The Experts below are selected from a list of 21 Experts worldwide ranked by ideXlab platform
Edmund T. Rolls - One of the best experts on this subject based on the ideXlab platform.
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CHEMOSENSORY LEARNING AND MEMORY - Chemosensory learning and memory
Frontiers in systems neuroscience, 2012Co-Authors: Milagros Gallo, Edmund T. RollsAbstract:The aim of this issue is to present an updated view of present knowledge and questions raised in the rapidly expanding field of chemosensory (taste and olfactory) learning. Taste is a powerful primary (unlearned) reinforcer, and topics such as olfactory-taste and visual taste association learning are covered in this issue. But the reinforcing properties of taste can themselves be modified, for example, by post-ingestive consequences, for example, in taste aversion learning, and this type of learning is also covered in this issue. In fact, research on the chemosensory systems has played an important role in advancing knowledge of the brain mechanisms of learning and memory. A well-known example is conditioned taste aversion (CTA). Since the time it was discovered (Garcia et al., 1955), the unique nature of CTA presented a challenge to the contemporary learning theory, and CTA contributed to present theoretical views of learning. CTA learning also became a useful tool for researchers on the neural mechanisms of learning and memory. Jan Bures was a leader in research on the brain mechanisms of CTA in Europe for several decades. We would like to dedicate this special issue to Jan Bures, who passed away on August 24, 2012, in Prague. The field of chemosensory learning is greatly saddened by the news (http://www.ctalearning.com/announcements.asp). He, together with his wife Olga Buresova, was a pioneer during the seventies in applying reversible brain inactivation techniques in order to identify the specific role of the areas forming the CTA circuits. Among other findings, he discovered the critical role of the parabrachial area in taste-Visceral Signal association, and the relevance of cortico-pontine connections in taste processing (Bures et al., 1998). In addition to his outstanding scientific contributions, Jan was a wonderful colleague and mentor for us and many of the contributors to the present issue and we will never forget him. The papers forming this issue are representative of the long history and great development of the field thanks to the use of different species and a variety of technical and theoretical approaches. The widely ranging review by Yamamoto and Ueji (2011) of flavor learning including both learned food preferences and aversions, and the paper by Scott (2011) reviewing classic knowledge on the brain mechanisms of CTA, highlight the advances in the field during the last decades. Wider and more complex brain systems than previously thought contribute to flavor learning, with age-dependent interactions between areas such as the insular cortex, amygdala, hippocampal, thalamic, and reward systems (Gamiz and Gallo, 2011). The evidence reported by Neseliler et al. (2011) using an in vivo genetically modified rodent model of hypercholinergic innervation is an example of the value of new approaches to support the hypothesis linking acetylcholine and CTA. As Guzman-Ramos and Bermudez-Rattoni (2011) describe, major research advances have been made on the cascade of molecular changes involved in the consolidation of CTA taking place during the post-acquisition period. Remarkable progress has also been made in the field of food preferences. de Araujo (2011) provides a review that includes data obtained both in rodents and Drosophila on the role of taste and energy-sensing systems receiving gastrointestinal and post-absorptive Signals in the formation of long-lasting preferences mediated by dopamine release. The elegant experimental work using a variety of techniques reported by Oliveira-Maia et al. (2012) adds evidence on this topic demonstrating the role of the insular cortex in detecting the postingestive effects of sucrose intake. Closely linked to taste learning in detecting chemical molecules is olfactory learning. As Sandoz (2011) shows in his review, the honeybee has been a model for applying behavioral, neurophysiological and neuroanatomical techniques to research on olfactory learning. Two separate models of the role in olfactory learning of the rat olfactory bulb (Auffarth et al., 2011) and the human glomerulus (Schaefer and Margrie, 2012) are presented. Finally, Rolls (2011) reviews evidence from primates including humans on the value of taste as a primary reinforcer and the role of the orbitofrontal cortex in building olfactory-taste, and visual-taste associations. He also shows how top–down cognition and attention influence taste and olfactory processing in ways that must involve learning, and also considers the cortical mechanisms involved in taking decisions about olfactory and taste stimuli.
