Abstract
It is well known that emotions can interfere with the perception of physical pain, as well as with the development and maintenance of painful conditions. On the other hand, somatic pain can have significant consequences on an individual’s affective behavior. Indeed, pain is defined as a complex and multidimensional experience, which includes both sensory and emotional components, thus exhibiting the features of a highly subjective experience. Over the years, neural pathways involved in the modulation of the different components of pain have been identified, indicating the existence of medial and lateral pain systems, which, respectively, project from medial or lateral thalamic nuclei to reach distinct cortex regions relating to specific functions. However, owing to the limited information concerning how mood state and painful input affect each other, pain treatment is frequently unsatisfactory. Different neuromodulators, including endogenous neuropeptides, appear to be involved in pain-related emotion and in its affective influence on pain perception, thus playing key roles in vulnerability and clinical outcome. Hence, this review article focuses on evidence concerning the modulation of the sensory and affective dimensions of pain, with particular attention given to some selected neuropeptidergic system contributions.
Highlights
Research conducted over the last 30 years has highlighted that pain, regardless of its nociceptive or neuropathic origin, is a complex and multidimensional experience, incorporating sensory-discriminative, affective-motivational and cognitive-emotional components [1,2]
A specific anxiety and aggression behavior was observed in pre-proenkephalin deficient mice [63]. According to these results, selected peptide or non-peptide delta-opioid receptors (DORs) agonists are highly effective in countering negative emotional states [64,65,66]. These results suggest a dual usefulness of DOR agonists in chronic pain, for their antinociceptive efficacy and for their action in the control of negative emotional states associated with persistent pain [67]
Another significant correlation between corticotropin-releasing factor (CRF) and the opioid system has been observed as regards the descending nociceptive control circuitry. It seems that the excitability of the central amygdala (CeA) neurons projecting to the periaqueductal gray matter (PAG), is strictly dependent on the nociceptin-orphanin FQ (N/OFQ) effect and CRF presence [77], since the N/OFQ perfusion of CeAM-PAG neurons causes the inhibition of the descending pain pathway through CRFergic neuron hyperpolarization [77]
Summary
Research conducted over the last 30 years has highlighted that pain, regardless of its nociceptive or neuropathic origin, is a complex and multidimensional experience, incorporating sensory-discriminative, affective-motivational and cognitive-emotional components [1,2]. The lateral pain system projects from the lateral thalamic nuclei to the primary and secondary somatosensory cortices (SSC) [7] This latter circuitry is mainly involved in the sensory-discriminative aspects of pain [8], including the localization and discrimination of pain intensity. The most recent optogenetic studies have shown that the activation of the PFC prelimbic region reduces nociceptive withdrawal latencies, and decreases aversive and affective responses [10,11], producing strong antinociceptive effects These results are in agreement with other observations, suggesting that the inhibition of PFC projection to the nucleus accumbens (NAc) enhances pain sensitivity [9]. In the present review we focused our attention on evidence concerning the modulation of the sensory and affective dimensions of pain, with particular attention to the neuropeptidergic contribution in the aforementioned brain regions
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