ezrin-positive (+) PAP, as well as the fraction of synaptic edge apposed by ezrin + PAP and the degree of its coverage of presynaptic axon terminals and postsynaptic dendrites increased significantly, (2) these effects were abolished by administration of the mGluR5 antagonist 2-methyl-6-(phenylethynyl) pyridine (MPEP). These findings indicate that PAP undergoes structural reorganization around the central synapses of sensory afferents following nerve injury, suggest that it may be mediated by mGluR5, and may represent the structural basis for enhancing astrocyte-neuron interaction in neuropathic pain.

Investigation of Oxidative Stress Parameters and Pro-Inflammatory Cytokines in a Neuropathy Model Created with Taraxacum Officinale L. Leaf Extract and Cisplatin

The aim of this study was to investigate the effect of Taraxacum officinale leaf extract, a plant known for its potent antioxidant and anti-inflammatory properties, on cisplatin-induced neurotoxicity. Cancer treatment has demonstrated platinum drugs, particularly cisplatin, as among the most effective treatments. However, the drug comes with serious side effects. The use of cisplatin is limited due to its cytotoxic effects, potentially preventing patients from benefiting optimally from anticancer agents. Taraxacum officinale has been used for various diseases for years, observed clinically in conditions such as dyspepsia, liver, gallbladder, and urinary disorders. Nowadays, Taraxacum officinale has entered our lives in various forms as a dietary supplement. However, this plant possesses many bioactivities, particularly potent anti-inflammatory, antioxidant, and hepatoprotective properties.In this study, chronic cisplatin administration was used to induce a peripheral neuropathy model, administered intraperitoneally (i.p) once a week for 5 weeks at a dose of 3 mg/kg. Taraxacum officinale leaf extract was administered intragastrically once daily at a dose of 500mg/kg for the same duration to determine its potential effects on cisplatin neuropathy. After drug administration, motor performance was evaluated using the rotarod test, while sensory transmission status was assessed using tail withdrawal and hot/cold plate tests. Oxidative stress parameters and proinflammatory cytokine markers were analyzed biochemically. In animals exposed to cisplatin, thermal hypoalgesia and cold hypoalgesia were observed (p&amp;lt;0.001), motor coordination balance was prolonged with the rotarod test (p&amp;lt;0.001), and tail withdrawal time was extended (p&amp;lt;0.001). Biochemically, oxidative stress parameters TOS (p&amp;lt;0.05), OSI (p&amp;lt;0.05), and MDA (p&amp;lt;0.05) levels significantly increased compared to the cisplatin control group. TAS levels provided a statistically significant increase compared to the cisplatin-administered group (p&amp;lt;0.05). Proinflammatory cytokine markers TNF-α (p&amp;lt;0.05), IL-6 (p&amp;lt;0.001), and NFKB (p&amp;lt;0.05) levels were found to be higher compared to the cisplatin control group. It was determined that Taraxacum officinale improved these side effects induced by cisplatin both behaviorally and biochemically. In conclusion, Taraxacum officinale leaf extract is a plant with potent antioxidant and anti-inflammatory activity.

Anandamide-Mediated Modulation of Nociceptive Transmission at the Spinal Cord Level.

Three decades ago, the first endocannabinoid, anandamide (AEA), was identified, and its analgesic effect was recognized in humans and preclinical models. However, clinical trial failures pointed out the complexity of the AEA-induced analgesia. The first synapses in the superficial laminae of the spinal cord dorsal horn represent an important modulatory site in nociceptive transmission and subsequent pain perception. The glutamatergic synaptic transmission at these synapses is strongly modulated by two primary AEA-activated receptors, cannabinoid receptor 1 (CB1) and transient receptor potential vanilloid 1 (TRPV1), both highly expressed on the presynaptic side formed by the endings of primary nociceptive neurons. Activation of these receptors can have predominantly inhibitory (CB1) and excitatory (TRPV1) effects that are further modulated under pathological conditions. In addition, dual AEA-mediated signaling and action may occur in primary sensory neurons and dorsal horn synapses. AEA application causes balanced inhibition and excitation of primary afferent synaptic input on superficial dorsal horn neurons in normal conditions, whereas peripheral inflammation promotes AEA-mediated inhibition. This review focuses mainly on the modulation of synaptic transmission at the spinal cord level and signaling in primary nociceptive neurons by AEA via CB1 and TRPV1 receptors. Furthermore, the spinal analgesic effect in preclinical studies and clinical aspects of AEA-mediated analgesia are considered.

