Ventral Pallidum

14,000,000 Leading Edge Experts on the ideXlab platform

Scan Science and Technology

Contact Leading Edge Experts & Companies

Scan Science and Technology

Contact Leading Edge Experts & Companies

The Experts below are selected from a list of 1809 Experts worldwide ranked by ideXlab platform

Kent C. Berridge - One of the best experts on this subject based on the ideXlab platform.

  • mapping excessive disgust in the brain Ventral Pallidum inactivation recruits distributed circuitry to make sweetness disgusting
    Cognitive Affective & Behavioral Neuroscience, 2020
    Co-Authors: Kevin R Urstadt, Hammad A Khan, Nina A Mostovoi, Kent C. Berridge
    Abstract:

    The Ventral Pallidum (VP) is an important structure in processing reward. The VP may be the only brain structure where localized lesions in rats replace normal facial “liking” expressions to sweetness with excessive “disgust” reactions, such as gapes and chin rubs, that are normally reserved for unpalatable tastes. The posterior half of the VP (pVP) contains a hedonic hot spot where opioid or related neurochemical stimulations can amplify positive “liking” reactions to sweet taste. This is the same site where lesions or pharmacological inactivations replace positive hedonic reactions to sucrose with intense negative “disgust.” In the present study, we aimed to identify brain networks recruited by pVP inactivation to generate excessive “disgust,” using neuronal Fos expression as a marker of neurobiological activation. Microinjections in pVP of inhibitory GABAA/B agonists (muscimol and baclofen) caused rats to exhibit excessive “disgust” reactions to sucrose. Excessive “disgust” was accompanied by recruitment of neural Fos activation in several subcortical structures, including the posterior medial shell of nucleus accumbens (which also contains another GABAergic “disgust”-inducing “hedonic cold spot”), the bed nucleus of stria terminalis, lateral habenula, hypothalamus, and midbrain Ventral tegmentum. Fos suppression was found in cortical limbic regions, including previously identified hedonic hot spots in the anteromedial orbitofrontal cortex and posterior insula. Finally, in addition to inducing excessive “disgust,” pVP inactivation abolished motivational “wanting” to eat palatable food, reduced positive social interactions, and reordered sensorimotor relations. Our findings identify potential “disgust” generators in the brain that are released into excitation by pVP inhibition and may serve as targets for future research.

  • Example photomicrographs of Fos recruited in distant brain structures.
    2018
    Co-Authors: Shannon L Cole, Mike J. F. Robinson, Kent C. Berridge
    Abstract:

    Images showing Fos core samples recruited by NAc laser illumination in D1 ChR2 or D2 ChR2 mice, or controls. Distant structures shown are basolateral amygdala (Top), caudal Ventral Pallidum (Middle) and lateral hypothalamus (Bottom). D1 ChR2, D2 ChR2, EYFP control, and surgically naïve mice are each shown. Brain region abbreviations: Basolateral Amygdala (BLA), caudal Ventral Pallidum (cVP), and lateral hypothalamus (LH).

  • Behavioral/Systems/Cognitive Opioid Limbic Circuit for Reward: Interaction between Hedonic Hotspots of Nucleus Accumbens and
    2016
    Co-Authors: Ventral Pallidum, Kyle S Smith, Kent C. Berridge
    Abstract:

    -Opioid stimulation of cubic millimeter hedonic hotspots in either the nucleus accumbens shell (NAc) or the Ventral Pallidum (VP) amplifies hedonic “liking ” reactions to sweetness andappetitive “wanting ” for food reward.Howdo these twoNAc–VPhotspots interact? To probe their interaction and limbic circuit properties, we assessedwhether opioid activation of one hotspot recruited the other hotspot (neurobiologically) and whether opioid hedonic and incentive motivational amplification by either opioid hotspot required permissive opioid coactivation in the other (behaviorally).We found that NAc andVP hotspots reciprocallymodulated Fos expression in each other and that the two hotspots were needed together to enhance sucrose “liking ” reactions, essentially cooperating within a single hedonic NAc–VP circuit. In contrast, theNAchotspot dominated for opioid stimulation of eating and food intake (“wanting”), independent ofVP activation. This pattern reveals differences between limbic opioid circuits that control reward “liking ” and “wanting ” functions. Key words: nucleus accumbens; Ventral Pallidum; opioid, hedonic; reward; motivation; eating; food intake; Fo

  • Behavioral/Systems/Cognitive Dynamic Computation of Incentive Salience: “Wanting” What Was Never “Liked”
    2016
    Co-Authors: Amy J Tindell, Kent C. Berridge, Kyle S Smith, Wayne J Aldridge
    Abstract:

