The neuropeptide that promotes hair growth in mice and causes premature catagen, neurogenic inflammation, and immune privilege collapse in human follicles—and the missing link between stress and hair loss

Substance P is an eleven-amino-acid neuropeptide—the very first neuropeptide ever discovered (von Euler and Gaddum, 1931)—released by sensory nerve fibers throughout the body. It signals pain, inflammation, and stress. In hair biology, it tells one of the most instructive stories in Cluster K: a compound where the mouse data and the human data point in opposite directions, and where understanding the biology matters more than the compound's therapeutic potential—because the therapeutic potential is essentially zero.

In mice, exogenous Substance P induces hair growth. In human hair follicles, it induces premature catagen (growth termination), neurogenic inflammation, mast cell degranulation, and the collapse of follicular immune privilege—the very process that underlies alopecia areata. The species difference is not subtle. It is categorical.

This article examines Substance P's role in human hair biology, explains why it is the leading mechanistic candidate for stress-induced hair loss, and makes the case that blocking Substance P signaling—not enhancing it—represents the unexplored therapeutic frontier.

Quick Facts: Substance P (Hair) at a Glance

What Is Substance P?

Pronunciation: SUB-stans pee

When you stub your toe, burn your finger, or sit through a meeting that makes your jaw clench, your sensory nerve endings release a tiny signaling molecule into the surrounding tissue. That molecule is Substance P. It is one of the oldest known neuropeptides—discovered in 1931 by Ulf von Euler and John Gaddum—and one of the most studied. Substance P signals pain, triggers inflammation, and recruits immune cells to sites of tissue stress. It is, in the simplest terms, a chemical alarm.

What makes Substance P relevant to hair biology is anatomy: sensory nerve fibers surround every hair follicle. During psychological stress, these perifollicular nerves release Substance P directly into the follicular microenvironment—the narrow zone of tissue where the hair growth machinery operates. This is not a long-distance hormonal signal (like cortisol traveling through the bloodstream). It is a local, direct delivery of an inflammatory neuropeptide to the exact tissue that controls hair growth.

In 2006, Arck and colleagues from the Paus laboratory tested what happens when Substance P reaches human hair follicles. The answer was unambiguous and damaging: premature termination of the growth phase, mast cell degranulation, collapse of follicular immune privilege, and activation of apoptosis pathways. Every measurable outcome was hair-negative.

Origins and Discovery

Substance P's discovery predates the entire field of neuropeptide biology. In 1931, Ulf von Euler and John Gaddum at the Karolinska Institute found that extracts of horse brain and intestine caused smooth muscle contraction and blood pressure changes. They called the active factor "Substance P" (P for "Preparation")—a placeholder name that stuck permanently because the molecule took decades to fully characterize.

The amino acid sequence was not determined until 1971 (Chang, Leeman, and Niall). The receptor (NK1R, neurokinin-1 receptor) was cloned in 1991. By that time, Substance P was established as the prototypical neuropeptide of pain and inflammation—a mediator of nociception, neurogenic inflammation, and immune cell activation.

The hair connection emerged from the Paus laboratory, which has produced more original research on neuropeptide-hair follicle interactions than any other group worldwide. In 1994, Paus et al. showed that capsaicin (which depletes SP from nerve endings) and exogenous SP both induced hair growth in mouse skin (PMID 7518880). This was interpreted as evidence that SP is a hair growth modulator.

But the 2006 human follicle study (Arck et al., PMID 18055548) reversed the narrative. When SP was applied to human scalp hair follicles maintained in organ culture, it did not promote growth. It terminated it. The species difference was not a matter of degree—it was a reversal of direction. This result reframed SP from a potential hair growth compound to the molecular explanation for stress-induced hair loss.

Mechanism of Action

Species-Dependent Effects—Why the Mouse Data Misleads

This section begins with the most important disclaimer in Cluster K: Substance P's effects on hair follicles are species-dependent. Mouse data and human data tell opposite stories. Any discussion of SP and hair that does not acknowledge this divergence is scientifically incomplete.

In mouse skin (C57BL/6, C3H models): SP at physiological concentrations accelerated anagen progression in murine skin organ culture (Peters et al., 2001; PMID 11179999). Capsaicin-induced SP release and exogenous SP both induced hair growth in telogen mouse skin (Paus et al., 1994; PMID 7518880). The effect involved mast cell degranulation and subsequent growth factor release. In mice, the inflammatory cascade triggered by SP tilts toward a pro-growth response.

