The Experts below are selected from a list of 1125 Experts worldwide ranked by ideXlab platform
Kobi Rosenblum - One of the best experts on this subject based on the ideXlab platform.
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Encoding of Conditioned Taste Aversion in Cortico-Amygdala Circuits
Cell reports, 2018Co-Authors: Karen Lavi, Kobi Rosenblum, Gilad A. Jacobson, Andreas LüthiAbstract:Avoidance of potentially toxic food by means of conditioned taste aversion is critical for survival of many animals. However, the underlying neuronal mechanisms are poorly understood. Here, using two-photon calcium imaging of defined Gustatory Cortex neurons in vivo, we show that conditioned taste aversion dynamically shifts neuronal population coding by stimulus-specific recruitment of neurons that project to the basolateral amygdala.
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mAChR-dependent decrease in proteasome activity in the Gustatory Cortex is necessary for novel taste learning.
Neurobiology of learning and memory, 2016Co-Authors: Tali Rosenberg, Alina Elkobi, Kobi RosenblumAbstract:Regulation of protein degradation via the ubiquitin proteasome system is crucial for normal learning and synaptic plasticity processes. While some studies reveal that increased proteasome degradation is necessary for different types of learning, others suggest the proteasome to be a negative regulator of plasticity. We aim to understand the molecular and cellular processes taking place in the Gustatory Cortex (GC), which underlie appetitive and aversive forms of taste learning. Previously, we have shown that N-methyl d-aspartic acid receptor (NMDAR)-dependent upregulation of proteasome activity 4h after novel taste learning is necessary for the association of novel taste with malaise and formation of conditioned taste aversion (CTA). Here, we first identify a correlative increase in proteasome activity in the GC immediately after novel taste learning and study the upstream and downstream effectors of this modulated proteasome activity. Interestingly, proteasome-mediated degradation was reduced in the GC, 20min after novel taste consumption in a muscarinic acetylcholine receptor (mAChR)-dependent and NMDAR-independent manner. This reduction in protein degradation led to an increased amount of p70 S6 kinase (p70S6k), which was abolished in the presence of mAChR antagonist scopolamine. Infusion of lactacystin, a proteasome inhibitor, to the GC precluded the amnestic effect of scopolamine. This study shows for the first time that following novel taste learning there is a cortical, mAChR-dependent reduced proteasome activity that enables the memory of taste familiarity. Moreover, inhibition of degradation in the GC attenuates novel taste learning and of p70 S6 kinase correlative increased expression. These results shed light on the complex regulation of protein synthesis and degradation machineries in the Cortex following novel taste experience.
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Fluid consumption and taste novelty determines transcription temporal dynamics in the Gustatory Cortex
Molecular Brain, 2016Co-Authors: Sharon Inberg, Eyal Jacob, Alina Elkobi, Efrat Edry, Akiva Rappaport, T. Ian Simpson, J. Douglas Armstrong, Metsada Pasmanik-chor, Noam Shomron, Kobi RosenblumAbstract:BackgroundNovel taste memories, critical for animal survival, are consolidated to form long term memories which are dependent on translation regulation in the Gustatory Cortex (GC) hours following acquisition. However, the role of transcription regulation in the process is unknown.ResultsHere, we report that transcription in the GC is necessary for taste learning in rats, and that drinking and its consequences, as well as the novel taste experience, affect transcription in the GC during taste memory consolidation. We show differential effects of learning on temporal dynamics in set of genes in the GC, including Arc/Arg3.1, known to regulate the homeostasis of excitatory synapses.ConclusionsWe demonstrate that in taste learning, transcription programs were activated following the physiological responses (i.e., fluid consumption following a water restriction regime, reward, arousal of the animal, etc.) and the specific information about a given taste (i.e., taste novelty). Moreover, the cortical differential prolonged kinetics of mRNA following novel versus familiar taste learning may represent additional novelty related molecular response, where not only the total amount, but also the temporal dynamics of transcription is modulated by sensory experience of novel information.
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Fluid consumption and taste novelty determines transcription temporal dynamics in the Gustatory Cortex
Molecular brain, 2016Co-Authors: Sharon Inberg, Eyal Jacob, Alina Elkobi, Efrat Edry, Akiva Rappaport, T. Ian Simpson, J. Douglas Armstrong, Metsada Pasmanik-chor, Noam Shomron, Kobi RosenblumAbstract:Background Novel taste memories, critical for animal survival, are consolidated to form long term memories which are dependent on translation regulation in the Gustatory Cortex (GC) hours following acquisition. However, the role of transcription regulation in the process is unknown.
