Abstract
Pathophysiological mechanisms involved in orofacial pain and their relationship with emotional disorders have emerged as an important research area for multidisciplinary studies. In particular, temporomandibular disorders (TMD) have been evaluated clinically from both physiological and psychological perspectives. We hypothesized that an altered neuronal activity occurs in the amygdala and the dorsal raphe nucleus (DR), encephalic regions involved in the modulation of painful and emotional information. Adult male Wistar rats were used in an experimental complete Freund's adjuvant (CFA)-induced temporomandibular joint (TMJ) inflammation model. CFA was applied for 1 or 10 days, and the animals were euthanized for brain samples dissection for FosB/ΔFosB and parvalbumin (PV) immunostaining. Our results were consistent in showing that the amygdala and DR were activated in the persistent inflammatory phase (10 days) and that the expression of PV+ interneurons in the amygdala was decreased. In contrast, in the DR, the expression of PV+ interneurons was increased in persistent states of CFA-induced TMJ inflammation. Moreover, at 10 days of inflammation, there was an increased co-localization of PV+ and FosB/ΔFosB+ neurons in the basolateral and central nucleus of the amygdala. Different nuclei of the amygdala, as well as portions of the DR, were activated in the persistent phase (10 days) of TMJ inflammation. In conclusion, altered activity of the amygdala and DR was detected during persistent inflammatory nociception in the temporomandibular joint. These regions may be essential for both sensory and affective dimensions of orofacial pain.
Highlights
One of the most common pain conditions experienced by adults is chronic orofacial pain
We investigated the role of CFAinduced temporomandibular joint (TMJ) inflammation on PV expression in the amygdala and dorsal raphe nucleus (DR), and on neuronal activation of the same regions as assessed by FosB/DFosB expression
In the dorsal raphe nucleus (DRL), we found significant effects on the number of FosB/DFosB+ neurons in the group with 10 days of complete Freund’s adjuvant (CFA)-induced inflammation compared with Day 10/saline and Day 1/CFA-induced inflammation groups (Po0.05, Figure 1F)
Summary
One of the most common pain conditions experienced by adults is chronic orofacial pain. Among the dysfunctions that affect the stomatognathic system, temporomandibular disorder (TMD) associated with myofascial pain is a usual cause for chronic orofacial pain development [1]. Preclinical and clinical studies have elucidated the direct relationship between TMD-induced pain with emotional alterations [2,3]. A consensus has formed regarding the need to clinically evaluate TMDs from both physical and psychological perspectives, and to consider both pharmacological and behavioral treatments [4]. This idea is not yet widely applied in clinical practice due to the lack of direct preclinical and clinical experimental evidence. The affective component of pain is mediated by circuits that are distinct from those mediating the sensorydiscriminative component [5] and research on neural mechanisms about emotional behavior in pain models can advance the knowledge on this line of research
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Schedule a callMore From: Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
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