In human scalp hair follicles (Arck et al., 2006; PMID 18055548): SP exposure produced a categorically different response. Every measured parameter was hair-negative. This is the study that matters for human relevance. The effects were:

Premature Catagen Induction

SP caused human follicles in organ culture to exit anagen (growth phase) prematurely and enter catagen (regression phase). This is the opposite of what every effective hair loss treatment does. Minoxidil, finasteride, and thymulin all prolong anagen. Substance P terminates it.

Neurogenic Inflammation

SP triggered degranulation of mast cells in the connective tissue sheath surrounding human follicles. Mast cells release histamine, TNF-α, and other pro-inflammatory mediators that damage the follicular environment. This neurogenic inflammation is distinct from the low-grade perifollicular microinflammation seen in androgenetic alopecia—it is acute, nerve-mediated, and directly triggered by SP.

Immune Privilege Collapse

Hair follicles maintain a specialized immune environment called "immune privilege"—they suppress the expression of molecules (MHC class I, β2-microglobulin) that would otherwise signal the immune system to inspect them. This is the same immune evasion strategy used by the cornea, the placenta, and the brain. When immune privilege collapses, the follicle's own immune system recognizes it as foreign and attacks—this is the pathological mechanism of alopecia areata.

SP upregulated MHC class I and β2-microglobulin expression in human follicular keratinocytes, causing ectopic antigen presentation. In genetically predisposed individuals, this collapse of immune privilege could trigger alopecia areata—autoimmune hair loss where the immune system destroys actively growing follicles.

Apoptosis Pathway Shift

SP altered the balance between two nerve growth factor (NGF) receptors in human follicles: it downregulated TrkA (the growth-promoting NGF receptor) and upregulated p75NTR (the apoptosis- and catagen-promoting NGF receptor). This receptor switch shifts the follicle's response to NGF from survival and growth toward programmed cell death and growth termination.

Negative Feedback Response

Notably, SP also caused downregulation of its own receptor (NK1R) and upregulation of neutral endopeptidase (NEP/CD10)—the enzyme that degrades SP. This suggests the human follicle is attempting to limit SP exposure, consistent with the interpretation that SP is a damaging signal in the human follicular context.

The Stress→Hair Loss Pathway

The most clinically important contribution of Substance P research is the mechanistic explanation for stress-induced hair loss:

Psychological stress activates the hypothalamic-pituitary-adrenal axis and sympathetic nervous system. Locally, stress activates sensory C-fiber nerve endings in the skin, causing SP release into the perifollicular environment. SP triggers mast cell degranulation and neurogenic inflammation. Inflammation damages the follicular microenvironment and can push follicles from anagen into catagen prematurely. In genetically predisposed individuals, SP-mediated immune privilege collapse may trigger alopecia areata.

This pathway was confirmed experimentally: sound-stressed mice showed premature catagen associated with increased perifollicular SP (Peters et al., 2003; PMID 12598315), and the NK1R antagonist RP67580 blocked the stress-induced hair loss entirely (Zhu et al., 2013; PMID 23637859). The therapeutic implication—blocking SP signaling, not enhancing it—has never been tested in humans for hair loss.

Key Research Findings

Human Follicle Organ Culture (Arck et al., 2006 — PMID 18055548)

Published in the American Journal of Pathology, this is the definitive study on Substance P and human hair follicles. The Paus group applied SP to human scalp hair follicles maintained in organ culture—living human tissue responding to a direct stimulus.

Every measured outcome was negative for hair: premature catagen induction, mast cell degranulation in the connective tissue sheath, upregulation of MHC class I and β2-microglobulin (immune privilege collapse), downregulation of TrkA (growth receptor), upregulation of p75NTR (death receptor), downregulation of NK1R (the follicle trying to protect itself), and upregulation of NEP (SP-degrading enzyme).

This single study fundamentally changed how hair biologists understand the stress-hair loss connection. It provided the first evidence-based biological explanation for how psychological stress might trigger both telogen effluvium and alopecia areata.

Mouse Anagen Induction (Paus et al., 1994 — PMID 7518880)

The study that initially suggested SP might promote hair growth. Capsaicin (which releases SP from nerve endings) and exogenous SP both induced anagen in telogen mouse back skin. The effect was associated with mast cell degranulation—the same process that damages human follicles.

This study is historically important but must be read with the caveat that the human follicle response (2006 study) was the opposite. The mouse result does not predict human outcomes for this compound.