Milagros Gallo - One of the best experts on this subject based on the ideXlab platform.
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CHEMOSENSORY LEARNING AND MEMORY - Chemosensory learning and memory
Frontiers in systems neuroscience, 2012Co-Authors: Milagros Gallo, Edmund T. RollsAbstract:The aim of this issue is to present an updated view of present knowledge and questions raised in the rapidly expanding field of chemosensory (taste and olfactory) learning. Taste is a powerful primary (unlearned) reinforcer, and topics such as olfactory-taste and visual taste association learning are covered in this issue. But the reinforcing properties of taste can themselves be modified, for example, by post-ingestive consequences, for example, in taste aversion learning, and this type of learning is also covered in this issue. In fact, research on the chemosensory systems has played an important role in advancing knowledge of the brain mechanisms of learning and memory. A well-known example is conditioned taste aversion (CTA). Since the time it was discovered (Garcia et al., 1955), the unique nature of CTA presented a challenge to the contemporary learning theory, and CTA contributed to present theoretical views of learning. CTA learning also became a useful tool for researchers on the neural mechanisms of learning and memory. Jan Bures was a leader in research on the brain mechanisms of CTA in Europe for several decades. We would like to dedicate this special issue to Jan Bures, who passed away on August 24, 2012, in Prague. The field of chemosensory learning is greatly saddened by the news (http://www.ctalearning.com/announcements.asp). He, together with his wife Olga Buresova, was a pioneer during the seventies in applying reversible brain inactivation techniques in order to identify the specific role of the areas forming the CTA circuits. Among other findings, he discovered the critical role of the parabrachial area in taste-Visceral Signal association, and the relevance of cortico-pontine connections in taste processing (Bures et al., 1998). In addition to his outstanding scientific contributions, Jan was a wonderful colleague and mentor for us and many of the contributors to the present issue and we will never forget him. The papers forming this issue are representative of the long history and great development of the field thanks to the use of different species and a variety of technical and theoretical approaches. The widely ranging review by Yamamoto and Ueji (2011) of flavor learning including both learned food preferences and aversions, and the paper by Scott (2011) reviewing classic knowledge on the brain mechanisms of CTA, highlight the advances in the field during the last decades. Wider and more complex brain systems than previously thought contribute to flavor learning, with age-dependent interactions between areas such as the insular cortex, amygdala, hippocampal, thalamic, and reward systems (Gamiz and Gallo, 2011). The evidence reported by Neseliler et al. (2011) using an in vivo genetically modified rodent model of hypercholinergic innervation is an example of the value of new approaches to support the hypothesis linking acetylcholine and CTA. As Guzman-Ramos and Bermudez-Rattoni (2011) describe, major research advances have been made on the cascade of molecular changes involved in the consolidation of CTA taking place during the post-acquisition period. Remarkable progress has also been made in the field of food preferences. de Araujo (2011) provides a review that includes data obtained both in rodents and Drosophila on the role of taste and energy-sensing systems receiving gastrointestinal and post-absorptive Signals in the formation of long-lasting preferences mediated by dopamine release. The elegant experimental work using a variety of techniques reported by Oliveira-Maia et al. (2012) adds evidence on this topic demonstrating the role of the insular cortex in detecting the postingestive effects of sucrose intake. Closely linked to taste learning in detecting chemical molecules is olfactory learning. As Sandoz (2011) shows in his review, the honeybee has been a model for applying behavioral, neurophysiological and neuroanatomical techniques to research on olfactory learning. Two separate models of the role in olfactory learning of the rat olfactory bulb (Auffarth et al., 2011) and the human glomerulus (Schaefer and Margrie, 2012) are presented. Finally, Rolls (2011) reviews evidence from primates including humans on the value of taste as a primary reinforcer and the role of the orbitofrontal cortex in building olfactory-taste, and visual-taste associations. He also shows how top–down cognition and attention influence taste and olfactory processing in ways that must involve learning, and also considers the cortical mechanisms involved in taking decisions about olfactory and taste stimuli.