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NMDAR-dependent proteasome activity in the Gustatory Cortex is necessary for conditioned taste aversion.
Neurobiology of learning and memory, 2016Co-Authors: Tali Rosenberg, Alina Elkobi, Daniela C. Dieterich, Kobi RosenblumAbstract:Taste information is processed in different brain structures in the mammalian brain, including the Gustatory Cortex (GC), which resides within the insular Cortex. N-methyl-d-aspartate receptor (NMDAR) activity in the GC is necessary for the acquisition of conditioned taste aversion (CTA) but not positive novel taste learning. Previous studies have shown that taste memory consolidation requires intact protein synthesis in the GC. In addition, the direct involvement of translation initiation and elongation factors was documented in the GC during taste learning. However, protein expression is defined by protein synthesis, degradation, and localization. Protein degradation is critical for the consolidation and reconsolidation of other forms of learning, such as fear learning and addiction behavior, but its role in cortical-dependent learning is not clear. Here, we show for the first time that proteasome activity is specifically increased in the GC 4h following experiencing of a novel taste. This increase in proteasome activity was abolished by local administration to the GC of the NMDA antagonist, APV, as well as a CaMKII inhibitor, at the time of acquisition. In addition, local application of lactacystin, a proteasome inhibitor, resulted in impaired CTA, but not novel taste learning. These results suggest that NMDAR-dependent proteasome activity in the GC participates in the association process between novel taste experience and negative visceral sensation.
Alan C. Spector - One of the best experts on this subject based on the ideXlab platform.
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Chemospecific deficits in taste sensitivity following bilateral or right hemispheric Gustatory Cortex lesions in rats
The Journal of comparative neurology, 2020Co-Authors: Michelle B. Bales, Alan C. SpectorAbstract:Our prior studies showed bilateral Gustatory Cortex (GC) lesions significantly impair taste sensitivity to salts (NaCl and KCl) and quinine ("bitter") but not to sucrose ("sweet"). The range of qualitative tastants tested here has been extended in a theoretically relevant way to include the maltodextrin, Maltrin, a preferred stimulus by rats thought to represent a unique taste quality, and the "sour" stimulus citric acid; NaCl was also included as a positive control. Male rats (Sprague-Dawley) with histologically confirmed neurotoxin-induced bilateral (BGCX, n = 13), or right (RGCX, n = 13) or left (LGCX, n = 9) unilateral GC lesions and sham-operated controls (SHAM, n = 16) were trained to discriminate a tastant from water in an operant two-response detection task. A mapping system was used to determine placement, size, and symmetry (when bilateral) of the lesion. BGCX significantly impaired taste sensitivity to NaCl, as expected, but not to Maltrin or citric acid, emulating our prior results with sucrose. However, in the case of citric acid, there was some disruption in performance at higher concentrations. Interestingly, RGCX, but not LGCX, also significantly impaired taste sensitivity, but only to NaCl, suggesting some degree of lateralized function. Taken together with our prior findings, extensive bilateral lesions in GC do not disrupt basic taste signal detection to all taste stimuli uniformly. Moreover, GC lesions do not preclude the ability of rats to learn and perform the task, clearly demonstrating that, in its absence, other brain regions are able to maintain sensory-discriminative taste processing, albeit with attenuated sensitivity for select stimuli.
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Extensive Gustatory Cortex Lesions Significantly Impair Taste Sensitivity to KCl and Quinine but Not to Sucrose in Rats.