Slit3 by PTH-Induced Osteoblast Secretion Repels Sensory Innervation in Spine Porous Endplates to Relieve Low Back Pain.

During aging, the spine undergoes degenerative changes, particularly with vertebral endplate bone expansion and sclerosis, that is associated with nonspecific low back pain (LBP). We reported that parathyroid hormone (PTH) treatment could reduce vertebral endplate sclerosis and improve pain behaviors in aging, SM/J and young lumbar spine instability (LSI) mice. Aberrant innervation noted in the vertebral body and endplate during spinal degeneration was reduced with PTH treatment in aging and LSI mice as quantified by PGP9.5 + and CGRP + nerve fibers, as well as CGRP expression in dorsal root ganglia (DRG). The neuronal repulsion factor Slit3 significantly increased in response to PTH treatment mediated by transcriptional factor FoxA2. PTH type1 receptor (PPR) and Slit3 deletion in osteoblasts prevented PTH-reduction of endplate porosity and improvement in behavior tests, whereas PPR deletion in chondrocytes continued to respond to PTH. Altogether, PTH stimulates Slit3 to repel sensory nerve innervation and provides symptomatic relief of LBP associated with spinal degeneration.

Role of minimal F-wave latency in the electrodiagnosis of polyneuropathy

Background and objective: Polyneuropathy is a debilitating condition that causes damage to more than two peripheral nerves in the body. The objective of this research was to detect the role of minimal F-wave latency as compared with other nerve conduction parameters for the electro-diagnosis of polyneuropathies. Methods: In this descriptive, prospective cross-sectional study, 80 consecutive patients with clinical diagnosis of polyneuropathy (both acute and chronic) between July and December 2023, presenting to the Neurology Department at King Edward Medical University were enrolled. Patients with clinical diagnosis of cervical/lumbar radiculopathies, plexopathies, compressive myelopathy , neuromuscular junction diseases, motor neuron disorders, or localized neuropathies were excluded from this research. NCS and EMG were carried out using conventional procedure. The results were recorded in the predesigned pro forma along with the history and demographic information. Statistical software SPSS 25.0 was used for the analysis of the recorded data. Results: F-wave abnormality was detected in 57 (71.3%) for median nerve, 57 (71.3%) for ulnar nerve, 79 (98.7%) for tibial nerve and in 79 (98.7%) patients for peroneal nerve. Nerve-specific motor nerve conduction study (MNCS) abnormality was found in 47 (58.8%) for median nerve, 43/80 (53.8%) for ulnar nerve, 59 (73.7%) for tibial nerve and in 57(71.3%) patients for peroneal nerve. Nerve-specific sensory nerve conduction study (SNCS) abnormality was present in 43 (53.3%) for median nerve, 43 (53.3%) for ulnar nerve, 50 (62.5%) for sural nerve, and in 49 (61.3%) patients for superficial peroneal nerve. Overall rate of abnormality was 85% for F-wave minimal latencies in comparison with 64% for MNCS and 56% for SNCS. Conclusion: Minimal F-wave latency can be an effective diagnostic parameter for detection of polyneuropathy. This can facilitate in early detection and management of polyneuropathy.