    Pavlovian cues for rewards become endowed with incentive salience, guiding “wanting ” to their learned reward. Usually, cues are “wanted ” only if their rewards have ever been “liked, ” but here we show that mesocorticolimbic systems can recompute “wanting ” de novo by integrating novel physiological signals with a cue’s preexisting associations to an outcome that lacked hedonic value. That is, a cue’s incentive salience can be recomputed adaptively. We demonstrate that this recomputation is encoded in neural signals coursing through the Ventral Pallidum. Ventral Pallidum neurons do not ordinarily fire vigorously to a cue that predicts the previously “disliked” taste of intense salt, although they do fire to a cue that predicts the taste of previously “liked ” sucrose. Yet we show that neural firing rises dramatically to the salt cue immediately and selectivelywhen that cue is encountered in anever-before-experienced state of physiological salt depletion. Crucially, robust neural firing to the salt cue occurred the first time it was encountered in the new depletion state (in cue-only extinction trials), evenbefore its associated intense saltinesshas everbeen tasted aspositively “liked ” (salt taste hadalwaysbeen “disliked”before). Theamplificationof incentive saliencedidnot require additional learningabout the cueor thenewlypositive salt taste. Thus dynamic recomputation of cue-triggered “wanting ” signals can occur in real time at themoment of cue re-encounter by combining previously learned Pavlovian associations with novel physiological information about a current state of specific appetite

  • lateral hypothalamus nucleus accumbens and Ventral Pallidum roles in eating and hunger interactions between homeostatic and reward circuitry
    Frontiers in Systems Neuroscience, 2015
    Co-Authors: Daniel C Castro, Shannon L Cole, Kent C. Berridge
    Abstract:

    The study of the neural bases of eating behavior, hunger, and reward has consistently implicated the lateral hypothalamus (LH) and its interactions with mesocorticolimbic circuitry, such as mesolimbic dopamine projections to nucleus accumbens (NAc) and Ventral Pallidum (VP), in controlling motivation to eat. The NAc and VP play special roles in mediating the hedonic impact (‘liking’) and motivational incentive salience (‘wanting’) of food rewards, and their interactions with LH help permit regulatory hunger/satiety modulation of food motivation and reward. Here, we review some progress that has been made regarding this circuitry and its functions: the identification of localized anatomical hedonic hotspots within NAc and VP for enhancing hedonic impact; interactions of NAc/VP hedonic hotspots with specific LH signals such as orexin; an anterior-posterior gradient of sites in NAc shell for producing intense appetitive eating versus intense fearful reactions; and anatomically distributed appetitive functions of dopamine and mu opioid signals in NAc shell and related structures. Such findings help improve our understanding of NAc, VP, and LH interactions in mediating affective and motivation functions, including ‘liking’ and ‘wanting’ for food rewards.

Kazue Semba - One of the best experts on this subject based on the ideXlab platform.

  • vesicular glutamate transporter 3 immunoreactivity is present in cholinergic basal forebrain neurons projecting to the basolateral amygdala in rat
    The Journal of Comparative Neurology, 2006
    Co-Authors: Amanda Nickerson Poulin, Salah El Mestikawy, Aline Guerci, Kazue Semba
    Abstract:

    The basal forebrain (BF) plays a role in behavioral and cortical arousal, attention, learning, and memory. It has been suggested that cholinergic BF neurons co-release glutamate, and some cholinergic BF neurons have been reported to contain vesicular glutamate transporter 3 (VGLUT3). We examined the distribution and projections of BF cholinergic neurons containing VGLUT3, by using dual-label immunofluorescence for choline acetyltransferase (ChAT) and VGLUT3, in situ hybridization, and retrograde tracing. Neurons immunoreactive (+) or containing mRNAs for both ChAT and VGLUT3 were mainly localized to the Ventral Pallidum and more caudal BF regions; the co-immunoreactive neurons represented 31% of cholinergic neurons in the Ventral Pallidum and 5-9% more caudally. Examination of cholinergic axon terminals in known target areas of BF projections indicated that the basolateral amygdaloid nucleus contained numerous terminals co-immunoreactive for ChAT and VGLUT3, whereas sampled areas of the olfactory bulb, neocortex, hippocampus, reticular thalamic nucleus, and interpeduncular nucleus were devoid of double-labeled terminals. The basolateral amygdala is innervated by cholinergic BF neurons lacking low-affinity p75 nerve growth factor receptors; many ChAT+VGLUT3+ BF neurons were immunonegative to this receptor. Twenty-five to 79% of ChAT+VGLUT3+ neurons in different BF regions were retrogradely labeled from the basolateral amygdala, up to 52% (Ventral Pallidum) of the retrogradely labeled ChAT+ neurons were VGLUT3+, and the largest number of amygdala-projecting ChAT+VGluT3+ neurons was found in the Ventral Pallidum. These findings indicate that BF cholinergic neurons containing VGLUT3 project to the basolateral amygdala and suggest that these neurons might have the capacity to release both acetylcholine and glutamate.

