Regulatory effect of nerve growth factor on release of substance P in cultured dorsal root ganglion neurons of rat.
ABSTRACT To investigate the regulatory effects of nerve growth factor (NGF) on basal and capsaicin-induced release of neuropeptide substance P (SP) in primary cultured embryonic rat dorsal root ganglion (DRG) neurons.
DRGs were dissected from 15-day-old embryonic Wistar rats. DRG neurons were dissociated and cultured, and then exposed to different concentrations of NGF (10 ng/mL, 30 ng/mL, or 100 ng/mL) for 72 h. The neurons cultured in media without NGF served as control. RT-PCR were used for detecting the mRNAs of SP and vanilloid receptor 1 (VR1) in the DRG neurons. The SP basal and capsaicin (100 nmol/L)-induced release in the culture were measured by radioimmunoassay (RIA).
SP mRNA and VR1 mRNA expression increased in primary cultured DRG neurons in a dose-dependent manner of NGF. Both basal release and capsaicin-evoked release of SP increased in NGF-treated DRG neurons compared with in control group. The capsaicin-evoked release of SP also increased in a dose-dependent manner of NGF.
NGF may promote both basal release and capsaicin-evoked release of SP. NGF might increase the sensitivity of nociceptors by increasing the SP mRNA or VR1 mRNA.
SourceAvailable from: Lorcan Mcgarvey[Show abstract] [Hide abstract]
ABSTRACT: Chronic cough is a common symptom that can be a daunting challenge for clinicians since treatment of the underlying cause does not always provide adequate relief, an obvious cause can remain elusive, and current antitussives have fairly poor efficacy and undesirable side-effects. Patients with chronic cough typically describe a range of sensory symptoms suggestive of upper-airway and laryngeal neural dysfunction. Additionally, patients often report cough triggered by low-level physical and chemical stimuli, which is suggestive of cough-reflex hyperresponsiveness. Pathophysiological mechanisms underlying peripheral and central augmentation of the afferent cough pathways have been identified, and compelling evidence exists for a neuropathy of vagal sensory nerves after upper-respiratory viral infections or exposure to allergic and non-allergic irritants. In this Personal View, we argue that chronic cough is a neuropathic disorder that arises from neural damage caused by a range of inflammatory, infective, and allergic factors. In support of this idea, we discuss evidence of successful treatment of chronic cough with agents used for treatment of neuropathic pain, such as gabapentin and amitriptyline. Regarding cough as a neuropathic disorder could lead to new, more effective antitussives.The Lancet Respiratory Medicine 07/2013; 1(5):414-22. DOI:10.1016/S2213-2600(13)70043-2
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ABSTRACT: Chronic cough is a common symptom that can be difficult to manage because associated causes may remain elusive and treatment of any associated cause may not provide relief. Current antitussives have limited efficacy and undesirable side-effects. Patients with chronic cough describe sensory symptoms suggestive of upper airway and laryngeal neural dysfunction, and report cough triggered by low-level physical and chemical stimuli supporting the concept of cough reflex hypersensitivity. Mechanisms underlying peripheral and central augmentation of the afferent cough pathways have been identified. Chronic cough is a neuropathic condition that could be secondary to sensory nerve damage caused by inflammatory, infective and allergic factors. Recent success in the treatment of chronic cough with agents used for treating neuropathic pain such as gabapentin and amitryptiline would also support this concept. Research into neuropathic cough may lead to the discovery of more effective antitussives.
Allergy, asthma & immunology research 09/2014; 6(5):373-5. DOI:10.4168/aair.2014.6.5.373 · 3.08 Impact Factor