Regulatory mechanisms orchestrating cellular diversity of Cd36+ olfactory sensory neurons revealed by scRNA-seq and scATAC-seq analysis

Recent discoveries have revealed remarkable complexity within olfactory sensory neurons (OSNs), including the existence of two OSN populations based on the expression of Cd36. However, the regulatory mechanisms governing this cellular diversity in the same cell type remain elusive. Here, we show the preferential expression of 79 olfactory receptors in Cd36+ OSNs and the anterior projection characteristics of Cd36+ OSNs, indicating the non-randomness of Cd36 expression. The integrated analysis of single-cell RNA sequencing (scRNA-seq) and scATAC-seq reveals that the differences in Cd36+/- OSNs occur at the immature OSN stage, with Mef2a and Hdac9 being important regulators of developmental divergence. We hypothesize that the absence of Hdac9 may affect the activation of Mef2a, leading to the up-regulation of Mef2a target genes, including teashirt zinc finger family member 1 (Tshz1), in the Cd36+ OSN lineage. We validate that Tshz1 directly promotes Cd36 expression through enhancer bindings. Our study unravels the intricate regulatory landscape and principles governing cellular diversity in the olfactory system.

Assessing the visual afferent pathway with the multifocal visual evoked potentials in the radiologically isolated syndrome

The early identification of individuals with radiologically isolated syndrome (RIS) who are at an elevated risk of progressing to multiple sclerosis (MS) is essential for making informed treatment decisions. This study aimed to evaluate the predictive potential of multifocal Visual Evoked Potentials (mfVEP) measures in individuals with RIS with respect to their conversion to MS. A prospective observational cohort study was conducted, involving 21 individuals with RIS recruited from a MS center. Baseline assessments, including mfVEP, magnetic resonance imaging (MRI), and clinical examinations, were performed, and participants were longitudinally followed for up to 24 months. The primary outcome measures were the conversion to MS. Over a clinical follow-up period of 24 months, five individuals (5/21) with RIS progressed to MS. MfVEP amplitude responses (interocular and monocular probability analysis) demonstrated abnormal cluster visual field defects in 47.6% of RIS eyes at baseline, whereas multifocal VEP latency analysis showed significant delays in 38.4%. A reduction in interocular amplitude [OR = 0.036, (95% CI 0.003–0.503); P = 0.014], monocular amplitude [OR = 0.083, (95% CI 0.007–0.982); P = 0.048], and a prolonged interocular latency [OR = 0.095, (95% CI 0.009–0.972); P = 0.047] were associated with a higher relative risk of clinical conversion at the 2-year follow-up. Multifocal VEP may serve as a novel and independent risk factor for predicting the conversion to MS in individuals with Radiologically Isolated Syndrome.

Damage-induced basal epithelial cell migration modulates the spatial organization of redox signaling and sensory neuron regeneration.

Epithelial damage leads to early reactive oxygen species (ROS) signaling, which regulates sensory neuron regeneration and tissue repair. How the initial type of tissue injury influences early damage signaling and regenerative growth of sensory axons remains unclear. Previously we reported that thermal injury triggers distinct early tissue responses in larval zebrafish. Here, we found that thermal but not mechanical injury impairs sensory axon regeneration and function. Real-time imaging revealed an immediate tissue response to thermal injury characterized by the rapid Arp2/3-dependent migration of keratinocytes, which was associated with tissue scale ROS production and sustained sensory axon damage. Isotonic treatment was sufficient to limit keratinocyte movement, spatially restrict ROS production, and rescue sensory neuron function. These results suggest that early keratinocyte dynamics regulate the spatial and temporal pattern of long-term signaling in the wound microenvironment during tissue repair.

Myeloid Cells and Sensory Nerves Mediate Peritendinous Adhesion Formation via Prostaglandin E2.