PloS one, 2015Co-Authors: Michelle B. Bales, Lindsey A. Schier, Ginger D. Blonde, Alan C. SpectorAbstract:Recently, we reported that large bilateral Gustatory Cortex (GC) lesions significantly impair taste sensitivity to salts in rats. Here we extended the tastants examined to include sucrose and quinine in rats with ibotenic acid-induced lesions in GC (GCX) and in sham-operated controls (SHAM). Presurgically, immediately after drinking NaCl, rats received a LiCl or saline injection (i.p.), but postsurgical tests indicated a weak conditioned taste aversion (CTA) even in controls. The rats were then trained and tested in gustometers to discriminate a tastant from water in a two-response operant taste detection task. Psychometric functions were derived for sucrose, KCl, and quinine. Our mapping system was used to determine placement, size, and symmetry of the lesions (~91% GC damage on average). For KCl, there was a significant rightward shift (ΔEC50 = 0.57 log10 units; p
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extensive Gustatory Cortex lesions significantly impair taste sensitivity to kcl and quinine but not to sucrose in rats
PLOS ONE, 2015Co-Authors: Michelle B. Bales, Lindsey A. Schier, Ginger D. Blonde, Alan C. SpectorAbstract:Recently, we reported that large bilateral Gustatory Cortex (GC) lesions significantly impair taste sensitivity to salts in rats. Here we extended the tastants examined to include sucrose and quinine in rats with ibotenic acid-induced lesions in GC (GCX) and in sham-operated controls (SHAM). Presurgically, immediately after drinking NaCl, rats received a LiCl or saline injection (i.p.), but postsurgical tests indicated a weak conditioned taste aversion (CTA) even in controls. The rats were then trained and tested in gustometers to discriminate a tastant from water in a two-response operant taste detection task. Psychometric functions were derived for sucrose, KCl, and quinine. Our mapping system was used to determine placement, size, and symmetry of the lesions (~91% GC damage on average). For KCl, there was a significant rightward shift (ΔEC50 = 0.57 log10 units; p<0.001) in the GCX psychometric function relative to SHAM, replicating our prior work. There was also a significant lesion-induced impairment (ΔEC50 = 0.41 log10 units; p = 0.006) in quinine sensitivity. Surprisingly, taste sensitivity to sucrose was unaffected by the extensive lesions and was comparable between GCX and SHAM rats. The fact that such large bilateral GC lesions did not shift sucrose psychometric functions relative to SHAM, but did significantly compromise quinine and KCl sensitivity suggests that the neural circuits responsible for the detection of specific taste stimuli are partially dissociable. Lesion-induced impairments were observed in expression of a postsurgical CTA to a maltodextrin solution as assessed in a taste-oriented brief-access test, but were not reflected in a longer term 46-h two-bottle test. Thus, deficits observed in rats after extensive damage to the GC are also dependent on the test used to assess taste function. In conclusion, the degree to which the GC is necessary for the maintenance of normal taste detectability apparently depends on the chemical and/or perceptual features of the stimulus.
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Unconditioned oromotor taste reactivity elicited by sucrose and quinine is unaffected by extensive bilateral damage to the Gustatory zone of the insular Cortex in rats
Brain research, 2014Co-Authors: Camille Tessitore King, Ginger D. Blonde, Koji Hashimoto, Alan C. SpectorAbstract:Abstract Rats display stereotypical oromotor and somatic responses to small volumes of intraorally infused taste solutions. These behaviors, known as taste reactivity, are categorized by their association with ingestion or rejection and are thought to reflect the palatability of the stimulus. Because supracollicular decerebrate rats display normal taste reactivity responses, it would appear that forebrain structures are not necessary for generating them. However, because moving the plane of transection rostrally, or damaging or manipulating specific ventral forebrain sites disrupts normal taste reactivity behavior, lesions of the Gustatory Cortex, a region that has been suggested to be involved with palatability processing, may do the same. In the current study, rats received two injections of either ibotenic acid ( N =12) or vehicle ( N =8), targeting the conventionally defined Gustatory Cortex in each hemisphere, and were implanted with intraoral cannulae. Following recovery, their responses to intraoral infusions (0.23 ml in 1 min) of d H 2 O, sucrose (1.0 M and 0.1 M), and quinine hydrochloride (3 mM and 0.3 mM) were video recorded. Analysis of brains with sufficient bilateral lesions ( N =10) revealed that, on average, approximately 94% of the Gustatory Cortex was destroyed. These extensive bilateral lesions had no significant effect on taste reactivity; the numbers of ingestive and aversive responses to sucrose and quinine were similar between groups. Though these findings do not rule out involvement of the Gustatory Cortex in palatability processing, they make evident that the region of insular Cortex destroyed is not necessary for the normal expression of unconditioned affective behavioral responses to taste stimuli.
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Restoration of quinine-stimulated Fos-immunoreactive neurons in the central nucleus of the amygdala and Gustatory Cortex following reinnervation or cross-reinnervation of the lingual taste nerves in rats.
