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Frontiers in Neurology 2023The male reproductive functions are largely regulated by the autonomic nervous system. Male sexual behavior and fertility primarily depend on the normal function of the... (Review)
Review
The male reproductive functions are largely regulated by the autonomic nervous system. Male sexual behavior and fertility primarily depend on the normal function of the higher neural centers related to the autonomic nervous system, the hypothalamic-pituitary-gonadal axis, the autonomic nervous components within the spinal cord and spinal nerves, and certain somatic nerves in the pelvic floor. In this review article, we will summarize the role of the autonomic nervous system in regulating male reproductive capabilities and fertility, its impact on male infertility under abnormal conditions, including the role of drug-induced autonomic nervous dysfunctions on male infertility. The main purpose of this article was to provide an overview of the effects of autonomic nervous dysfunction on male reproductive function and shed light on the potential therapeutic target for male infertility.
PubMed: 38125834
DOI: 10.3389/fneur.2023.1277795 -
Journal of Translational Medicine Aug 2023Brachial plexus root avulsion (BPRA), a disabling peripheral nerve injury, induces substantial motoneuron death, motor axon degeneration and denervation of biceps...
BACKGROUND
Brachial plexus root avulsion (BPRA), a disabling peripheral nerve injury, induces substantial motoneuron death, motor axon degeneration and denervation of biceps muscles, leading to the loss of upper limb motor function. Acetylglutamine (N-acetyl-L-glutamine, NAG) has been proven to exert neuroprotective and anti-inflammatory effects on various disorders of the nervous system. Thus, the present study mainly focused on the influence of NAG on motor and sensory recovery after BPRA in rats and the underlying mechanisms.
METHODS
Male adult Sprague Dawley (SD) rats were subjected to BPRA and reimplantation surgery and subsequently treated with NAG or saline. Behavioral tests were conducted to evaluate motor function recovery and the mechanical pain threshold of the affected forelimb. The morphological appearance of the spinal cord, musculocutaneous nerve, and biceps brachii was assessed by histological staining. Quantitative real-time PCR (qRT‒PCR) was used to measure the mRNA levels of remyelination and regeneration indicators in myocutaneous nerves. The protein levels of inflammatory and pyroptotic indicators in the spinal cord anterior horn were measured using Western blotting.
RESULTS
NAG significantly accelerated the recovery of motor function in the injured forelimbs, enhanced motoneuronal survival in the anterior horn of the spinal cord, inhibited the expression of proinflammatory cytokines and pyroptosis pathway factors, facilitated axonal remyelination in the myocutaneous nerve and alleviated atrophy of the biceps brachii. Additionally, NAG attenuated neuropathic pain following BPRA.
CONCLUSION
NAG promotes functional motor recovery and alleviates neuropathic pain by enhancing motoneuronal survival and axonal remyelination and inhibiting the pyroptosis pathway after BPRA in rats, laying the foundation for the use of NAG as a novel treatment for BPRA.
Topics: Male; Rats; Animals; Rats, Sprague-Dawley; Neuralgia; Spinal Cord; Atrophy; Brachial Plexus
PubMed: 37612586
DOI: 10.1186/s12967-023-04399-7 -
Journal of Translational Medicine Aug 2023Peripheral nerve injury can cause neuroinflammation and neuromodulation that lead to mitochondrial dysfunction and neuronal apoptosis in the dorsal root ganglion (DRG)...
BACKGROUND
Peripheral nerve injury can cause neuroinflammation and neuromodulation that lead to mitochondrial dysfunction and neuronal apoptosis in the dorsal root ganglion (DRG) and spinal cord, contributing to neuropathic pain and motor dysfunction. Hyperbaric oxygen therapy (HBOT) has been suggested as a potential therapeutic tool for neuropathic pain and nerve injury. However, the specific cellular and molecular mechanism by which HBOT modulates the development of neuropathic pain and motor dysfunction through mitochondrial protection is still unclear.
METHODS
Mechanical and thermal allodynia and motor function were measured in rats following sciatic nerve crush (SNC). The HBO treatment (2.5 ATA) was performed 4 h after SNC and twice daily (12 h intervals) for seven consecutive days. To assess mitochondrial function in the spinal cord (L2-L6), high-resolution respirometry was measured on day 7 using the OROBOROS-O2k. In addition, RT-PCR and Immunohistochemistry were performed at the end of the experiment to assess neuroinflammation, neuromodulation, and apoptosis in the DRG (L3-L6) and spinal cord (L2-L6).
RESULTS
HBOT during the early phase of the SNC alleviates mechanical and thermal hypersensitivity and motor dysfunction. Moreover, HBOT modulates neuroinflammation, neuromodulation, mitochondrial stress, and apoptosis in the DRG and spinal cord. Thus, we found a significant reduction in the presence of macrophages/microglia and MMP-9 expression, as well as the transcription of pro-inflammatory cytokines (TNFa, IL-6, IL-1b) in the DRG and (IL6) in the spinal cord of the SNC group that was treated with HBOT compared to the untreated group. Notable, the overexpression of the TRPV1 channel, which has a high Ca permeability, was reduced along with the apoptosis marker (cleaved-Caspase3) and mitochondrial stress marker (TSPO) in the DRG and spinal cord of the HBOT group. Additionally, HBOT prevents the reduction in mitochondrial respiration, including non-phosphorylation state, ATP-linked respiration, and maximal mitochondrial respiration in the spinal cord after SNC.
