oxytocin and Peripheral-Nerve-Injuries

Oxytocin reduces primary sensory afferent excitability and produces analgesia in part through a peripheral mechanism, yet its actions on physiologically characterized, mechanically sensitive afferents in normal and neuropathic conditions are unknown. We recorded intracellularly from L4 dorsal root ganglion neurons characterized as low-threshold mechanoreceptors (LTMRs) or high-threshold mechanoreceptors (HTMRs) in female rats 1 week after L5 partial spinal nerve injury or sham control (n = 24 rats/group) before, during, and after ganglionic perfusion with oxytocin, 1 nM. Nerve injury desensitized and hyperpolarized LTMRs (membrane potential [Em] was -63 ± 1.8 mV in sham vs -76 ± 1.4 mV in nerve injury; P < 0.001), and sensitized HTMRs without affecting Em. In nerve-injured rats, oxytocin depolarized LTMRs towards normal (Em = -69 ± 1.9 mV) and, in 6 of 21 neurons, resulted in spontaneous action potentials. By contrast, oxytocin hyperpolarized HTMRs (Em = -68 ± 2.7 mV before vs -80 ± 3.2 mV during oxytocin exposure; P < 0.01). These effects were reversed after removal of oxytocin, and oxytocin had minimal effects in neurons from sham surgery animals. Sensory afferent neurons immunopositive for the vasopressin 1a receptor were larger (34 ± 6.3 μm, range 16-57 μm) than immunonegative neurons (26 ± 3.4 μm, range 15-43 μm; P < 0.005). These data replicate findings that neuropathic injury desensitizes LTMRs while sensitizing HTMRs and show rapid and divergent oxytocin effects on these afferent subtypes towards normal, potentially rebalancing input to the central nervous system. Vasopressin 1a receptors are present on medium to large diameter afferent neurons and could represent oxytocin's target.

Topics: Action Potentials; Afferent Pathways; Animals; Disease Models, Animal; Electric Stimulation; Female; Ganglia, Spinal; Mechanoreceptors; Nociceptors; Oxytocin; Pain Threshold; Peripheral Nerve Injuries; Rats; Rats, Sprague-Dawley; Receptors, Vasopressin; Sensory Receptor Cells; Touch

To provide evidence-based guidelines for safe and effective assisted vaginal birth.. Prerequisites, indications, contraindications, along with maternal and neonatal morbidity associated with assisted vaginal birth.. Medline database was searched for articles published from January 1, 1985, to February 28, 2018 using the key words "assisted vaginal birth," "instrumental vaginal birth," "operative vaginal delivery," "forceps delivery," "vacuum delivery," "ventouse delivery." The quality of evidence is described using the Evaluation of Evidence criteria outlined in the Report of the Canadian Task Force on Preventive Health Care.. These guidelines were approved by the Clinical Practice Obstetrics Committee and the Board of the Society of Obstetricians and Gynaecologists of Canada.

Topics: Analgesia, Epidural; Birth Injuries; Brachial Plexus; Canada; Cardiotocography; Clinical Competence; Episiotomy; Extraction, Obstetrical; Facial Injuries; Female; Humans; Labor Presentation; Labor Stage, Second; Lacerations; Obstetrical Forceps; Oxytocics; Oxytocin; Peripheral Nerve Injuries; Pregnancy; Puerperal Disorders; Scalp; Shoulder Dystocia; Soft Tissue Injuries; Stress Disorders, Post-Traumatic; Time Factors; Vacuum Extraction, Obstetrical; Version, Fetal

Growth factors such as nerve growth factor (NGF) and insulin-like growth factor-1 (IGF-1) have been shown to play a role in the healing process of nerve injury. Recent researches have also shown that oxytocin administration activates these growth factors of importance for the healing of nerve tissue. The objective of the present study was to evaluate the effects of oxytocin on peripheral nerve regeneration in rats.. Twenty-four male Sprague-Dawley rats were underwent transection damage model on the right sciatic nerve and defective damage model on the left sciatic nerve. The animals were assigned to one of two groups: control group or treatment group (received 80 mg/kg oxytocin intraperitoneally for 12 weeks). The sciatic nerve was examined, both functionally (on the basis of climbing platform test) and histologically (on the basis of axon count), 3, 6, 9, and 12 weeks after the injury. Also, stereomicroscopic and electrophysiological evaluations were carried out.. Significantly greater improvements in electrophysiological recordings and improved functional outcome measures were presented in the treatment group at 12-week follow-up. Stereomicroscopic examinations disclosed prominent increases in vascularization on proximal cut edges in the oxytocin group in comparison with the control group. Higher axon counts were also found in this group.. Intraperitoneal oxytocin administration resulted in accelerated functional, histological, and electrophysiological recovery after different sciatic injury models in rats.

