Migraine headaches are theorized to cause aura and symptoms via spreading cortical depression that ultimately results in substance P release, alterations in blood flow, and neurogenic inflammation.
Through activation of NK<sub>1</sub>R, substance P modulates a wide variety of physiological and disease processes including nociception, inflammation, and depression.
Our results show a significant upregulation of MAOA and TAC1 in the medial area frontopolaris which is a node in the limbic-cortical network and known to be susceptible for gray matter loss and behavioral dysfunction in patients with depression.
We quantified Tacr1 (neurokinin-1 receptor gene) and Avp (vasopressin peptide gene) mRNA in brain regions involved in depression, addiction and social behavior.
We consider our findings to contribute to the neurobiological evidence on the association between SP and brain structural changes in depression, which may be related with the pathophysiology and treatment of MDD.
The study aimed at assessing the concentrations of ADMA, carbonyl groups, CAT and NKA in patients with varying levels of depression severity, PTSD, and depression concurrent with PTSD.
In this review, we update the involvement of the SP/NK-1 receptor system in the physiopathology of the above-mentioned pathologies and we suggest valuable future therapeutic interventions involving the use of NK-1 receptor antagonists, particularly in the treatment of emesis, depression, cancer, neural degeneration, inflammatory bowel disease, viral infection and pruritus, in which that system is upregulated.
The present studies indicate that alterations in substance P/NK1 receptor system underlie, at least in part, the behavioural and monoaminergic changes in this animal model of depression.
Taken together, these data are in line with behavioural experiments showing ameliorating effects of NK1 and NK2 receptor antagonists against anxiety and depression-like symptoms in rodents, and therefore further implicate the tachykinin systems in the pathophysiology of depression and adult life psychopathology.
Increasing evidence suggests that substance P (SP) neurokinin-1 (NK1) receptors are involved in stress and emotional responses, representing a potential target for the treatment of anxiety and depression in humans.
Because of the possible antidepressant effects of SP antagonists, the influence of SP on both pathophysiology and mitigation of depression has been hypothesized.
This review summarizes the pre-clinical evidence derived from pharmacological and transgenic animal studies that suggests an important role for the substance P/neurokinin 1 system in anxiety and depression.