The neural basis of footshock analgesia: The role of specific ventral medullary nuclei
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Mechanisms of placebo analgesia: A dual-process model informed by insights from cross-species comparisons
2018, Progress in NeurobiologyCitation Excerpt :While the specific role of endogenous cannabinoids within the amygdala in FCA is unclear, the amygdala is an important hub for generating FCA (Helmstetter, 1992; Helmstetter and Bellgowan, 1993) and relays signals to the PAG that serve to initiate descending pain control mechanisms (Finnegan et al., 2005; Millan, 2002). Within the brainstem, lesions of the RVM, dorsolateral PAG (dlPAG) or ventral/ventrolateral PAG (vPAG) can reduce FCA (Helmstetter and Tershner, 1994; Kinscheck et al., 1984; Watkins et al., 1983). Though all of these structures play a role in FCA, the neurochemical systems involved vary by region.
The dorsomedial hypothalamus mediates stress-induced hyperalgesia and is the source of the pronociceptive peptide cholecystokinin in the rostral ventromedial medulla
2013, NeuroscienceCitation Excerpt :Extreme stress can inhibit pain, producing “stress-induced analgesia,” whereas mild or prolonged stress often heightens pain, giving rise to “stress-induced hyperalgesia” (SIH). The rostral ventromedial medulla (RVM) is a brainstem region shown to be critical for some forms of stress-induced analgesia (Watkins et al., 1983; Butler and Finn, 2009), but has also been implicated in SIH (Imbe et al., 2006; Reynolds et al., 2011). The RVM integrates somatic information with influences from higher structures, and can facilitate nociception via activation of the pronociceptive “ON-cells” (Porreca et al., 2002; Heinricher and Ingram, 2008).
Selective ablation of mu-opioid receptor expressing neurons in the rostral ventromedial medulla attenuates stress-induced mechanical hypersensitivity
2011, Life SciencesCitation Excerpt :Specific classes of RVM neurons have been shown to either inhibit (off-cells) or facilitate (on-cells) nociceptive transmission (Fields et al., 1983, 1991). The contribution of the RVM to SIA has been demonstrated in conditioned fear paradigms, in which conditioned fear-induced analgesia can be blocked by inactivation or microinjection of specific mu-opioid receptor antagonists into the RVM (Fields, 2000; Foo and Helmstetter, 1999; Helmstetter and Tershner, 1994; Watkins and Mayer, 1982; Watkins et al., 1983). More recently, the RVM has been implicated in SIH.
Acute inflammation induces segmental, bilateral, supraspinally mediated opioid release in the rat spinal cord, as measured by μ-opioid receptor internalization
2009, NeuroscienceCitation Excerpt :An alternative possibility is that, in fact, noxious stimuli do not release enough endogenous opioids to overcome their degradation by peptidases and produce analgesia. If this is the case, then opioid release of physiological significance may require additional supraspinal signals caused by states like stress (Watkins et al., 1982, 1983, 1984). Indeed, early studies (El-Sobky et al., 1976; Grevert and Goldstein, 1978) found that systemic injections of naloxone did not change pain perception in humans, and intrathecal injections of naloxone did not change tail-flick responses in rats (Zorman et al., 1982).
The Brainstem and Nociceptive Modulation
2008, The Senses: A Comprehensive Reference