The Journal of comparative neurology, 2014Co-Authors: Camille Tessitore King, Mircea Garcea, Alan C. SpectorAbstract:Remarkably, when lingual Gustatory nerves are surgically re-routed to inappropriate taste fields in the tongue, some taste functions recover. We previously demonstrated that quinine-stimulated oromotor rejection reflexes and neural activity (assessed by Fos-immunoreactivity) in subregions of hindbrain Gustatory nuclei were restored if the posterior tongue, which contains receptor cells that respond strongly to bitter compounds, was cross-reinnervated by the chorda tympani nerve. Such functional recovery was not seen if instead, the anterior tongue, where receptor cells are less responsive to bitter compounds, was cross-reinnervated by the glossopharyngeal nerve, despite that this nerve typically responds robustly to bitter substances. Thus, recovery depended more on the taste field being reinnervated than on the nerve itself. Here, the distribution of quinine-stimulated Fos-immunoreactive neurons in two taste-associated forebrain areas was examined in these same rats. In the central nucleus of the amygdala (CeA), a rostrocaudal gradient characterized the normal quinine-stimulated Fos response, with the greatest number of labeled cells rostrally situated. Quinine-stimulated neurons were found throughout the Gustatory Cortex but a ‘hot spot’ was observed in its anterior-posterior center in subregions approximating the dysgranular/agranular layers. Fos neurons here and in the rostral CeA were highly correlated with quinine-elicited gapes. Denervation of the posterior tongue eliminated, and its reinnervation by either nerve restored, numbers of quinine-stimulated labeled cells in the rostral-most CeA and in the subregion approximating dysgranular Gustatory Cortex. These results underscore the remarkable plasticity of the Gustatory system and also help clarify the functional anatomy of neural circuits activated by bitter taste stimulation.
Alina Elkobi - One of the best experts on this subject based on the ideXlab platform.
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mAChR-dependent decrease in proteasome activity in the Gustatory Cortex is necessary for novel taste learning.
Neurobiology of learning and memory, 2016Co-Authors: Tali Rosenberg, Alina Elkobi, Kobi RosenblumAbstract:Regulation of protein degradation via the ubiquitin proteasome system is crucial for normal learning and synaptic plasticity processes. While some studies reveal that increased proteasome degradation is necessary for different types of learning, others suggest the proteasome to be a negative regulator of plasticity. We aim to understand the molecular and cellular processes taking place in the Gustatory Cortex (GC), which underlie appetitive and aversive forms of taste learning. Previously, we have shown that N-methyl d-aspartic acid receptor (NMDAR)-dependent upregulation of proteasome activity 4h after novel taste learning is necessary for the association of novel taste with malaise and formation of conditioned taste aversion (CTA). Here, we first identify a correlative increase in proteasome activity in the GC immediately after novel taste learning and study the upstream and downstream effectors of this modulated proteasome activity. Interestingly, proteasome-mediated degradation was reduced in the GC, 20min after novel taste consumption in a muscarinic acetylcholine receptor (mAChR)-dependent and NMDAR-independent manner. This reduction in protein degradation led to an increased amount of p70 S6 kinase (p70S6k), which was abolished in the presence of mAChR antagonist scopolamine. Infusion of lactacystin, a proteasome inhibitor, to the GC precluded the amnestic effect of scopolamine. This study shows for the first time that following novel taste learning there is a cortical, mAChR-dependent reduced proteasome activity that enables the memory of taste familiarity. Moreover, inhibition of degradation in the GC attenuates novel taste learning and of p70 S6 kinase correlative increased expression. These results shed light on the complex regulation of protein synthesis and degradation machineries in the Cortex following novel taste experience.