  • vesicular glutamate transporter 3 immunoreactivity is present in cholinergic basal forebrain neurons projecting to the basolateral amygdala in rat
    The Journal of Comparative Neurology, 2006
    Co-Authors: Amanda Nickerson Poulin, Salah El Mestikawy, Aline Guerci, Kazue Semba
    Abstract:

    The basal forebrain (BF) plays a role in behavioral and cortical arousal, attention, learning, and memory. It has been suggested that cholinergic BF neurons co-release glutamate, and some cholinergic BF neurons have been reported to contain vesicular glutamate transporter 3 (VGLUT3). We examined the distribution and projections of BF cholinergic neurons containing VGLUT3, by using dual-label immunofluorescence for choline acetyltransferase (ChAT) and VGLUT3, in situ hybridization, and retrograde tracing. Neurons immunoreactive (+) or containing mRNAs for both ChAT and VGLUT3 were mainly localized to the Ventral Pallidum and more caudal BF regions; the co-immunoreactive neurons represented 31% of cholinergic neurons in the Ventral Pallidum and 5–9% more caudally. Examination of cholinergic axon terminals in known target areas of BF projections indicated that the basolateral amygdaloid nucleus contained numerous terminals co-immunoreactive for ChAT and VGLUT3, whereas sampled areas of the olfactory bulb, neocortex, hippocampus, reticular thalamic nucleus, and interpeduncular nucleus were devoid of double-labeled terminals. The basolateral amygdala is innervated by cholinergic BF neurons lacking low-affinity p75 nerve growth factor receptors; many ChAT+VGLUT3+ BF neurons were immunonegative to this receptor. Twenty-five to 79% of ChAT+VGLUT3+ neurons in different BF regions were retrogradely labeled from the basolateral amygdala, up to 52% (Ventral Pallidum) of the retrogradely labeled ChAT+ neurons were VGLUT3+, and the largest number of amygdala-projecting ChAT+VGluT3+ neurons was found in the Ventral Pallidum. These findings indicate that BF cholinergic neurons containing VGLUT3 project to the basolateral amygdala and suggest that these neurons might have the capacity to release both acetylcholine and glutamate. J. Comp. Neurol. 498:690–711, 2006. © 2006 Wiley-Liss, Inc.

Aline Guerci - One of the best experts on this subject based on the ideXlab platform.

  • vesicular glutamate transporter 3 immunoreactivity is present in cholinergic basal forebrain neurons projecting to the basolateral amygdala in rat
    The Journal of Comparative Neurology, 2006
    Co-Authors: Amanda Nickerson Poulin, Salah El Mestikawy, Aline Guerci, Kazue Semba
    Abstract:

    The basal forebrain (BF) plays a role in behavioral and cortical arousal, attention, learning, and memory. It has been suggested that cholinergic BF neurons co-release glutamate, and some cholinergic BF neurons have been reported to contain vesicular glutamate transporter 3 (VGLUT3). We examined the distribution and projections of BF cholinergic neurons containing VGLUT3, by using dual-label immunofluorescence for choline acetyltransferase (ChAT) and VGLUT3, in situ hybridization, and retrograde tracing. Neurons immunoreactive (+) or containing mRNAs for both ChAT and VGLUT3 were mainly localized to the Ventral Pallidum and more caudal BF regions; the co-immunoreactive neurons represented 31% of cholinergic neurons in the Ventral Pallidum and 5-9% more caudally. Examination of cholinergic axon terminals in known target areas of BF projections indicated that the basolateral amygdaloid nucleus contained numerous terminals co-immunoreactive for ChAT and VGLUT3, whereas sampled areas of the olfactory bulb, neocortex, hippocampus, reticular thalamic nucleus, and interpeduncular nucleus were devoid of double-labeled terminals. The basolateral amygdala is innervated by cholinergic BF neurons lacking low-affinity p75 nerve growth factor receptors; many ChAT+VGLUT3+ BF neurons were immunonegative to this receptor. Twenty-five to 79% of ChAT+VGLUT3+ neurons in different BF regions were retrogradely labeled from the basolateral amygdala, up to 52% (Ventral Pallidum) of the retrogradely labeled ChAT+ neurons were VGLUT3+, and the largest number of amygdala-projecting ChAT+VGluT3+ neurons was found in the Ventral Pallidum. These findings indicate that BF cholinergic neurons containing VGLUT3 project to the basolateral amygdala and suggest that these neurons might have the capacity to release both acetylcholine and glutamate.