Stress-Hair Loss Mechanism (Peters et al., 2003 — PMID 12598315)

Sound stress in mice caused premature catagen via SP-dependent neurogenic inflammation. This established the causal chain: stress → nerve activation → SP release → perifollicular inflammation → premature hair growth termination. The mechanism has been widely cited in the dermatology literature as the best current explanation for stress-induced telogen effluvium.

NK1R Antagonist Rescue (Zhu et al., 2013 — PMID 23637859)

Chronic restraint stress in mice inhibited hair growth via a SP → mast cell → reactive oxygen species (ROS) pathway. The NK1R antagonist RP67580 blocked the SP signal and normalized the hair cycle. The antioxidant Tempol also rescued hair growth by neutralizing the ROS generated downstream. This study demonstrates that the SP pathway is druggable—the damage can be prevented by blocking the receptor.

Alopecia Areata Amplification (Siebenhaar et al., 2007 — PMID 17273166)

In the C3H/HeJ mouse model of alopecia areata, SP-immunoreactive nerve fibers increased during early disease development. SP treatment increased granzyme B expression in CD8+ T cells—the cytotoxic lymphocytes that directly destroy hair follicles in alopecia areata. This places SP as an amplifier of the autoimmune attack, not merely a bystander.

Safety Profile

Exogenous Substance P—Contraindicated for Hair

Based on the human follicle organ culture data, exogenous Substance P applied to the scalp would be expected to worsen hair loss, not improve it. The compound induces premature catagen, neurogenic inflammation, and immune privilege collapse in human follicles. Self-experimentation with SP for hair growth is not merely unsupported—it is contraindicated by the available evidence.

SP's Endogenous Role

Substance P is an endogenous neuropeptide that the body produces continuously. The concern is not exogenous SP (which no one should be applying for hair)—it is excessive endogenous SP release during chronic stress. The safety question for hair is about stress management, not compound administration.

NK1R Antagonist Safety (Aprepitant)

Aprepitant (Emend) has a well-characterized safety profile from its approved use in chemotherapy-induced nausea: common side effects include fatigue, dizziness, and constipation. It is a CYP3A4 inhibitor with drug interactions. Chronic use for a cosmetic indication would require different risk-benefit analysis than acute use for chemotherapy support—but the drug itself is well-tolerated.

Claims vs. Evidence

We currently don’t have any vetted partners for this compound. Check back soon.

The Human Evidence Landscape

There is no human clinical evidence for Substance P in hair—no interventional trial, no observational study, no case report of SP administration for hair growth or SP blockade for hair loss.

The human evidence that does exist is ex vivo: the Arck et al. (2006) study used human scalp hair follicles maintained in organ culture. This is the highest-quality preclinical evidence available—it uses human tissue, not animal models—but it is not the same as treating patients. Organ culture cannot replicate the full in vivo scalp environment: vascular supply, neural networks, systemic hormones, immune surveillance, and sebaceous gland interactions are all absent.

The animal evidence is extensive and mechanistically coherent—five controlled studies from three research groups spanning 1994 to 2013, all consistently demonstrating SP's role in hair cycle modulation and stress-induced alopecia. The NK1R antagonist rescue data (2013) is the most clinically promising finding in the entire Substance P literature for hair.

What is conspicuously absent: any clinical trial testing NK1R antagonists for hair loss in humans. Aprepitant has been FDA-approved since 2003 for chemotherapy-induced nausea. The drug exists, the mechanistic rationale exists, the animal proof-of-concept exists. The clinical trial does not.

Legal and Regulatory Status

Substance P is available from peptide vendors as a research reagent. It is not sold, marketed, or positioned for hair growth—and the evidence base actively argues against such use.

NK1R antagonists (aprepitant/Emend, fosaprepitant/Ivemend) are prescription drugs approved for chemotherapy-induced nausea and vomiting. Off-label use for hair loss would require a prescription and would be entirely without clinical evidence—no dermatology guideline recommends it.

WADA does not list Substance P or NK1R antagonists on the Prohibited List.

Research Protocols

Human Follicle Organ Culture (Arck et al., 2006)

Human scalp hair follicles obtained from cosmetic surgery were microdissected and maintained in supplemented Williams' E medium. Anagen VI follicles were treated with Substance P (10⁻⁸ M) or vehicle for up to 6 days. Endpoints: hair cycle staging (catagen conversion), mast cell degranulation (toluidine blue staining), MHC class I and β2-microglobulin expression (immunohistochemistry), TrkA and p75NTR expression, NK1R expression, and NEP expression.