Peritendinous adhesion that forms after tendon injury substantially limits daily life. The pathology of adhesion involves inflammation and the associated proliferation. However, the current studies on this condition are lacking, previous studies reveal that cyclooxygenase-2 (COX2) gene inhibitors have anti-adhesion effects through reducing prostaglandin E2 (PGE2) and the proliferation of fibroblasts, are contrary to the failure in anti-adhesion through deletion of EP4 (prostaglandin E receptor 4) gene in fibroblasts in mice of another study. In this study, single-cell RNA sequencing analysis of human and mouse specimens are combined with eight types of conditional knockout mice and further reveal that deletion of COX2 in myeloid cells and deletion of EP4 gene in sensory nerves decrease adhesion and impair the biomechanical properties of repaired tendons. Furthermore, the COX2 inhibitor parecoxib reduces PGE2 but impairs the biomechanical properties of repaired tendons. Interestingly, PGE2 local treatment improves the biomechanical properties of the repaired tendons. These findings clarify the complex role of PGE2 in peritendinous adhesion formation (PAF) and tendon repair.

Damage-induced basal epithelial cell migration modulates the spatial organization of redox signaling and sensory neuron regeneration

Damage-induced basal epithelial cell migration modulates the spatial organization of redox signaling and sensory neuron regeneration

Sensory nerves drive migration of dental pulp stem cells via the CGRP-Ramp1 axis in pulp repair

Dental pulp stem cells (DPSCs) are responsible for maintaining pulp structure and function after pulp injury. DPSCs migrate directionally to the injury site before differentiating into odontoblast-like cells, which is a prerequisite and a determinant in pulp repair. Increasing evidence suggests that sensory neuron-stem cell crosstalk is critical for maintaining normal physiological functions, and sensory nerves influence stem cells mainly by neuropeptides. However, the role of sensory nerves on DPSC behaviors after pulp injury is largely unexplored. Here, we find that sensory nerves released significant amounts of calcitonin gene-related peptide (CGRP) near the injury site, acting directly on DPSCs via receptor activity modifying protein 1 (RAMP1) to promote collective migration of DPSCs to the injury site, and ultimately promoting pulp repair. Specifically, sensory denervation leads to poor pulp repair and ectopic mineralization, in parallel with that DPSCs failed to be recruited to the injury site. Furthermore, in vitro evidence shows that sensory nerve-deficient microenvironment suppressed DPSC migration prominently among all related behaviors. Mechanistically, the CGRP-Ramp1 axis between sensory neurons and DPSCs was screened by single-cell RNA-seq analysis and immunohistochemical studies confirmed that the expression of CGRP rather than Ramp1 increases substantially near the damaged site. We further demonstrated that CGRP released by sensory nerves binds the receptor Ramp1 on DPSCs to facilitate cell collective migration by an indirect co-culture system using conditioned medium from trigeminal neurons, CGRP recombinant protein and antagonists BIBN4096. The treatment with exogenous CGRP promoted the recruitment of DPSCs, and ultimately enhanced the quality of pulp repair. Targeting the sensory nerve could therefore provide a new strategy for stem cell-based pulp repair and regeneration.

Swimming training prevents obesity installation and normalizes hypothalamic expressions of GLP1 and leptin receptors in adult offspring born in small litters.

Glucagon-like peptide-1 (GLP1) and leptin (Lep) are afferent signals that regulate energy metabolism. Lactational hypernutrition results in hyperphagia and adiposity in adult life, and these events can be prevented by exercise. We evaluated the effects of swimming training on hypothalamic (GLP1-R) and Lep receptor (Lep-R) gene expressions in lactational hypernutrition-induced obesity. On the 3rd postnatal day, the litter sizes of lactating dams were adjusted to small litters (SL; 3 pups/dams) or normal litters (NL; 9 pups/dams). After weaning (21 days), NL and SL male rats were randomly distributed to sedentary (Sed) and exercised (Exe) groups. Exercised mice swam (30 min/3 times/week) for 68 days. Food intake and body weight gain were registered. At 92 days, intraperitoneal glucose and insulin tolerance tests were performed and rats were euthanized at 93 days; adipose tissue depots were weighed, and blood counts and plasma biochemical analyses performed. Hypothalamus were isolated to evaluate Lep-R and GLP1-R gene expressions. Small litters sedentary rats presented increased body weight gain, adiposity, insulin sensibility and higher fasting values of glucose and triglycerides, besides higher hypothalamic gene expressions of Lep-R and GLP1-R, compared to NLSed animals. SLExe rats did not develop obesity or metabolic abnormalities and Lep-R and GLP1-R hypothalamic gene expressions were normalized. Lactational hypernutrition induces obesity and metabolic dysfunction in adult life, in association with higher hypothalamic expressions of the Lep-R and GLP1-R genes. Exercise prevented obesity and improved metabolic state in SL overnourished rats, and normalized their hypothalamic Lep-R and GLP1-R gene expressions.

