Changes in phrenic nerve compound muscle action potential in streptozotocin-induced diabetic rats

Ferrari, Marcelo C; Peixoto, João Victor Capelli; Fogaça, Rosalvo Hochmueller; Dias, Fernando Augusto Lavezzo

doi:10.1016/j.resp.2022.103923

Cited by 3 publications

(5 citation statements)

References 13 publications

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“…It has been reported that diabetic neuropathy has a relationship with axonal changes manifested in a decrease of peripheral nerve conduction velocity, which affects the F-wave presence and lengthens its latency, which explains, in part the demyelination and axonal damage of the phrenic nerve in diabetic rats [29,35]. Furthermore, it is possible that the affectation of NMJ is related to the time of diabetes evolution and hyperglycemia [36].…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, it is possible that the affectation of NMJ is related to the time of diabetes evolution and hyperglycemia [36]. However, to date, there exist scarce studies that examine the functional and morphological in NMJ [35]. One of the reports suggests that diabetes could affect the phrenic nerve, causing respiratory complications [37].…”

Section: Discussionmentioning

confidence: 99%

“…One of the reports suggests that diabetes could affect the phrenic nerve, causing respiratory complications [37]. In addition, a significative reduction in the transversal surface of the phrenic nerve has been observed in diabetic animal models [35,38], and a diaphragm with lipid accumulation in the red fibers associated with partial atrophy of the white fibers but no evaluation of the diaphragmatic function was performed before animal euthanasia [38]. The physiological implication in the animal is not well understood, which is a focus line for future studies.…”

Section: Discussionmentioning

confidence: 99%

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Increased Frequency of Giant Miniature End-Plate Potentials at the Neuromuscular Junction in Diabetic Rats

Martínez-Sánchez,

Cárdenas,

Trujillo

et al. 2023

Biomedicines

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There is a need for research addressing the functional characteristics of the motor end-plate in diabetes to identify mechanisms contributing to neuromuscular dysfunction. Here, we investigated the effect of diabetes on spontaneous acetylcholine release in the rat neuromuscular junction. We studied two randomized groups of male Wistar rats (n = 7 per group, 350 ± 50 g, 12–16 weeks of age): one with streptozotocin-induced experimental diabetes, and a healthy control group without diabetes. After 8 weeks of monitoring after diabetes induction, rats in both groups were anesthetized with pentobarbital. Then, the diaphragm muscle was dissected for electrophysiological recordings of miniature end-plate potentials (MEPPs) using a single electrode located at the region of the muscle end-plate. All experiments were conducted at environmental temperature (20–22 °C) in rat Ringer solution with constant bubbling carbogen (95% O2, 5% CO2). Compared to healthy controls, in the diaphragm neuromuscular end-plate derived from diabetic rats, the MEPPs were higher in amplitude and frequency, and the proportion of giant MEPPs was elevated (7.09% vs. 1.4% in controls). Our results showed that diabetes affected the acetylcholine MEPP pattern and increased the number of giant potentials compared to healthy controls.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Increased Frequency of Giant Miniature End-Plate Potentials at the Neuromuscular Junction in Diabetic Rats

Martínez-Sánchez,

Cárdenas,

Trujillo

et al. 2023

Biomedicines

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“…We suggest that the effect of LKB1 in delaying muscle atrophy may be achieved by CRMP1 stimulation to regenerate and repair the injured sciatic nerve. The electrophysiological properties of nerve are closely related to the function of nerve, including NCV (Limbu et al., 2022), action potential latency, and CMAP (Ferrari et al., 2022). NCV can directly reflect the number, lamellar structure, and thickness of the regenerated myelin sheath.…”

Section: Discussionmentioning

confidence: 99%

LKB1 and CRMP1 cooperatively promote the repair of the sciatic nerve injury

Liu,

2023

Developmental Neurobiology

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After peripheral nervous system injury, Schwann cells (SCs) can repair axons by providing a growth‐promoting microenvironment. The aim of this study is to explore the effects and mechanisms of LKB1 and CRMP1 on the repair of sciatic nerve injury (SNI). The expressions of LKB1 and CRMP1 were changed in rats with SNI from 12 h to 4 weeks by hematoxylin–eosin staining, RT‐PCR assay, immunohistochemical staining, and western blotting. Immunofluorescence results show that LKB1 and CRMP1 are co‐localized in the regenerated axons of the sciatic nerve tissue of SNI rats. Co‐immunoprecipitation indicates that LKB1 interacts with CRMP1. LKB1 interference suppresses the phosphorylation level of CRMP1. Overexpression of LKB1 and CRMP1 promotes the invasion and migration of SCs, and nerve cell protuberance extends. The structure of the myelin sheath in the sciatic nerve of the model group was found to be loose and disordered. Rats in the model group had higher pain thresholds and heat sensitivity response times than those in the control group. Nerve conduction velocity, the latency of action potential, and the peak value of compound muscle action potential in the SNI group were significantly lower than those in the control group, and the muscle atrophy was severe. Overexpression of LKB1 may significantly improve the above conditions. However, the function of LKB1 to improve SNI is abolished by the interference of CRMP1. In summary, the interaction between LKB1 and CRMP promotes the migration and differentiation of SCs and the extension of neurons, thereby improving the repair of nerve injury.

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“…One of the most probable causes of diaphragmatic atrophy is a systemic alteration of the reninangiotensin system [18]. The diaphragm can suffer lesions due to paralysis of the phrenic nerve due to surgery, interscalene blocks, direct trauma to the chest, the presence of tumor masses, or systemic pathologies that damage the integrity of the nerve [19][20][21][22][23]. Despite these traumatic circumstances, the patient or clinician is not always aware of the existence of a lesion to the phrenic nerve, with paralysis of one side of the diaphragm (rarely bilaterally), whose symptoms are not immediately related to dysfunctional breathing [24].…”

Section: Introductionmentioning

confidence: 99%

Symptoms Arising From the Diaphragm Muscle: Function and Dysfunction

Bordoni,

Kotha,

Escher

2024

Cureus

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There can be many reasons that damage the function of the diaphragm, either transiently or permanently, involving one hemilate or both muscle portions. The diaphragm is associated only with breathing, but many other functions are related to it. The patient is not always aware of the presence of diaphragmatic dysfunction, and it is not always immediate to identify non-respiratory diaphragmatic symptoms. Pseudoanginal pain, night sweats, difficulty memorizing, or muscular and visceral problems of the pelvic floor are just some of the disorders linked to reduced diaphragmatic contractility. A decline in respiratory contractile force can be the basis for further pathological conditions that can increase the rate of mortality and morbidity. The article reviews the possible symptoms that may be presented by the patient, which are not necessarily related to lung function.

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Changes in phrenic nerve compound muscle action potential in streptozotocin-induced diabetic rats

Cited by 3 publications

References 13 publications

Increased Frequency of Giant Miniature End-Plate Potentials at the Neuromuscular Junction in Diabetic Rats

Increased Frequency of Giant Miniature End-Plate Potentials at the Neuromuscular Junction in Diabetic Rats

LKB1 and CRMP1 cooperatively promote the repair of the sciatic nerve injury

Symptoms Arising From the Diaphragm Muscle: Function and Dysfunction

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