Evaluation of reward from pain relief (original) (raw)
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Hedonic and motivational responses to food reward are unchanged in rats with neuropathic pain
Pain, 2016
Rewards influence responses to acute painful stimuli, but the relationship of chronic pain to hedonic or motivational aspects of reward is not well understood. We independently evaluated hedonic qualities of sweet or bitter tastants and motivation to seek food reward in rats with experimental neuropathic pain induced by L5/6 spinal nerve ligation. Hedonic response was measured by implantation of intraoral catheters to allow passive delivery of liquid solutions, and “liking/disliking” responses were scored according to a facial reactivity scale. Spinal nerve ligation rats did not differ from controls in either “liking” or “disliking” reactions to intraoral sucrose or quinine, respectively, at postsurgery day 21, suggesting no differences in perceived hedonic value of sweet or bitter tastants. To assess possible motivational deficits during acute and chronic pain, we used fixed- and progressive-ratio response paradigms of sucrose pellet presentation in rats with transient inflammatory...
Behavioral Pharmacology of Pain
Current topics in behavioral neurosciences, 2014
Behavioral methods are extensively used in pain research. Rodent modeling tends to rely on evoked responses but there is a growing interest in behavioral readouts that may capture elements of ongoing pain and disability, reflecting the major clinical signs and symptoms. Clinically, analgesics show greater efficacy in acute pain after standard surgery than in chronic conditions but are never completely effective on a population basis. In contrast, experimental pharmacological studies in rodents often demonstrate full efficacy, but there is variability in sensitivity between models and readouts. Full efficacy is rarely seen when more complex or multiple readouts are used to quantify behavior, especially after acute surgery or in studies of clinical pain in animals. Models with excellent sensitivity for a particular drug class exist and are suitable for screening mechanistically similar drugs. However, if used to compare drugs with different modes of action or to predict magnitude of clinical efficacy, these models will be misleading. Effective use of behavioral pharmacology in pain research is thus dependent on selection and validation of the best models for the purpose.
Proceedings of the National Academy of Sciences, 2012
Relief of pain is rewarding. Using a model of experimental postsurgical pain we show that blockade of afferent input from the injury with local anesthetic elicits conditioned place preference, activates ventral tegmental dopaminergic cells, and increases dopamine release in the nucleus accumbens. Importantly, place preference is associated with increased activity in midbrain dopaminergic neurons and blocked by dopamine antagonists injected into the nucleus accumbens. The data directly support the hypothesis that relief of pain produces negative reinforcement through activation of the mesolimbic reward-valuation circuitry. motivated behavior | incision | in vivo microdialysis | immunohistochemistry | ventral tegmental area
Reward Circuitry Plasticity in Pain Perception and Modulation
Frontiers in pharmacology, 2017
Although pain is a widely known phenomenon and an important clinical symptom that occurs in numerous diseases, its mechanisms are still barely understood. Owing to the scarce information concerning its pathophysiology, particularly what is involved in the transition from an acute state to a chronic condition, pain treatment is frequently unsatisfactory, therefore contributing to the amplification of the chronic pain burden. In fact, pain is an extremely complex experience that demands the recruitment of an intricate set of central nervous system components. This includes cortical and subcortical areas involved in interpretation of the general characteristics of noxious stimuli. It also comprises neural circuits that process the motivational-affective dimension of pain. Hence, the reward circuitry represents a vital element for pain experience and modulation. This review article focuses on the interpretation of the extensive data available connecting the major components of the rewar...