CONCLUSION
Mitochondrial dysfunction in peripheral neuropathic pain was found to be mediated by neuroinflammation and neuromodulation. Strikingly, our findings indicate that HBOT during the critical period of the nerve injury modulates the transition from acute to chronic pain via reducing neuroinflammation and protecting mitochondrial function, consequently preventing neuronal apoptosis in the DRG and spinal cord.
Topics: Rats; Animals; Peripheral Nerve Injuries; Rats, Sprague-Dawley; Neuroinflammatory Diseases; Neuralgia; Hyperalgesia; Sciatic Nerve; Spinal Cord; Mitochondria
PubMed: 37582750
DOI: 10.1186/s12967-023-04414-x -
Current Pain and Headache Reports Mar 2024Intervertebral disc degeneration is the primary etiology of low back pain and radicular pain. This review examines the roles of crucial chemokines in different stages of... (Review)
Review
PURPOSE OF REVIEW
Intervertebral disc degeneration is the primary etiology of low back pain and radicular pain. This review examines the roles of crucial chemokines in different stages of degenerative disc disease, along with interventions targeting chemokine function to mitigate disc degeneration.
RECENT FINDINGS
The release of chemokines from degenerated discs facilitates the infiltration and activation of immune cells, thereby intensifying the inflammatory cascade response. The migration of immune cells into the venous lumen is concomitant with the emergence of microvascular tissue and nerve fibers. Furthermore, the presence of neurogenic factors secreted by disc cells and immune cells stimulates the activation of pain-related cation channels in the dorsal root ganglion, potentially exacerbating discogenic and neurogenic pain and intensifying the degenerative cascade response mediated by chemokines. Gaining a deeper comprehension of the functions of chemokines and immune cells in these processes involving catabolism, angiogenesis, and injury detection could offer novel therapeutic avenues for managing symptomatic disc disease.
Topics: Humans; Intervertebral Disc Degeneration; Intervertebral Disc; Low Back Pain; Chemokines; Ganglia, Spinal
PubMed: 37976014
DOI: 10.1007/s11916-023-01188-1 -
Seminars in Pediatric Surgery Feb 2024Diaphragm pacing is a ventilation strategy in respiratory failure. Most of the literature on pacing involves adults with common indications being spinal cord injury and... (Review)
Review
Diaphragm pacing is a ventilation strategy in respiratory failure. Most of the literature on pacing involves adults with common indications being spinal cord injury and amyotrophic lateral sclerosis (ALS). Previous reports in pediatric patients consist of case reports or small series; most describe direct phrenic nerve stimulation for central hypoventilation syndrome. This differs from adult reports that focus most commonly on spinal cord injuries and the rehabilitative nature of diaphragm pacing. This review describes the current state of diaphragm pacing in pediatric patients. Indications, current available technologies, surgical techniques, advantages, and pitfalls/problems are discussed.
Topics: Child; Humans; Amyotrophic Lateral Sclerosis; Diaphragm; Phrenic Nerve; Respiratory Insufficiency
PubMed: 38245992
DOI: 10.1016/j.sempedsurg.2024.151386 -
Cell Reports Sep 2023Primary somatosensory axons stop regenerating as they re-enter the spinal cord, resulting in incurable sensory loss. What arrests them has remained unclear. We...
Primary somatosensory axons stop regenerating as they re-enter the spinal cord, resulting in incurable sensory loss. What arrests them has remained unclear. We previously showed that axons stop by forming synaptic contacts with unknown non-neuronal cells. Here, we identified these cells in adult mice as oligodendrocyte precursor cells (OPCs). We also found that only a few axons stop regenerating by forming dystrophic endings, exclusively at the CNS:peripheral nervous system (PNS) borderline where OPCs are absent. Most axons stop in contact with a dense network of OPC processes. Live imaging, immuno-electron microscopy (immuno-EM), and OPC-dorsal root ganglia (DRG) co-culture additionally suggest that axons are rapidly immobilized by forming synapses with OPCs. Genetic OPC ablation enables many axons to continue regenerating deep into the spinal cord. We propose that sensory axons stop regenerating by encountering OPCs that induce presynaptic differentiation. Our findings identify OPCs as a major regenerative barrier that prevents intraspinal restoration of sensory circuits following spinal root injury.
Topics: Mice; Animals; Oligodendrocyte Precursor Cells; Spinal Cord; Axons; Spinal Nerve Roots; Ganglia, Spinal; Nerve Regeneration
PubMed: 37656624
DOI: 10.1016/j.celrep.2023.113068 -
The Journal of Hand Surgery, European... Jun 2024Distal nerve transfer is a refined surgical technique involving the redirection of healthy sacrificable nerves from one part of the body to reinstate function in another... (Review)
Review
Distal nerve transfer is a refined surgical technique involving the redirection of healthy sacrificable nerves from one part of the body to reinstate function in another area afflicted by paralysis or injury. This approach is particularly valuable when the original nerves are extensively damaged and standard repair methods, such as direct suturing or grafting, may be insufficient. As the nerve coaptation is close to the recipient muscles or skin, distal nerve transfers reduce the time to reinnervation. The harvesting of nerves for transfer should usually result in minimal or no donor morbidity, as any anticipated loss of function is compensated for by adjacent muscles or overlapping cutaneous territory. Recent years have witnessed notable progress in nerve transfer procedures, markedly enhancing the outcomes of upper limb reconstruction for conditions encompassing peripheral nerve, brachial plexus and spinal cord injuries.
Topics: Humans; Nerve Transfer; Peripheral Nerve Injuries; Brachial Plexus; Upper Extremity
PubMed: 38296247
DOI: 10.1177/17531934231226169