1990
DOI: 10.1016/0006-8993(90)91512-f
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Effect of noxious somesthetic stimulation on the activity of neurons of the nucleus centralis of the amygdala

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Cited by 55 publications
(13 citation statements)
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“…In accordance with neuroadaptations described in the previous section, converging lines of evidence suggest that pain-induced levels of CRF modify the electrophysiological properties of nociceptive CeA neurons (Bernard, Huang, & Besson, 1990) to promote pain sensitization (Neugebauer, Li, Bird, & Han, 2004). Rats placed in a state of arthritic inflammatory pain exhibit increased CeA excitability that is alleviated by CRF1R antagonism (Ji & Neugebauer, 2007).…”
Section: Sensitization Of Pain-related Negative Affect In Addictionsupporting
confidence: 80%
“…In accordance with neuroadaptations described in the previous section, converging lines of evidence suggest that pain-induced levels of CRF modify the electrophysiological properties of nociceptive CeA neurons (Bernard, Huang, & Besson, 1990) to promote pain sensitization (Neugebauer, Li, Bird, & Han, 2004). Rats placed in a state of arthritic inflammatory pain exhibit increased CeA excitability that is alleviated by CRF1R antagonism (Ji & Neugebauer, 2007).…”
Section: Sensitization Of Pain-related Negative Affect In Addictionsupporting
confidence: 80%
“…The CeA is an autonomic-projecting region, which has been suggested to constitute a “visceromotor striatum” (Swanson and Petrovich 1998). Since both the jcBNST (Dong et al, 2000) and the CeA receive nociceptive information (Bernard and Besson 1990; Bernard et al 1990), changes in the excitability of the jcBNST in rats with history of morphine dependence are likely to contribute to the hyperalgesia observed in these rats. Allostatic adaptation of circuits involving the BNST and the CeA are expected to affect descending regulation of the periaqueductal gray matter (PAG) in the brainstem and its role in integrating nociceptive inputs arriving from the ascending pain pathways (Elman et al 2013; Hayes and Northoff 2012)…”
Section: Discussionmentioning
confidence: 99%
“…Strong evidence suggests that the neural substrates associated with addiction may also overlap with substrates of emotional aspects of nociceptive processing in areas such as the central amygdala (Neugebauer et al, 2004), cingulate cortex (Vogt, 2005), and nucleus accumbens (Gear and Levine, 1995; Barrot et al, 2002), where ascending pain pathways connect for processing the emotional components of pain perception. Specifically, pain-responsive neurons are abundant in the lateral part of the central amygdala (also known as the “nociceptive amygdala”; Bernard and Besson, 1990). As a potentially powerful negative motivational symptom, pain represents a subjective experience that can have a substantial influence on drug reinforcement, possibly facilitating the transition to drug addiction (Miller and Gold, 2007).…”
Section: Discussionmentioning
confidence: 99%