Mouse Stress Models (Peters et al., 2003; Zhu et al., 2013)

Sound stress (Peters): C57BL/6 mice exposed to sonic stress for 24 hours. Hair cycle assessed by skin color, histology, and immunohistochemistry for SP, CGRP, and NGF.

Chronic restraint stress (Zhu): Mice subjected to 12 hours daily restraint for 15 days. SP, NK1R, mast cell density, and ROS measured in skin. NK1R antagonist RP67580 and antioxidant Tempol administered to intervention groups.

Dosing in Published Research

The following table summarizes dosing protocols for Substance P (Hair) as reported in published clinical and preclinical research. These reflect study designs, not treatment recommendations.

Organ Culture Concentration (Arck et al., 2006)

Animal Dosing (NK1R Antagonist — Zhu et al., 2013)

Dosing — Community Protocols

WHY NEARLY EMPTY

Substance P is not used in the peptide community for hair growth. No community protocol exists. No vendor markets SP for hair applications. This section is intentionally minimal because the available evidence indicates that exogenous Substance P would worsen, not improve, hair loss based on human follicle data.

Peptidings includes Substance P in Cluster K because understanding what damages hair follicles is as important as understanding what helps them. If you are searching for a compound to promote hair growth, Substance P is not it. If you are searching for an explanation of why stress causes hair loss, you are in the right place.

Combination Stacks

Research into Substance P (Hair) combination protocols is limited. The stacking practices described below are drawn from community reports and have not been validated in controlled studies.

If you are considering combining Substance P (Hair) with other compounds, consult a qualified healthcare provider. Interactions between peptides and other substances are poorly characterized in the literature.

Frequently Asked Questions

Summary of Key Findings

Substance P is the most unusual entry in Cluster K—a compound included not for its therapeutic potential but for its explanatory power. It does not belong on anyone's list of hair growth compounds. It belongs in a biology textbook under the chapter on why hair falls out.

The narrative arc is instructive: mouse studies in the 1990s suggested SP promotes hair growth, generating early excitement. Human follicle studies in the 2000s showed the opposite—premature catagen, neurogenic inflammation, immune privilege collapse. The species difference was not subtle. It was a reversal. This is exactly the kind of translational failure that evidence-based reporting exists to document.

The clinically valuable insight is the stress-hair loss mechanism. Substance P provides the strongest mechanistic explanation for how psychological stress causes telogen effluvium and may trigger alopecia areata. The pathway—stress → nerve activation → SP release → mast cell degranulation → follicular damage—has been confirmed in animal models and is consistent with human follicle data.

The untapped therapeutic frontier is blocking SP signaling, not enhancing it. NK1R antagonists rescued the hair cycle in stressed mice. An FDA-approved NK1R antagonist (aprepitant) already exists. The clinical trial testing it for hair loss does not.

Verdict Recapitulation

Verdict: Thin Ice. Exogenous Substance P is actively harmful to human hair follicles based on the best available evidence. Mouse data suggesting hair growth promotion does not translate. The compound is included in Cluster K for biological understanding, not therapeutic recommendation. The one promising direction—NK1R antagonist blockade—remains completely untested in humans.

For readers considering Substance P (Hair), the evidence above represents the current state of knowledge. As always, consult a qualified healthcare provider before making any decisions about peptide use.