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Fluid consumption and taste novelty determines transcription temporal dynamics in the Gustatory Cortex
Molecular Brain, 2016Co-Authors: Sharon Inberg, Eyal Jacob, Alina Elkobi, Efrat Edry, Akiva Rappaport, T. Ian Simpson, J. Douglas Armstrong, Metsada Pasmanik-chor, Noam Shomron, Kobi RosenblumAbstract:BackgroundNovel taste memories, critical for animal survival, are consolidated to form long term memories which are dependent on translation regulation in the Gustatory Cortex (GC) hours following acquisition. However, the role of transcription regulation in the process is unknown.ResultsHere, we report that transcription in the GC is necessary for taste learning in rats, and that drinking and its consequences, as well as the novel taste experience, affect transcription in the GC during taste memory consolidation. We show differential effects of learning on temporal dynamics in set of genes in the GC, including Arc/Arg3.1, known to regulate the homeostasis of excitatory synapses.ConclusionsWe demonstrate that in taste learning, transcription programs were activated following the physiological responses (i.e., fluid consumption following a water restriction regime, reward, arousal of the animal, etc.) and the specific information about a given taste (i.e., taste novelty). Moreover, the cortical differential prolonged kinetics of mRNA following novel versus familiar taste learning may represent additional novelty related molecular response, where not only the total amount, but also the temporal dynamics of transcription is modulated by sensory experience of novel information.
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Fluid consumption and taste novelty determines transcription temporal dynamics in the Gustatory Cortex
Molecular brain, 2016Co-Authors: Sharon Inberg, Eyal Jacob, Alina Elkobi, Efrat Edry, Akiva Rappaport, T. Ian Simpson, J. Douglas Armstrong, Metsada Pasmanik-chor, Noam Shomron, Kobi RosenblumAbstract:Background Novel taste memories, critical for animal survival, are consolidated to form long term memories which are dependent on translation regulation in the Gustatory Cortex (GC) hours following acquisition. However, the role of transcription regulation in the process is unknown.
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NMDAR-dependent proteasome activity in the Gustatory Cortex is necessary for conditioned taste aversion.
Neurobiology of learning and memory, 2016Co-Authors: Tali Rosenberg, Alina Elkobi, Daniela C. Dieterich, Kobi RosenblumAbstract:Taste information is processed in different brain structures in the mammalian brain, including the Gustatory Cortex (GC), which resides within the insular Cortex. N-methyl-d-aspartate receptor (NMDAR) activity in the GC is necessary for the acquisition of conditioned taste aversion (CTA) but not positive novel taste learning. Previous studies have shown that taste memory consolidation requires intact protein synthesis in the GC. In addition, the direct involvement of translation initiation and elongation factors was documented in the GC during taste learning. However, protein expression is defined by protein synthesis, degradation, and localization. Protein degradation is critical for the consolidation and reconsolidation of other forms of learning, such as fear learning and addiction behavior, but its role in cortical-dependent learning is not clear. Here, we show for the first time that proteasome activity is specifically increased in the GC 4h following experiencing of a novel taste. This increase in proteasome activity was abolished by local administration to the GC of the NMDA antagonist, APV, as well as a CaMKII inhibitor, at the time of acquisition. In addition, local application of lactacystin, a proteasome inhibitor, resulted in impaired CTA, but not novel taste learning. These results suggest that NMDAR-dependent proteasome activity in the GC participates in the association process between novel taste experience and negative visceral sensation.
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Biphasic Activation of the mTOR Pathway in the Gustatory Cortex Is Correlated with and Necessary for Taste Learning
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009Co-Authors: Katya Belelovsky, Alina Elkobi, Hanoch Kaphzan, Kobi RosenblumAbstract:Different forms of memories and synaptic plasticity require synthesis of new proteins at the time of acquisition or immediately after. We are interested in the role of translation regulation in the Cortex, the brain structure assumed to store long-term memories. The mammalian target of rapamycin, mTOR (also known as FRAP and RAFT-1), is part of a key signal transduction mechanism known to regulate translation of specific subset of mRNAs and to affect learning and synaptic plasticity. We report here that novel taste learning induces two waves of mTOR activation in the Gustatory Cortex. Interestingly, the first wave can be identified both in synaptoneurosomal and cellular fractions, whereas the second wave is detected in the cellular fraction but not in the synaptic one. Inhibition of mTOR, specifically in the Gustatory Cortex, has two effects. First, biochemically, it modulates several known downstream proteins that control translation and reduces the expression of postsynaptic density-95 in vivo. Second, behaviorally, it attenuates long-term taste memory. The results suggest that the mTOR pathway in the Cortex modulates both translation factor activity and protein expression, to enable normal taste memory consolidation.
Donald B. Katz - One of the best experts on this subject based on the ideXlab platform.
