Clinical and Experimental Dermatology
Depression- and anxiety-like behaviour is related to BDNF/TrkB
signalling in a mouse model of psoriasis
and L. Jing
Neurology, Second Afﬁliated Hospital, Medical School of Xi’an Jiaotong University, Xi’an 710004, Shaanxi Province,
Background. The prevalence of anxiety and depression is signiﬁcantly higher in
individuals with psoriasis than in the general population. Clinical data also show
that anti-anxiety and antidepression drugs can reduce skin lesions in patients with
psoriasis, but the actual mechanism is still poorly understood.
Aim. To investigate whether brain-derived neurotrophic factor (BDNF) and tropo-
myosin receptor kinase B (TrKB) signalling plays a role in the mechanism under-
lying psoriasis with depression and anxiety behaviours.
Methods. Expression of BDNF and tropomyosin receptor kinase B (TrKB) in the
K5.Stat3C mouse, an animal model of psoriasis, were investigated by reverse tran-
scription PCR and Western blotting. Anxiety-like behaviours in the elevated-plus
maze test and changes in BDNF/TrkB that have been implicated in depression and
anxiety behaviours were measured. Skin lesions induced by 12-O-tetradecanoyl
phorbol-13-acetate (TPA) were also measured when the mice were administered ﬂu-
oxetine and K252a, an antagonist of TrkB.
Results. The antidepression and anti-anxiety drug ﬂuoxetine reduced TPA-induced
skin lesions and increased expression of BDNF and TrkB in K5.Stat3C mice. More
importantly, the effects of ﬂuoxetine were reversed by the TrkB antagonist K252a.
Conclusions. BDNF/TrkB signalling participates in the pathological mechanism of
depression and anxiety behaviours in psoriasis. Our ﬁndings provide a new thera-
peutic strategy for the treatment of skin lesions in psoriasis.
Psoriasis is a common chronic skin disease, and much
evidence shows that there is a close correlation
between this disease and anxiety/depression.
Epidemiological studies strongly suggest that patients
with psoriasis have a signiﬁcant prevalence of anxiety
and conversely, anxiety and depres-
sion can increase the prevalence of psoriasis.
more, clinical data also suggest that anti-anxiety and
antidepression drugs can reduce skin lesions in
patients with psoriasis.
Thus, psoriasis is also
referred to as a psychocutaneous disorder. Neuroen-
docrine dysfunction and disturbances in autoimmune
inﬂammatory reactions in the skin and enhanced
levels of T-cell inﬁltrates are among several mecha-
nisms that are thought to be the underlying causes
connecting psoriasis with anxiety and depression,
but the exact molecular mechanisms are still poorly
In recent years, there has been growing evidence to
show that the brain-derived neurotrophic factor
(BDNF)/TrKB pathway can modulate serotonin
(5-hydroxytryptamine; 5-HT) and other neurotrans-
mitters, and this pathway has been implicated in the
pathophysiology and treatment of depression and anxi-
Clinical data have also revealed epigenetic
Correspondence: Dr Sun Hong, Department of Dermatology, Second
Afﬁliated Hospital, Medical School of Xi’an Jiaotong University, NO.157
West 5 Road, Xi’an 710004, Shaanxi Province, China
Conﬂict of interest: the authors declare that they have no conﬂicts of
Accepted for publication 23 January 2017
ª 2018 British Association of Dermatologists
Clinical and Experimental Dermatology (2018) 43, pp254–261