Topics: Animals; Axons; Disease Models, Animal; Drug Evaluation, Preclinical; Electromyography; Male; Nerve Regeneration; Oxytocin; Peripheral Nerve Injuries; Rats, Sprague-Dawley; Recovery of Function; Sciatic Nerve

Topics: Animals; Delivery, Obstetric; Female; Humans; Hypersensitivity; Oxytocics; Oxytocin; Pain; Parturition; Peripheral Nerve Injuries

Physical injury, including surgery, can result in chronic pain; yet chronic pain following childbirth, including cesarean delivery in women, is rare. The mechanisms involved in this protection by pregnancy or delivery have not been explored.. We examined the effect of pregnancy and delivery on hypersensitivity to mechanical stimuli of the rat hindpaw induced by peripheral nerve injury (spinal nerve ligation) and after intrathecal oxytocin, atosiban, and naloxone. Additionally, oxytocin concentration in lumbar spinal cerebrospinal fluid was determined.. Spinal nerve ligation performed at mid-pregnancy resulted in similar hypersensitivity to nonpregnant controls, but hypersensitivity partially resolved beginning after delivery. Removal of pups after delivery prevented this partial resolution. Cerebrospinal fluid concentrations of oxytocin were greater in normal postpartum rats prior to weaning. To examine the effect of injury at the time of delivery rather than during pregnancy, spinal nerve ligation was performed within 24 h of delivery. This resulted in acute hypersensitivity that partially resolved over the next 2-3 weeks. Weaning of pups resulted only in a temporary return of hypersensitivity. Intrathecal oxytocin effectively reversed the hypersensitivity following separation of the pups. Postpartum resolution of hypersensitivity was transiently abolished by intrathecal injection of the oxytocin receptor antagonist, atosiban.. These results suggest that the postpartum period rather than pregnancy protects against chronic hypersensitivity from peripheral nerve injury and that this protection may reflect sustained oxytocin signaling in the central nervous system during this period.

Topics: Animals; Behavior, Animal; Disease Models, Animal; Female; Hormone Antagonists; Hypersensitivity; Injections, Spinal; Naloxone; Narcotic Antagonists; Oxytocics; Oxytocin; Peripheral Nerve Injuries; Physical Stimulation; Postpartum Period; Rats; Rats, Sprague-Dawley; Spinal Nerves; Vasotocin; Weaning

To examine the salubrious role of social interaction in modulating the development of allodynia (increased sensitivity to typically innocuous physical stimuli) and depressive-like behavior post peripheral nerve injury in mice. The determination of potential mechanisms that mediate social influences on the behavioral and physiological response to peripheral nerve injury.. Mice were pair housed or socially isolated for 2 weeks before spared nerve injury (SNI). Animals were cannulated; socially isolated animals were centrally treated with oxytocin; and socially paired animals were centrally treated with an oxytocin receptor antagonist. Animals were subsequently monitored for the development of mechanical allodynia and depressive-like behavior, and tissue was collected for analysis of the central levels of the cytokine interleukin 1 beta (IL-1beta).. Depressive-like behavior was assessed via the Porsolt forced swim test, developed only among socially isolated mice with nerve injury. Socially isolated mice with nerve injury also were the only experimental group to exhibit increased frontal cortex IL-1beta gene expression on day 7 post injury. Moreover, central treatment of socially isolated mice with oxytocin, a neuropeptide associated with social bonding, attenuated the effects of SNI on depressive-like behavior and reduced frontal cortex IL-1beta protein levels in socially isolated animals. Conversely, pair-housed animals treated with a selective oxytocin receptor antagonist developed depressive-like behavior equivalent to that of socially isolated animals and displayed increased IL-1beta protein levels within the frontal cortex.. These data suggest that social interaction significantly alters the affective and neuroinflammatory responses to SNI through a mechanism that could involve oxytocin.

Topics: Animals; Behavior, Animal; Depressive Disorder; Disease Models, Animal; Female; Gene Expression; Interleukin-1beta; Male; Mice; Mice, Inbred C57BL; Oxytocin; Pain Threshold; Peripheral Nerve Injuries; Physical Exertion; Prefrontal Cortex; Receptors, Oxytocin; Social Behavior; Social Environment; Social Isolation; Swimming