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Perturbation of amygdala-cortical projections reduces ensemble coherence of palatability coding in Gustatory Cortex
2020Co-Authors: Jian-you Lin, Narendra Mukherjee, Max J. Bernstein, Donald B. KatzAbstract:ABSTRACT Taste palatability is centrally involved in consumption decisions—we ingest foods that taste good and reject those that don’t. Gustatory Cortex (GC) and basolateral amygdala (BLA) almost certainly work together to mediate palatability-driven behavior, but the precise nature of their interplay during taste decision-making is still unknown. Here, we take a step toward filling this gap in our knowledge, by investigating the specific role that activity in the BLA→GC pathway plays in the emergence of palatability-related firing in GC response dynamics (which influence consumption decisions). We implanted electrode/optical-fiber probes in virally-prepared female Long-Evans rats, such that we could optogenetically hyperpolarize BLA→GC axons, perturbing activity in these axons without affecting BLA and GC somas, while recording GC neural responses to intra-oral presentations of a diverse taste battery. This inter-regional axonal perturbation strongly altered GC taste responses, but despite the laser illumination being tonic for the first 2s that the taste was on the tongue, the alterations were far from monolithic: rather than changing all moments of the response equally, or causing a simple exponential decay of changes, the perturbation was most strongly felt at the onset times of previously-described response epochs; furthermore, the effect was epoch-specific—perturbations had little impact on the amount of taste identity information in the “middle epoch” of the responses, but reduced evidence of palatability-related activity in the “late-epoch.” Finally, BLA→GC axon inhibition affected the nature of the epochal dynamics themselves, such that the normal abruptness of the behaviorally-relevant ensemble transitions into the palatability-related epoch was greatly diminished. These results suggest that BLA “organizes” behavior-related GC taste dynamics.
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Single and population coding of taste in the Gustatory Cortex of awake mice.
Journal of neurophysiology, 2019Co-Authors: David Levitan, Narendra Mukherjee, Joseph Wachutka, Sacha B. Nelson, Jian-you Lin, Donald B. KatzAbstract:Here, we analyzed taste-related spiking activity in awake mouse Gustatory cortical (GC) neural ensembles, revealing deep similarities between mouse cortical taste processing and that repeatedly dem...
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Impact of precisely-timed inhibition of Gustatory Cortex on taste behavior depends on single-trial ensemble dynamics.
eLife, 2019Co-Authors: Narendra Mukherjee, Joseph Wachutka, Donald B. KatzAbstract:Sensation and action are necessarily coupled during stimulus perception – while tasting, for instance, perception happens while an animal decides to expel or swallow the substance in the mouth (the former via a behavior known as ‘gaping’). Taste responses in the rodent Gustatory Cortex (GC) span this sensorimotor divide, progressing through firing-rate epochs that culminate in the emergence of action-related firing. Population analyses reveal this emergence to be a sudden, coherent and variably-timed ensemble transition that reliably precedes gaping onset by 0.2–0.3s. Here, we tested whether this transition drives gaping, by delivering 0.5s GC perturbations in tasting trials. Perturbations significantly delayed gaping, but only when they preceded the action-related transition - thus, the same perturbation impacted behavior or not, depending on the transition latency in that particular trial. Our results suggest a distributed attractor network model of taste processing, and a dynamical role for Cortex in driving motor behavior.
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Single and population coding of taste in the Gustatory-Cortex of awake mice
2019Co-Authors: David Levitan, Narendra Mukherjee, Joseph Wachutka, Sacha B. Nelson, Jian-you Lin, Donald B. KatzAbstract:Abstract A great deal is known about the broad coding and neural ensemble dynamics characterizing forebrain taste processing in awake rats, and about the relationship between these firing rate dynamics and behavior. With regard to mice, in contrast, data concerning cortical taste coding are few, inconclusive, and largely restricted to imaging— a technique that as of now lacks the temporal sensitivity necessary for evaluation of fast response dynamics. Here we have recorded the spiking activity of ensembles of Gustatory cortical (GC) single neurons while presenting representatives of the basic taste modalities (sweet, salty, sour and bitter) to awake mice. Our results reveal deep similarities between rat and mouse taste processing: many recorded murine GC neurons (∼66%) responded distinctly to different tastes, and entropy analysis (which measures the breadth of taste coding) confirmed that the majority in fact responded to 3 or 4 tastes; temporal coding analyses further revealed that single mouse GC neurons sequentially code taste identity and palatability—the latter responses emerging ∼0.5s after the former—a dynamic that population analysis suggested reflects a reliable sequence of network states activated by taste delivery (i.e., ensembles of simultaneously-recorded neurons transitioned suddenly and coherently from coding taste identity to coding taste palatability). All of the above results held across the anterior-posterior and dorsal-ventral axes of GC—neither between-nor within-mouse mapping revealed regions of narrow or temporally simple taste responses. In conclusion, our data indicates that mouse GC, like rat GC, codes multiple aspects of taste in a coarse, time-varying manner. Significance Taste is a useful system with which to study the electrophysiology of cortical coding in relation to behavior. Given the likely contribution of genetics to this subject, it is surprising that there has been almost no work done on the electrophysiology of mouse taste (and that the few imaging studies done on mouse Gustatory Cortex (GC) have failed to provide consensus on basic features of taste coding). Here we provide the first thorough analysis of taste-related spiking activity in ensembles of awake mouse GC neurons. This analysis reveals deep, abiding similarities between mouse cortical taste processing and that repeatedly demonstrated in rat: mouse GC codes multiple aspects of taste in a coarse, time-varying manner that is essentially invariant across the spatial dimensions of the GC. Mice engage in distributed cortical network processing of taste, rather than coding each specific taste in an all or non-fashion in specific anatomical locations.