Perspective Nociception, Pain, Negative Moods, and Behavior Selection
Recent neuroimaging studies suggest that the brain adapts with pain, as well as imparts risk for developing chronic pain. Within this context, we revisit the concepts for nociception, acute and chronic pain, and negative moods relative to behavior selection. We redefine nociception as the mechanism protecting the organism from injury, while acute pain as failure of avoidant behavior, and a mesolimbic threshold process that gates the transformation of nociceptive activity to conscious pain. Adaptations in this threshold process are envisioned to be critical for development of chronic pain. We deconstruct chronic pain into four distinct phases, each with specific mechanisms, and outline current state of knowledge regarding these mechanisms: the limbic brain imparting risk, and the mesolimbic learning processes reorganizing the neocortex into a chronic pain state. Moreover, pain and negative moods are envisioned as a continuum of aversive behavioral learning, which enhance survival by protecting against threats. Introduction Classically, pain has been conceptualized from the narrow viewpoint of nociceptive processing. The field has generated extensive knowledge regarding the transduction, transmission, and spinal cord processing of nociceptive signals related to acute and chronic pain; similarly, animal studies have unraveled properties of primary afferents, their spinal cord circuitry, and related specialized pathways in the brain that mediate pain-like behavior. Post-nerve injury reorganization of nociceptive afferents and spinal cord circuitry, in particular, has been extensively characterized in rodent models, with the tacit assumption that acute and chronic pain is best understood through this circuitry. In parallel, human brain imaging studies have identified nociceptive brain circuits. However, recent human brain imaging studies examining a variety of pain conditions indicate that the brain plays an active role in acute and clinical pain perception (Figure 1), leading to a heated debate regarding the respective importance of peripheral afferents versus the brain's interpretation of afferent signals. Here we review implications of these competing concepts in light of emerging evidence. The standard definition of pain emphasizes its subjectivity. Subjectivity, in turn, implies a conscious experience. A central goal of our perspective is to revise the understanding of conscious pain perception by incorporating nociception, acute and chronic pain, and negative moods into the unifying framework of behavior selection, where behavioral selections encompass the full range of possible actions for stimuli, whether internal or external, conscious or subconscious, and voluntary or involuntary. This viewpoint calls for a re-examination of the definitions we have inherited, because their narrow meanings have limited the types of questions posed within the field. Furthermore, we will introduce a novel interpretation of supraspinal processing
Applied Animal Behaviour Science, 2014
The understanding and recognition of pain in laboratory rats and mice has advanced considerably in recent times. However, there is evidence that despite these advances, analgesics are still relatively underutilised in these species. One possible contributing influence to this is the difficulty in assessing pain reliably and objectively in these prey species. This review presents the current scientific knowledge on behavioural methods of pain assessment in laboratory rats and mice. The focus is on measures of spontaneous behaviour, since these will find greatest utility in clinical pain management.
Proceedings of the National Academy of Sciences of the United States of America, 2001
Numerous human and animal studies indirectly implicate neurons in the anterior cingulate cortex (ACC) in the encoding of the affective consequences of nociceptor stimulation. No causal evidence, however, has been put forth linking the ACC specifically to this function. Using a rodent pain assay that combines the hindpaw formalin model with the place-conditioning paradigm, we measured a learned behavior that directly reflects the affective component of pain in the rat (formalin-induced conditioned place avoidance) concomitantly with ''acute'' formalin-induced nociceptive behaviors (paw lifting, licking, and flinching) that reflect the intensity and localization of the nociceptive stimulus. Destruction of neurons originating from the rostral, but not caudal, ACC reduced formalin-induced conditioned place avoidance without reducing acute pain-related behaviors. These results provide evidence indicating that neurons in the ACC are necessary for the ''aversiveness'' of nociceptor stimulation.
Behavioral neuroscience of psychological pain
Neuroscience and biobehavioral reviews, 2015
Pain is a common word used to refer to a wide range of physical and mental states sharing hedonic aversive value. Three types of pain are distinguished in this article: Physical pain, an aversive state related to actual or potential injury and disease; social pain, an aversive emotion associated to social exclusion; and psychological pain, a negative emotion induced by incentive loss. This review centers on psychological pain as studied in nonhuman animals. After covering issues of terminology, the article briefly discusses the daily-life significance of psychological pain and then centers on a discussion of the results originating from two procedures involving incentive loss: successive negative contrast-the unexpected devaluation of a reward-and appetitive extinction-the unexpected omission of a reward. The evidence reviewed points to substantial commonalities, but also some differences and interactions between physical and psychological pains. This evidence is discussed in relati...
Pain, 2014
Preclinical assessment of pain has increasingly explored operant methods that may allow behavioral assessment of ongoing pain. In animals with incisional injury, peripheral nerve block produces conditioned place preference (CPP) and activates the mesolimbic dopaminergic reward pathway. We hypothesized that activation of this circuit could serve as a neurochemical output measure of relief of ongoing pain. Medications commonly used clinically, including gabapentin and nonsteroidal anti-inflammatory drugs (NSAIDs), were evaluated in models of post-surgical (1 day after incision) or neuropathic (14 days after spinal nerve ligation [SNL]) pain to determine whether the clinical efficacy profile of these drugs in these pain conditions was reflected by extracellular dopamine (DA) release in the nucleus accumbens (NAc) shell. Microdialysis was performed in awake rats. Basal DA levels were not significantly different between experimental groups, and no significant treatment effects were seen in sham-operated animals. Consistent with clinical observation, spinal clonidine produced CPP and produced a dose-related increase in net NAc DA release in SNL rats. Gabapentin, commonly used to treat neuropathic pain, produced increased NAc DA in rats with SNL but not in animals with incisional, injury. In contrast, ketorolac or naproxen produced increased NAc DA in animals with incisional but not neuropathic pain. Increased extracellular NAc DA release was consistent with CPP and was observed selectively with treatments commonly used clinically for post-surgical or neuropathic pain. Evaluation of NAc DA efflux in animal pain models may represent an objective neurochemical assay that may serve as a biomarker of efficacy for novel pain-relieving mechanisms.