Compound	Type	Primary Target	Half-Life	FDA Status	WADA Status	Evidence Tier	Primary Tissue Target	Route	Human Evidence Status	Key Differentiator
BPC-157	Synthetic pentadecapeptide (15 amino acids, derived from gastric protective protein BPC)	VEGF / Nitric oxide (proposed multi-target)	~2–6 hours	Not FDA-approved	Prohibited — S0 (Non-Approved Substances)	Tier 3 — Pilot / Limited Human Data	Musculoskeletal, tendon, ligament, GI tract, CNS	Subcutaneous injection + Oral (both routes studied)	3 published human pilot studies (~30 subjects combined); no RCTs	Broadest tissue tropism in cluster. Only injury-repair peptide with both oral and injectable evidence. Most evidence in rodent models
TB-500	Synthetic 4-amino-acid fragment (residues 17–23 of Thymosin Beta-4)	Actin binding (cell migration, angiogenesis)	~2–3 hours	Not FDA-approved	Prohibited — S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics)	Tier 4 — Preclinical Only	Musculoskeletal (muscle, tendon, ligament), cardiac, neurological	Subcutaneous injection	Zero published human clinical trials; animal models and cell culture only	Smallest fragment studied; synthetic derivative of endogenous Thymosin Beta-4. Actin sequestration may drive cell migration
Thymosin Beta-4	Endogenous 43-amino-acid peptide (ubiquitous actin-sequestering protein)	Actin binding, cell migration, angiogenesis	~2–4 hours	Not FDA-approved	Prohibited — S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics)	Tier 3 — Pilot / Limited Human Data	Broad: muscle, cardiac, neurological, immune, epithelial	Subcutaneous injection + Topical (cosmetics)	Few human studies; cardiac regeneration in early-stage human data; cosmetic formulations	Full-length parent peptide of TB-500. Endogenous compound; ubiquitous in mammalian tissues. More potent than TB-500 fragment in vitro
GHK-Cu	Synthetic tripeptide-copper complex (Gly-His-Lys chelated to Cu2+)	Collagen synthesis, wound healing, TGF-beta modulation	~2 hours topical; ~4–6 hours systemic (estimated)	Not FDA-approved (topical in cosmetics; injectable investigational)	Prohibited — S0 (injectable as growth factor analog); topical unregulated	Tier 5 — It's Complicated	Dermal (collagen, elastin remodeling); broad systemic effects proposed but unverified	Topical (cosmetics — extensive evidence) vs. Subcutaneous injection (preclinical only)	Topical: 30+ years cosmetic use data; Injectable: zero human trials	Route-dependent evidence: topical skin rejuvenation well-established, but injectable claims extrapolate from fundamentally different delivery
AHK-Cu	Synthetic copper tripeptide variant (Ala-His-Lys chelated to Cu2+)	Copper chelation, extracellular matrix remodeling, growth factor signaling	~2–4 hours (estimated)	Not FDA-approved	Not WADA-listed	Tier 4 — Preclinical Only	Dermal (hair follicle, scalp), cosmetic	Topical (cosmetics)	No human clinical trials; in vitro and cosmetic formulation data only	GHK-Cu structural analog with alanine substitution. Primarily studied for hair growth. Less evidence base than GHK-Cu
LL-37	Human cathelicidin antimicrobial peptide (37 amino acids)	Antimicrobial, wound healing, angiogenesis, vitamin D-regulated immune modulation	~2–4 hours	Not FDA-approved	Not WADA-listed	Tier 3 — Pilot / Limited Human Data	Skin, mucosal surfaces, immune system	Subcutaneous injection, Topical	Limited human data; antimicrobial efficacy well-characterized in vitro; wound healing in animal models	Endogenous host defense peptide. Dual role: direct antimicrobial activity + immune modulation. Vitamin D pathway regulates expression
KPV	Alpha-MSH C-terminal tripeptide (Lys-Pro-Val)	NF-kB inhibition, anti-inflammatory (no melanocortin receptor activation)	~1–2 hours (estimated)	Not FDA-approved	Not WADA-listed	Tier 4 — Preclinical Only	GI tract (colitis models), skin, immune system	Subcutaneous injection, Oral (investigational)	No published human clinical trials; animal models (colitis, dermatitis) only	Smallest anti-inflammatory peptide in cluster (3 amino acids). NF-kB pathway without melanocortin receptor binding. GI-focused research
VIP	Endogenous 28-amino-acid neuropeptide (vasoactive intestinal peptide)	VPAC1/VPAC2 receptor agonism; vasodilation, immunomodulation, bronchodilation	~1–2 minutes (extremely short)	Not FDA-approved (aviptadil in clinical trials)	Not WADA-listed	Tier 2 — Clinical Trials	Pulmonary, GI tract, immune system, neurological	Subcutaneous injection, IV infusion, Intranasal	Multiple Phase 2 trials (ARDS, pulmonary hypertension, sarcoidosis); aviptadil in FDA pipeline	Shortest half-life in cluster. CIRS protocol use. Aviptadil (synthetic VIP) is furthest along FDA pathway among non-approved compounds here
KGF / Palifermin	Recombinant keratinocyte growth factor (FGF-7)	FGFR2b receptor; keratinocyte proliferation, epithelial barrier repair	~3–5 hours	FDA-approved (Kepivance for oral mucositis)	Not WADA-listed	Tier 1 — Approved Drug	Epithelial surfaces (oral mucosa, GI tract, skin)	Intravenous injection (FDA-approved route)	FDA-approved for chemo-induced oral mucositis; multiple Phase 2/3 trials	Only FDA-approved compound in Cluster B. Specific to epithelial tissues. IV-only approved route limits off-label accessibility
Substance P	Endogenous 11-amino-acid tachykinin neuropeptide	NK1 receptor agonism; fibroblast migration, angiogenesis, immune activation	~1–2 minutes	Not FDA-approved	Not WADA-listed	Tier 3 — Pilot / Limited Human Data	Corneal epithelium, skin, nervous system	Topical (corneal), Subcutaneous injection	Human data primarily in corneal wound healing; limited systemic human studies	Endogenous pain signaling peptide repurposed for tissue repair. Strongest human evidence in corneal healing. Dual role: nociception + repair
PRP	Autologous platelet-rich plasma (concentrated growth factor preparation)	PDGF, VEGF, TGF-beta release via platelet degranulation	N/A (not a single molecule)	FDA-cleared devices (not drug-approved)	Prohibited — M1 (Manipulation of Blood and Blood Components)	Tier 2 — Clinical Trials	Musculoskeletal (tendon, cartilage, bone), dermal, hair	Injection (local to injury site)	Hundreds of RCTs across orthopedic, dermatologic, and dental applications	Non-peptide. Autologous preparation — no synthetic manufacturing. Largest clinical evidence base in cluster but high study heterogeneity
ARA-290	Synthetic 11-amino-acid peptide (cibinetide; EPO-derived tissue-protective peptide)	Innate Repair Receptor (EPOR/CD131 heterodimer) selective agonist	~2–4 hours	Not FDA-approved (Phase 2b completed)	Not WADA-listed	Tier 2 — Clinical Trials	Peripheral nerves, retina, cardiac, immune system	Subcutaneous injection (1–8 mg daily in trials); IV infusion (early trials)	Phase 2b complete (sarcoidosis SFN — DOSARA trial); Phase 2 (diabetic neuropathy, diabetic macular edema)	EPO-derived but does NOT bind classical EPO receptor. No erythropoietic activity. Tissue protection without blood doping risk. Furthest clinical development for neuropathy