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Impact of precisely-timed inhibition of Gustatory Cortex on taste behavior depends on single-trial ensemble dynamics
2018Co-Authors: Narendra Mukherjee, Joseph Wachukta, Donald B. KatzAbstract:Abstract The purpose of perception is the driving of action. During tasting, for instance, every stimulus must be either swallowed or rejected (the latter via a behavior known as “gaping”). Taste responses in the rodent Gustatory Cortex (GC) span this sensorimotor divide, progressing through a series of firing-rate epochs that culminate in action-related firing. Population analyses reveal this emergence to be a sudden, coherent ensemble transition that, despite varying in latency between trials, reliably precedes gaping onset by 0.2-0.3s. Here, we tested whether this transition drives gaping, by delivering 0.5s GC perturbations at various time-points in tasting trials. Perturbations significantly delayed gaping, but only when they preceded the variably-timed action-related transition - thus, the same perturbation might have an impact or not, depending on the transition latency in that particular trial. Our results suggest a distributed attractor network model of taste processing, and a dynamical role for Cortex in driving motor behavior.
Sharon Inberg - One of the best experts on this subject based on the ideXlab platform.
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Fluid consumption and taste novelty determines transcription temporal dynamics in the Gustatory Cortex
Molecular Brain, 2016Co-Authors: Sharon Inberg, Eyal Jacob, Alina Elkobi, Efrat Edry, Akiva Rappaport, T. Ian Simpson, J. Douglas Armstrong, Metsada Pasmanik-chor, Noam Shomron, Kobi RosenblumAbstract:BackgroundNovel taste memories, critical for animal survival, are consolidated to form long term memories which are dependent on translation regulation in the Gustatory Cortex (GC) hours following acquisition. However, the role of transcription regulation in the process is unknown.ResultsHere, we report that transcription in the GC is necessary for taste learning in rats, and that drinking and its consequences, as well as the novel taste experience, affect transcription in the GC during taste memory consolidation. We show differential effects of learning on temporal dynamics in set of genes in the GC, including Arc/Arg3.1, known to regulate the homeostasis of excitatory synapses.ConclusionsWe demonstrate that in taste learning, transcription programs were activated following the physiological responses (i.e., fluid consumption following a water restriction regime, reward, arousal of the animal, etc.) and the specific information about a given taste (i.e., taste novelty). Moreover, the cortical differential prolonged kinetics of mRNA following novel versus familiar taste learning may represent additional novelty related molecular response, where not only the total amount, but also the temporal dynamics of transcription is modulated by sensory experience of novel information.
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Fluid consumption and taste novelty determines transcription temporal dynamics in the Gustatory Cortex
Molecular brain, 2016Co-Authors: Sharon Inberg, Eyal Jacob, Alina Elkobi, Efrat Edry, Akiva Rappaport, T. Ian Simpson, J. Douglas Armstrong, Metsada Pasmanik-chor, Noam Shomron, Kobi RosenblumAbstract:Background Novel taste memories, critical for animal survival, are consolidated to form long term memories which are dependent on translation regulation in the Gustatory Cortex (GC) hours following acquisition. However, the role of transcription regulation in the process is unknown.