  • vesicular glutamate transporter 3 immunoreactivity is present in cholinergic basal forebrain neurons projecting to the basolateral amygdala in rat
    The Journal of Comparative Neurology, 2006
    Co-Authors: Amanda Nickerson Poulin, Salah El Mestikawy, Aline Guerci, Kazue Semba
    Abstract:

    The basal forebrain (BF) plays a role in behavioral and cortical arousal, attention, learning, and memory. It has been suggested that cholinergic BF neurons co-release glutamate, and some cholinergic BF neurons have been reported to contain vesicular glutamate transporter 3 (VGLUT3). We examined the distribution and projections of BF cholinergic neurons containing VGLUT3, by using dual-label immunofluorescence for choline acetyltransferase (ChAT) and VGLUT3, in situ hybridization, and retrograde tracing. Neurons immunoreactive (+) or containing mRNAs for both ChAT and VGLUT3 were mainly localized to the Ventral Pallidum and more caudal BF regions; the co-immunoreactive neurons represented 31% of cholinergic neurons in the Ventral Pallidum and 5–9% more caudally. Examination of cholinergic axon terminals in known target areas of BF projections indicated that the basolateral amygdaloid nucleus contained numerous terminals co-immunoreactive for ChAT and VGLUT3, whereas sampled areas of the olfactory bulb, neocortex, hippocampus, reticular thalamic nucleus, and interpeduncular nucleus were devoid of double-labeled terminals. The basolateral amygdala is innervated by cholinergic BF neurons lacking low-affinity p75 nerve growth factor receptors; many ChAT+VGLUT3+ BF neurons were immunonegative to this receptor. Twenty-five to 79% of ChAT+VGLUT3+ neurons in different BF regions were retrogradely labeled from the basolateral amygdala, up to 52% (Ventral Pallidum) of the retrogradely labeled ChAT+ neurons were VGLUT3+, and the largest number of amygdala-projecting ChAT+VGluT3+ neurons was found in the Ventral Pallidum. These findings indicate that BF cholinergic neurons containing VGLUT3 project to the basolateral amygdala and suggest that these neurons might have the capacity to release both acetylcholine and glutamate. J. Comp. Neurol. 498:690–711, 2006. © 2006 Wiley-Liss, Inc.

Amanda Nickerson Poulin - One of the best experts on this subject based on the ideXlab platform.

  • vesicular glutamate transporter 3 immunoreactivity is present in cholinergic basal forebrain neurons projecting to the basolateral amygdala in rat
    The Journal of Comparative Neurology, 2006
    Co-Authors: Amanda Nickerson Poulin, Salah El Mestikawy, Aline Guerci, Kazue Semba
    Abstract:

    The basal forebrain (BF) plays a role in behavioral and cortical arousal, attention, learning, and memory. It has been suggested that cholinergic BF neurons co-release glutamate, and some cholinergic BF neurons have been reported to contain vesicular glutamate transporter 3 (VGLUT3). We examined the distribution and projections of BF cholinergic neurons containing VGLUT3, by using dual-label immunofluorescence for choline acetyltransferase (ChAT) and VGLUT3, in situ hybridization, and retrograde tracing. Neurons immunoreactive (+) or containing mRNAs for both ChAT and VGLUT3 were mainly localized to the Ventral Pallidum and more caudal BF regions; the co-immunoreactive neurons represented 31% of cholinergic neurons in the Ventral Pallidum and 5-9% more caudally. Examination of cholinergic axon terminals in known target areas of BF projections indicated that the basolateral amygdaloid nucleus contained numerous terminals co-immunoreactive for ChAT and VGLUT3, whereas sampled areas of the olfactory bulb, neocortex, hippocampus, reticular thalamic nucleus, and interpeduncular nucleus were devoid of double-labeled terminals. The basolateral amygdala is innervated by cholinergic BF neurons lacking low-affinity p75 nerve growth factor receptors; many ChAT+VGLUT3+ BF neurons were immunonegative to this receptor. Twenty-five to 79% of ChAT+VGLUT3+ neurons in different BF regions were retrogradely labeled from the basolateral amygdala, up to 52% (Ventral Pallidum) of the retrogradely labeled ChAT+ neurons were VGLUT3+, and the largest number of amygdala-projecting ChAT+VGluT3+ neurons was found in the Ventral Pallidum. These findings indicate that BF cholinergic neurons containing VGLUT3 project to the basolateral amygdala and suggest that these neurons might have the capacity to release both acetylcholine and glutamate.