Physiological effects of field concentrations and sublethal concentrations of sulfoxaflor on Apis mellifera.

Bees (Apis mellifera), as important pollinators of agricultural crops, are at risk when pesticides are used. Sulfoxaflor is a new insecticide which acts on the nicotinic acetylcholine receptor (nAChR) in a similar way to neonicotinoids. The goal of this study is to evaluate the toxicity of sulfoxaflor and its effect on the A. mellifera exposure. Initially, developmental indicators such as larval survival, pupation, and eclosion were inhibited by 5.0 mg/L (field concentration) sulfoxaflor. In the pupal stage, fat content was significantly increased, while the glycogen content decreased. In addition, A. mellifera heads were treated with 2.0 mg/L (sublethal concentration) of sulfoxaflor and analyzed by RNA sequencing. The transcriptome results indicated that 2.0 mg/L amounts of sulfoxaflor have adverse effects on the immune, digestive, and nervous systems. Sulfoxaflor down-regulated the expression of many genes involved in immunity, detoxification, the myosin cytoskeleton, sensory neurons, and odor-binding proteins. Field concentration and sublethal concentration were used for the combined analysis of honeybees. The effect of sublethal concentration of sulfoxaflor on honeybees was studied for the first time from the perspective of transcriptome sequencing of honeybee head. A preliminary study was carried out on the stress of sulfoxaflor at sublethal concentration on honeybee workers, which has certain research significance and can provide theoretical basis for the use of sulfoxaflor in the field environment. © 2024 Society of Chemical Industry.

Simultaneous recordings from vestibular Type I hair cells and their calyceal afferents in mice.

The vestibular hair cell receptors of anamniotes, designated Type II, are presynaptic to bouton endings of vestibular nerve distal neurites. An additional flask-shaped hair cell receptor, Type I, is present in amniotes, and communicates with a chalice-shaped afferent neuritic ending that surrounds the entire hair cell except its apical neck. Since the full repertoire of afferent fiber dynamics and sensitivities observed throughout the vertebrate phyla can be accomplished through Type II hair cell-bouton synapses, the functional contribution(s) of Type I hair cells and their calyces to vestibular performance remains a topic of great interest. The goal of the present study was to investigate electrical coupling between the Type I hair cell and its enveloping calyx in the mouse semicircular canal crista ampullaris. Since there are no gap junctions between these two cells, evidence for electrical communication would necessarily involve other mechanisms. Simultaneous recordings from the two cells of the synaptic pair were used initially to verify the presence of orthodromic quantal synaptic transmission from the hair cell to the calyx, and then to demonstrate bi-directional communication due to the slow accumulation of potassium ions in the synaptic cleft. As a result of this potassium ion accretion, the equilibrium potentials of hair cell conductances facing the synaptic cleft become depolarized to an extent that is adequate for calcium influx into the hair cell, and the calyx inner face becomes depolarized to a level that is near the threshold for spike initiation. Following this, paired recordings were again employed to characterize fast bi-directional electrical coupling between the two cells. In this form of signaling, cleft-facing conductances in both the hair cell and calyx increase, which strengthens their coupling. Because this mechanism relies on the cleft resistance, we refer to it as resistive coupling. We conclude that the same three forms of hair cell-calyceal transmission previously demonstrated in the turtle are present in the mammalian periphery, providing a biophysical basis for the exceptional temporal fidelity of the vestibular system.