Richard J. Traub - One of the best experts on this subject based on the ideXlab platform.
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Spinal estrogen receptor alpha mediates estradiol-induced pronociception in a Visceral pain model in the rat
Pain, 2011Co-Authors: Bin Tang, Richard J. TraubAbstract:We previously reported that 17β-estradiol (E2) is pronociceptive in a Visceral pain model in the rat. Subcutaneously (s.c.) administered E2 reversed the decrease in the colorectal distention (CRD)-evoked visceromotor response produced by ovariectomy (OVx) and CRD-induced nociceptive responses were greater in proestrous rats compared with met/diestrous rats. The site of action, the type of estrogen receptors activated, and the possible intracellular Signaling pathway involved are yet to be established. In the present study, intrathecal (i.t.) E2 administered to OVx rats mimicked the effects of s.c. E2, suggesting that spinal estrogen receptors are involved. This is further supported by the observations that the anti-estrogen ICI 182,780 injected i.t. in intact female rats significantly decreased the visceromotor response to CRD, the response of colonic afferents was not affected by OVx, and colonic afferents did not label for estrogen receptor α (ERα). The ERα selective agonist, 4,4',4''-[4-propyl-(1H)-pyrazole-1,3,5-triyl]tris-phenol (PPT; s.c. or i.t.) facilitated the visceromotor response similar to E2, suggesting ERα activation is involved in mediating the pronociceptive effect of E2. PPT (s.c. or i.t.) increased the response of spinal dorsal horn neurons to CRD, indicating a spinal site of action. In addition, s.c. E2 or PPT increased CRD-induced spinal extracellular Signal-regulated kinase (ERK) phosphorylation that was not observed in OVx rats and a mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitor blocked facilitation of the visceromotor response by PPT. Taken together, the present study demonstrates that spinal ERα mediates the pronociceptive effect of E2 on Visceral Signal processing through activation of the MAPK pathway.
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Modulatory effects of estrogen and progesterone on colorectal hyperalgesia in the rat.
Pain, 2005Co-Authors: Bin Tang, Richard J. TraubAbstract:Abstract The contribution of estrogen and progesterone to colorectal hyperalgesia was examined in female rats. The electromyogram recorded from the abdominal wall (visceromotor response, vmr) and the discharge of lumbosacral dorsal horn neurons to colorectal distention (CRD) were measured in intact female, ovariectomized (OVx) and estradiol replaced OVx (E2; 50 μg, 48 h) rats with and without colonic inflammation. Colorectal hyperalgesia was transient in intact rats, but persisted at least 4 h in E2 and OVx rats. The magnitude of hyperalgesia in E2 rats was greater than OVx which was greater than intact rats. Dorsal horn neurons that responded to CRD with an Abrupt (on and off with stimulus) excitatory discharge showed similar sensitivity to estradiol as the vmr following colonic inflammation. In contrast, inflammation did not increase the magnitude of response of excitatory neurons with sustained afterdischarges in any of the treatment groups. Intact female rats have a comparable plasma estrogen concentration to E2 rats, suggesting the difference in responses may have been due to antinociceptive effects of progesterone. This was tested by administering E2± progesterone (1 mg) and measuring the vmr. Progesterone reduced the facilitation of the vmr produced by E2 before and following colonic inflammation. The present study suggests that estrogen replacement enhances Visceral Signal processing following colonic inflammation. Furthermore, progesterone may counteract the effects of estrogen on colorectal sensitivity.
Bin Tang - One of the best experts on this subject based on the ideXlab platform.