  • vesicular glutamate transporter 3 immunoreactivity is present in cholinergic basal forebrain neurons projecting to the basolateral amygdala in rat
    The Journal of Comparative Neurology, 2006
    Co-Authors: Amanda Nickerson Poulin, Salah El Mestikawy, Aline Guerci, Kazue Semba
    Abstract:

    The basal forebrain (BF) plays a role in behavioral and cortical arousal, attention, learning, and memory. It has been suggested that cholinergic BF neurons co-release glutamate, and some cholinergic BF neurons have been reported to contain vesicular glutamate transporter 3 (VGLUT3). We examined the distribution and projections of BF cholinergic neurons containing VGLUT3, by using dual-label immunofluorescence for choline acetyltransferase (ChAT) and VGLUT3, in situ hybridization, and retrograde tracing. Neurons immunoreactive (+) or containing mRNAs for both ChAT and VGLUT3 were mainly localized to the Ventral Pallidum and more caudal BF regions; the co-immunoreactive neurons represented 31% of cholinergic neurons in the Ventral Pallidum and 5–9% more caudally. Examination of cholinergic axon terminals in known target areas of BF projections indicated that the basolateral amygdaloid nucleus contained numerous terminals co-immunoreactive for ChAT and VGLUT3, whereas sampled areas of the olfactory bulb, neocortex, hippocampus, reticular thalamic nucleus, and interpeduncular nucleus were devoid of double-labeled terminals. The basolateral amygdala is innervated by cholinergic BF neurons lacking low-affinity p75 nerve growth factor receptors; many ChAT+VGLUT3+ BF neurons were immunonegative to this receptor. Twenty-five to 79% of ChAT+VGLUT3+ neurons in different BF regions were retrogradely labeled from the basolateral amygdala, up to 52% (Ventral Pallidum) of the retrogradely labeled ChAT+ neurons were VGLUT3+, and the largest number of amygdala-projecting ChAT+VGluT3+ neurons was found in the Ventral Pallidum. These findings indicate that BF cholinergic neurons containing VGLUT3 project to the basolateral amygdala and suggest that these neurons might have the capacity to release both acetylcholine and glutamate. J. Comp. Neurol. 498:690–711, 2006. © 2006 Wiley-Liss, Inc.

Gary Astonjones - One of the best experts on this subject based on the ideXlab platform.

  • designer receptors show role for Ventral Pallidum input to Ventral tegmental area in cocaine seeking
    Nature Neuroscience, 2014
    Co-Authors: Stephen V Mahler, Karl Deisseroth, Elena M Vazey, Jacob T Beckley, Colby Keistler, Ellen M Mcglinchey, Jennifer Kaufling, Steven P Wilson, John J Woodward, Gary Astonjones
    Abstract:

    The authors show that rostral Ventral Pallidum projections to the Ventral tegmental area (VTA) are activated during cue-induced reinstatement of cocaine seeking, and DREADD inhibition of these projections blocks this behavior. In contrast, projections from the caudal Ventral Pallidum are necessary for cocaine-primed, but not cue-induced, reinstatement of cocaine seeking.

  • designer receptors show role for Ventral Pallidum input to Ventral tegmental area in cocaine seeking
    Nature Neuroscience, 2014
    Co-Authors: Stephen V Mahler, Karl Deisseroth, Elena M Vazey, Jacob T Beckley, Colby Keistler, Ellen M Mcglinchey, Jennifer Kaufling, Steven P Wilson, John J Woodward, Gary Astonjones
    Abstract:

    The Ventral Pallidum is centrally positioned within mesocorticolimbic reward circuits, and its dense projection to the Ventral tegmental area (VTA) regulates neuronal activity there. However, the Ventral Pallidum is a heterogeneous structure, and how this complexity affects its role within wider reward circuits is unclear. We found that projections to VTA from the rostral Ventral Pallidum (RVP), but not the caudal Ventral Pallidum (CVP), were robustly Fos activated during cue-induced reinstatement of cocaine seeking--a rat model of relapse in addiction. Moreover, designer receptor-mediated transient inactivation of RVP neurons, their terminals in VTA or functional connectivity between RVP and VTA dopamine neurons blocked the ability of drug-associated cues (but not a cocaine prime) to reinstate cocaine seeking. In contrast, CVP neuronal inhibition blocked cocaine-primed, but not cue-induced, reinstatement. This double dissociation in Ventral Pallidum subregional roles in drug seeking is likely to be important for understanding the mesocorticolimbic circuits underlying reward seeking and addiction.