Figure 2 - uploaded by Armen N Akopian
Content may be subject to copyright.
Source publication
Surgical procedures lead to profound and sustained (up to 1–2 weeks) activation of the pituitary gland, resulting in changes in endocrine function. Questions remain on whether activation of the pituitary influences the threshold and development time-course of postoperative pain. To address these questions, we evaluated postoperative hypersensitivit...
Contexts in source publication
Context 1
... hypophysectomy substantially decreases gonadal hormone production, we separately evaluated roles of gonad-produced hormones on postoperative hypersensitivity in female and male rats. OVX lowers estradiol levels three-fold and testosterone to levels that are not detectable (Table 1). Besides gonadal hormone, OVX results in reduction of some pituitary hormones, such as serum PRL [35] (Table 1). Baseline (BL) thermal and mechanical nociception was not affected by OVX (Figure 2A and 2B). OVX rats did not differ from intact female rats (in estrous phase) in levels of thermal ( Figure 2A) and mechanical ( Figure 2B)postoperative hypersensitivity. For both OVX and intact female rats, postoperative hypersensitivity receded to almost pre- operated levels at 7 days post-surgery (Figure 2A and ...
Context 2
... hypophysectomy substantially decreases gonadal hormone production, we separately evaluated roles of gonad-produced hormones on postoperative hypersensitivity in female and male rats. OVX lowers estradiol levels three-fold and testosterone to levels that are not detectable (Table 1). Besides gonadal hormone, OVX results in reduction of some pituitary hormones, such as serum PRL [35] (Table 1). Baseline (BL) thermal and mechanical nociception was not affected by OVX (Figure 2A and 2B). OVX rats did not differ from intact female rats (in estrous phase) in levels of thermal ( Figure 2A) and mechanical ( Figure 2B)postoperative hypersensitivity. For both OVX and intact female rats, postoperative hypersensitivity receded to almost pre- operated levels at 7 days post-surgery (Figure 2A and ...
Context 3
... hypophysectomy substantially decreases gonadal hormone production, we separately evaluated roles of gonad-produced hormones on postoperative hypersensitivity in female and male rats. OVX lowers estradiol levels three-fold and testosterone to levels that are not detectable (Table 1). Besides gonadal hormone, OVX results in reduction of some pituitary hormones, such as serum PRL [35] (Table 1). Baseline (BL) thermal and mechanical nociception was not affected by OVX (Figure 2A and 2B). OVX rats did not differ from intact female rats (in estrous phase) in levels of thermal ( Figure 2A) and mechanical ( Figure 2B)postoperative hypersensitivity. For both OVX and intact female rats, postoperative hypersensitivity receded to almost pre- operated levels at 7 days post-surgery (Figure 2A and ...
Context 4
... hypophysectomy substantially decreases gonadal hormone production, we separately evaluated roles of gonad-produced hormones on postoperative hypersensitivity in female and male rats. OVX lowers estradiol levels three-fold and testosterone to levels that are not detectable (Table 1). Besides gonadal hormone, OVX results in reduction of some pituitary hormones, such as serum PRL [35] (Table 1). Baseline (BL) thermal and mechanical nociception was not affected by OVX (Figure 2A and 2B). OVX rats did not differ from intact female rats (in estrous phase) in levels of thermal ( Figure 2A) and mechanical ( Figure 2B)postoperative hypersensitivity. For both OVX and intact female rats, postoperative hypersensitivity receded to almost pre- operated levels at 7 days post-surgery (Figure 2A and ...
Similar publications
Gonadic deficiency and corticotherapy are important risk factors in the pathogenesis of osteoporosis. This study was outlined to assess the effects of combined orchidectomy (ORX) and corticosteroid (cortisol; CS) administration on bone remodeling and metabolism. Twenty-week-old male Swiss mice were randomized into four groups: either sham operated...
Citations
... However, the HPA axis does not show clear effects on pain conditions in which stress and inflammation are not present. For instance, hypophysectomy does not alter postoperative pain responses in females or males (Green et al., 2016). Surgery briefly upregulates ACTH (Srinivasan et al., 2011), but this does not enhance surgery-triggered inflammation. ...
Clinical and basic research on regulation of pituitary hormones, extra-pituitary release of these hormones, distribution of their receptors and cell signaling pathways recruited upon receptor binding suggests that pituitary hormones can regulate mechanisms of nociceptive transmission in multiple orofacial pain conditions. Moreover, many pituitary hormones either regulate glands that produce gonadal hormones (GnH) or are regulated by GnH. This implies that pituitary hormones may be involved in sex-dependent mechanisms of orofacial pain and could help explain why certain orofacial pain conditions are more prevalent in women than men. Overall, regulation of nociception by pituitary hormones is a relatively new and emerging area of pain research. The aims of this review article are to: (1) present an overview of clinical conditions leading to orofacial pain that are associated with alterations of serum pituitary hormone levels; (2) discuss proposed mechanisms of how pituitary hormones could regulate nociceptive transmission; and (3) outline how pituitary hormones could regulate nociception in a sex-specific fashion. Pituitary hormones are routinely used for hormonal replacement therapy, while both receptor antagonists and agonists are used to manage certain pathological conditions related to hormonal imbalance. Administration of these hormones may also have a place in the treatment of pain, including orofacial pain. Hence, understanding the involvement of pituitary hormones in orofacial pain, especially sex-dependent aspects of such pain, is essential to both optimize current therapies as well as provide novel and sex-specific pharmacology for a diversity of associated conditions.
Many clinical and preclinical studies report higher prevalence and severity of chronic pain in females. We used hyperalgesic priming with interleukin 6 (IL-6) priming and PGE2 as a second stimulus as a model for pain chronicity. Intraplantar IL-6 induced hypersensitivity was similar in magnitude and duration in both males and females, while both paw and intrathecal PGE2 hypersensitivity was more persistent in females. This difference in PGE2 response was dependent on both circulating estrogen and translation regulation signaling in the spinal cord. In males, the duration of hypersensitivity was regulated by testosterone. Since the prolactin receptor (Prlr) is regulated by reproductive hormones and is female-selectively activated in sensory neurons, we evaluated whether Prlr signaling contributes to hyperalgesic priming. Using DPRL, a competitive Prlr antagonist, and a mouse line with ablated Prlr in the Nav1.8 sensory neuronal population, we show that Prlr in sensory neurons is necessary for the development of hyperalgesic priming in female, but not male, mice. Overall, sex-specific mechanisms in the initiation and maintenance of chronic pain are regulated by the neuroendocrine system and, specifically, sensory neuronal Prlr signaling.
