Abstract
Depression is a prominent complex psychiatric disorder, usually complicated through expression of comorbid conditions, with chronic pain being among the most prevalent. This comorbidity is consistently associated with a poor prognosis and has been shown to negatively impact patient outcomes. With a global rise in this condition presenting itself, the importance of discovering long-term, effective, and affordable treatments is crucial. Electroacupuncture has demonstrated renowned success in its use for the treatment of pain and is a widely recognized therapy in clinical practice for the treatment of various psychosomatic disorders, most notably depression. Our study aimed to investigate the effects and mechanisms of Acid-Saline (AS) inducing states of chronic pain and depression comorbidity in the cerebellum, using the ST36 acupoint as the therapeutic intervention. Furthermore, the role of TRPV1 was relatedly explored through the use of TRPV1−/− mice (KO). The results indicated significant differences in the four behavioral tests used to characterize pain and depression states in mice. The AS and AS + SHAM group showed significant differences when compared to the Control and AS + EA groups in the von Frey and Hargreaves’s tests, as well as the Open-Field and Forced Swimming tests. This evidence was further substantiated in the protein levels observed in immunoblotting, with significant differences between the AS and AS + SHAM groups when compared to the AS + EA and AS + KO groups being identified. In addition, immunofluorescence visibly served to corroborate the quantitative outcomes. Conclusively these findings suggest that AS-induced chronic pain and depression comorbidity elicits changes in the cerebellum lobules VI, VII, VIII, which are ameliorated through the use of EA at ST36 via its action on TRPV1 and related molecular pathways. The action of TRPV1 is not singular in CPDC, which would suggest other potential targets such as acid-sensing ion channel subtype 3 (ASIC3) or voltage-gated sodium channels (Navs) that could be explored in future studies.
Highlights
Neuropsychiatric disorders display a complex relationship with the physical manifestations of disease in patients, often presenting with corresponding clinical signs and common pathological pathways [1]
The neurobiological correlates of chronic pain and depression comorbidity (CPDC) can be observed through widespread expression of Transient receptor potential vanilloid 1 (TRPV1) [10], with a resultant pathological cascade implicating signaling molecules that are well-established in neuronal plasticity, central sensitization, neuroinflammation, nociception, and various cognitive aptitudes
Chronic pain and depression are considered to be extremely detrimental, long-lasting, disabling conditions that significantly reduce the quality of life, and when presenting as comorbidity, an observable increase in the number of individuals presenting with this disorder underlines the urgent need to improve the management and treatment of these patients [31]
Summary
Neuropsychiatric disorders display a complex relationship with the physical manifestations of disease in patients, often presenting with corresponding clinical signs and common pathological pathways [1]. Understanding and identifying the underlying molecular processes involved in CPDC provides potential therapeutic targets to address the clinical manifestations thereof. To this end, the similarity of symptomatic presentations between chronic pain and depression underline shared biological mechanisms, such as neuroinflammation and central sensitization [4]. Transient receptor potential vanilloid 1 (TRPV1) is a widely accepted marker of inflammation observed in various nociceptive responses [7]. The neurobiological correlates of CPDC can be observed through widespread expression of TRPV1 [10], with a resultant pathological cascade implicating signaling molecules that are well-established in neuronal plasticity, central sensitization, neuroinflammation, nociception, and various cognitive aptitudes
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