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Spinal estrogen receptor alpha mediates estradiol-induced pronociception in a Visceral pain model in the rat
Pain, 2011Co-Authors: Bin Tang, Richard J. TraubAbstract:We previously reported that 17β-estradiol (E2) is pronociceptive in a Visceral pain model in the rat. Subcutaneously (s.c.) administered E2 reversed the decrease in the colorectal distention (CRD)-evoked visceromotor response produced by ovariectomy (OVx) and CRD-induced nociceptive responses were greater in proestrous rats compared with met/diestrous rats. The site of action, the type of estrogen receptors activated, and the possible intracellular Signaling pathway involved are yet to be established. In the present study, intrathecal (i.t.) E2 administered to OVx rats mimicked the effects of s.c. E2, suggesting that spinal estrogen receptors are involved. This is further supported by the observations that the anti-estrogen ICI 182,780 injected i.t. in intact female rats significantly decreased the visceromotor response to CRD, the response of colonic afferents was not affected by OVx, and colonic afferents did not label for estrogen receptor α (ERα). The ERα selective agonist, 4,4',4''-[4-propyl-(1H)-pyrazole-1,3,5-triyl]tris-phenol (PPT; s.c. or i.t.) facilitated the visceromotor response similar to E2, suggesting ERα activation is involved in mediating the pronociceptive effect of E2. PPT (s.c. or i.t.) increased the response of spinal dorsal horn neurons to CRD, indicating a spinal site of action. In addition, s.c. E2 or PPT increased CRD-induced spinal extracellular Signal-regulated kinase (ERK) phosphorylation that was not observed in OVx rats and a mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitor blocked facilitation of the visceromotor response by PPT. Taken together, the present study demonstrates that spinal ERα mediates the pronociceptive effect of E2 on Visceral Signal processing through activation of the MAPK pathway.
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Modulatory effects of estrogen and progesterone on colorectal hyperalgesia in the rat.
Pain, 2005Co-Authors: Bin Tang, Richard J. TraubAbstract:Abstract The contribution of estrogen and progesterone to colorectal hyperalgesia was examined in female rats. The electromyogram recorded from the abdominal wall (visceromotor response, vmr) and the discharge of lumbosacral dorsal horn neurons to colorectal distention (CRD) were measured in intact female, ovariectomized (OVx) and estradiol replaced OVx (E2; 50 μg, 48 h) rats with and without colonic inflammation. Colorectal hyperalgesia was transient in intact rats, but persisted at least 4 h in E2 and OVx rats. The magnitude of hyperalgesia in E2 rats was greater than OVx which was greater than intact rats. Dorsal horn neurons that responded to CRD with an Abrupt (on and off with stimulus) excitatory discharge showed similar sensitivity to estradiol as the vmr following colonic inflammation. In contrast, inflammation did not increase the magnitude of response of excitatory neurons with sustained afterdischarges in any of the treatment groups. Intact female rats have a comparable plasma estrogen concentration to E2 rats, suggesting the difference in responses may have been due to antinociceptive effects of progesterone. This was tested by administering E2± progesterone (1 mg) and measuring the vmr. Progesterone reduced the facilitation of the vmr produced by E2 before and following colonic inflammation. The present study suggests that estrogen replacement enhances Visceral Signal processing following colonic inflammation. Furthermore, progesterone may counteract the effects of estrogen on colorectal sensitivity.
Suzanne Higgs - One of the best experts on this subject based on the ideXlab platform.
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Aversive Viscerally referred states and thirst accompanying the sating of hunger motivation by rapid digestion of glucosaccharides
Physiology & Behavior, 2010Co-Authors: David A Booth, Gemma O’leary, Suzanne HiggsAbstract:Associative conditioning of satiety indicates that concentrated maltodextrin (cMD) may induce a mildly aversive Visceral Signal within 20 min of its ingestion, as well as satiating normally. Individuals' awareness of this adverse state was tested on ratings of statistically distinct descriptions of factors liable to suppress hunger, whether distressing or comfortably satisfying. Wanted amount of a food and the pleasantness of eating it correlated highly for each of five foods, once again refuting the widespread presumption that “pleasant” refers to sensory pleasure; hence, as in previous reports, suppression of hunger was measured as a reduction of the averaged pleasantness of functionally related foods. At 20 min after the start of ingestion of a small meal on a near-empty stomach, cMD reliably reduced hunger. The greatest influence on hunger, besides normal sating, was thirst, but there were also tendencies to nausea and bloat, although all less than after a full sized meal. Visceral processes shortly after a meal can create dissociable conscious states, only one of which is satiety for food.