Where to Source Substance P (Hair)

Further Reading and Resources

If you want to go deeper on Substance P (Hair), the evidence landscape for hair & follicle peptides, or the methodology behind how we evaluate this research, these are the places worth your time.

ON PEPTIDINGS

• Hair & Follicle Research Hub — Overview of all compounds in this cluster
• Reconstitution Guide — How to properly prepare injectable peptides
• Storage and Handling Guide — Proper storage to maintain peptide stability
• About Peptidings — Our editorial methodology and evidence framework

EXTERNAL RESOURCES

• PubMed: Substance P (Hair) — All indexed publications
• ClinicalTrials.gov — Active and completed trials

Selected References and Key Studies

1. Arck PC, Handjiski B, Peters EMJ, Peter AS, Hagen E, Fischer A, Klapp BF, Paus R. Stress inhibits hair growth in mice by mechanisms involving substance P–dependent neurogenic inflammation. Am J Pathol. 2006;168(4):1164-1172. PMID 18055548
2. Paus R, Heinzelmann T, Schultz KD, Furkert J, Fechner K, Czarnetzki BM. Hair growth induction by substance P. Lab Invest. 1994;71(1):134-140. PMID 7518880
3. Peters EMJ, Botchkarev VA, Botchkareva NV, Tobin DJ, Paus R. Hair-cycle-associated remodeling of the peptidergic innervation of murine skin, and hair growth modulation by neuropeptides. J Invest Dermatol. 2001;116(2):236-245. PMID 11179999
4. Peters EMJ, Arck PC, Paus R. Hair growth inhibition by psychoemotional stress: a mouse model for neural mechanisms in hair growth control. Am J Pathol. 2003;162(3):803-814. PMID 12598315
5. Siebenhaar F, Sharov AA, Peters EMJ, Sharova TY, Syska W, Mardaryev AN, Freyschmidt-Paul P, Sundberg JP, Maurer M, Botchkarev VA. Substance P as an immunomodulatory neuropeptide in a murine model for autoimmune hair loss (alopecia areata). J Invest Dermatol. 2007;127(6):1489-1497. PMID 17273166
6. Zhu HL, Gao YH, Yang JQ, Li JB, Gao J. Serenity in the midst of a busy life: a brief analysis of the effect of NK1R antagonist and antioxidant on chronic restraint stress–induced hair loss. PLoS ONE. 2013;8(4):e61574. PMID 23637859

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