biology

Neurogenic inflammation

Neurogenic inflammation is a biology topic covered in the lgStudy science library. This page brings together a partial reference excerpt, illustrations, worked examples, real-world applications and a short study plan, so you can understand Neurogenic inflammation rather than just read about it. In short: Neurogenic inflammation is inflammation arising from the local release by afferent neurons of inflammatory mediators such as substance P, calcitonin gene-related peptide (CGRP), neurokinin A (NKA), and endothelin-3 (ET-3). For example, release of neuropeptides can increase vasodilatation and capillary permeability of vascular endothelial and smooth muscle cells.

Key takeaways

Neurogenic inflammation belongs to biology; place it in that map before memorising details.
Learn the definition first, then one example that makes the definition concrete.
Connect Neurogenic inflammation to a quantity you can measure, compute or draw — that is where exam questions come from.
Reproduce the core statement of Neurogenic inflammation from memory before moving on to harder problems.

Reference excerpt

Neurogenic inflammation is inflammation arising from the local release by afferent neurons of inflammatory mediators such as substance P, calcitonin gene-related peptide (CGRP), neurokinin A (NKA), and endothelin-3 (ET-3). For example, release of neuropeptides can increase vasodilatation and capillary permeability of vascular endothelial and smooth muscle cells. The release of pro-inflammatory mediators is thought to be triggered by the activation of ion channels that are the principal detectors of noxious environmental stimuli. The heat/capsaicin receptor TRPV1 and the wasabi receptor TRPA1. TRPA1 channels stimulated by lipopolysaccharides may also cause acute neurogenic inflammation. Once released, these neuropeptides induce the release of histamine from nearby mast cells. In turn, histamine evokes the release of substance P and CGRP; thus, a bidirectional link between histamine and neuropeptides in neurogenic inflammation is established. Neurogenic inflammation appears to play a role in the pathogenesis of numerous disorders, including migraine, psoriasis, asthma, vasomotor rhinitis, fibromyalgia, eczema, rosacea, dystonia, and multiple chemical sensitivity. In migraine, stimulation of the trigeminal nerve causes neurogenic inflammation via the release of neuropeptides, including substance P, nitric oxide, vasoactive intestinal polypeptide, 5-HT, neurokinin A, and CGRP.

Prevention Magnesium deficiency causes neurogenic inflammation in a rat model. Researchers have theorized that since substance P which appears at day five of induced magnesium deficiency, is known to stimulate in turn the production of other inflammatory cytokines including Interleukin 1 (IL-1), interleukin 6 (IL-6), and tumor necrosis factor alpha (TNFα), which begin a sharp rise at day 12, substance P is a key in the path from magnesium deficiency to the subsequent cascade of neuro-inflammation. In a later study, researchers provided rats dietary levels of magnesium that were reduced but still within the range of dietary intake found in the human population, and observed an increase in substance P, TNFα, and interleukin-1 beta (IL-1β), followed by exacerbated bone loss. These and other data suggest that deficient dietary magnesium intake, even at levels not uncommon in humans, may trigger neurogenic inflammation and lead to an increased risk of osteoporosis.

Treatment In 2018, three CGRP blockers were approved by the FDA for the prevention of migraine: erenumab; fremanezumab; and galcanezumab. The calcitonin gene-related peptide (CGRP) is a therapeutic target in migraine because of its hypothesized role in mediating trigeminovascular pain transmission and the vasodilatory component of neurogenic inflammation. In 2018, the US Food and Drug Administration (FDA) approved the CGRP antagonists erenumab, fremanezumab, and galcanezumab for migraine prevention. Additional CGRP blockers are progressing through clinical trials. Anticipating later botox therapy for migraine, early work by Jancsó et al. found some success in treatment using denervation or pretreatment with capsaicin to prevent uncomfortable symptoms of neurogenic inflammation. A 2010 study of the treatment of migraine with CGRP blockers had shown promise for CGRP blockers. In early trials, the first oral nonpeptide CGRP antagonist, MK-0974 (Telcagepant), was shown effective in the treatment of migraine attacks, but elevated liver enzymes in two participants were found. Other therapies and other links in the neurogenic inflammatory pathway for interruption of disease are under study, including migraine therapies. Noting that botulinum toxin has been shown to have an effect on inhibiting neurogenic inflammation, and evidence suggesting the role of neurogenic inflammation in the pathogenesis of psoriasis, the University of Minnesota has a pilot clinical trial underway to follow up on the observation that patients treated with botulinum toxin for dystonia had dramatic improvement in psoriasis. Astelin (Azelastine) "is indicated for symptomatic treatment of vasomotor rhinitis including rhinorrhea, nasal congestion, and post nasal drip in adults and children 12 years of age and older." Statins appear to "decrease expression of the proinflammatory neuropeptides calcitonin gene-related peptide and substance P in sensory neurons," and so might be of use in treating diseases presenting with predominant neurogenic inflammation.

Research In a 2012 article in Nature Neuroscience Chiu et al. discuss the development of science related to neurogenic inflammation and provide a graphic illustrating key discoveries leading toward the current understanding of neurogenic inflammation, its mechanisms, and the conditions caused by its disorder.

References

Worked examples

Example 1 — a first encounter with Neurogenic inflammation

Start with the simplest possible case. Write down what Neurogenic inflammation claims or describes in one sentence, then invent the smallest concrete situation in which that sentence is true. In biology, the smallest case is usually a single object, a single equation or a single measurement. Check that every symbol or term in your sentence has a meaning in that case.

Example 2 — changing one variable

Take the situation from Example 1 and change exactly one quantity: double it, halve it, or set it to zero. Predict what should happen to Neurogenic inflammation before you calculate. Comparing your prediction with the result is the fastest way to find out whether you understand the idea or only the words.

Example 3 — an exam-style question

Typical questions about Neurogenic inflammation ask you to (a) state it precisely, (b) apply it to given data, and (c) explain a limitation. Practise writing all three answers in under five minutes; the third part is what separates a full-mark answer from an average one.

Applications of Neurogenic inflammation

In research: Neurogenic inflammation appears in biology research whenever the underlying quantities have to be modelled precisely. Papers usually cite it as a starting assumption and then explore where it breaks down.
In technology and industry: Engineering practice reuses Neurogenic inflammation in design rules, simulations and safety margins. Knowing the idea lets you read a specification sheet and understand why the numbers look the way they do.
In the classroom: Neurogenic inflammation is common in secondary-school and first-year university syllabi. It links to neighbouring topics Inflammations, so understanding it makes those chapters shorter.
In everyday life: Look for Neurogenic inflammation outside the textbook — in sport, cooking, traffic, electronics or the sky above you. An example you found yourself is remembered far longer than one you were given.

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How to study Neurogenic inflammation in 20 minutes

Read the reference excerpt below once, without taking notes.
Close the page and write down what Neurogenic inflammation means in your own words.
Compare your version with the excerpt and mark what you missed.
Work through the three examples above with pen and paper.
Explain Neurogenic inflammation out loud to somebody else — or to Teacher Smith in the lgStudy chat.

Frequently asked questions

What is Neurogenic inflammation in simple terms?

Why does Neurogenic inflammation matter?

Because it connects several biology ideas at once: it gives you a definition you can apply, a quantity you can calculate, and a way to check whether a result is plausible.

How should I study Neurogenic inflammation?

Read the excerpt, restate it from memory, then work through the examples and applications listed on this page. The five-step study plan above takes about twenty minutes.

What does this page cover?

It gives you a compact reference excerpt plus original lgStudy explanations, examples, applications and study material on Neurogenic inflammation.