Nucleus Accumbens Shell

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Charles J Billington - One of the best experts on this subject based on the ideXlab platform.

  • orexin signaling in rostral lateral hypothalamus and Nucleus Accumbens Shell in the control of spontaneous physical activity in high and low activity rats
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2017
    Co-Authors: Claudio E Perezleighton, Charles J Billington, Morgan R Little, Martha K Grace, Catherine M Kotz
    Abstract:

    Spontaneous physical activity (SPA) describes activity outside of formal exercise and shows large inter-individual variability. The hypothalamic orexin/hypocretin peptides are key regulators of SPA. Orexins drive SPA within multiple brain sites, including rostral lateral hypothalamus (LH) and Nucleus Accumbens Shell (NAcSh). Rats with high basal SPA (high activity, HA) show higher orexin mRNA expression and SPA after injection of orexin-A in rostral LH compared to low activity (LA) rats. Here we explored the contribution of orexin signaling in rostral LH and NAcSh to the HA/LA phenotype. We found that HA rats have higher sensitivity to SPA after injection of orexin-A in rostral LH, but not in NAcSh. HA and LA rats showed similar levels of orexin receptor expression in rostral LH and activation of orexin producing neurons after orexin-A injection in rostral LH. Also, in HA and LA rats the co-injection of orexin-A in rostral LH and NAcSh failed to further increase SPA beyond the effects of orexin-A in rostral LH. Pre-treatment with muscimol, a GABA(A) receptor agonist, in NAcSh potentiated SPA produced by orexin-A injection in rostral LH in HA but not in LA rats. Our results suggest that a feedback loop from orexin responsive neurons in rostral LH to orexin neurons and a NAcSh - orexin neuron - rostral LH circuit regulate SPA. Overall, our data suggest that differences in orexin sensitivity in rostral LH and its modulation by GABA afferents from NAcSh contribute to individual SPA differences.

  • orexin signaling in rostral lateral hypothalamus and Nucleus Accumbens Shell in the control of spontaneous physical activity in high and low activity rats
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2017
    Co-Authors: Claudio E Perezleighton, Charles J Billington, Morgan R Little, Martha K Grace, Catherine M Kotz
    Abstract:

    Spontaneous physical activity (SPA) describes activity outside of formal exercise and shows large interindividual variability. The hypothalamic orexin/hypocretin peptides are key regulators of SPA. Orexins drive SPA within multiple brain sites, including rostral lateral hypothalamus (LH) and Nucleus Accumbens Shell (NAcSh). Rats with high basal SPA (high activity, HA) show higher orexin mRNA expression and SPA after injection of orexin-A in rostral LH compared with low-activity (LA) rats. Here, we explored the contribution of orexin signaling in rostral LH and NAcSh to the HA/LA phenotype. We found that HA rats have higher sensitivity to SPA after injection of orexin-A in rostral LH, but not in NAcSh. HA and LA rats showed similar levels of orexin receptor expression in rostral LH, and activation of orexin-producing neurons after orexin-A injection in rostral LH. Also, in HA and LA rats, the coinjection of orexin-A in rostral LH and NAcSh failed to further increase SPA beyond the effects of orexin-A in rostral LH. Pretreatment with muscimol, a GABAA receptor agonist, in NAcSh potentiated SPA produced by orexin-A injection in rostral LH in HA but not in LA rats. Our results suggest that a feedback loop from orexin-responsive neurons in rostral LH to orexin neurons and a the NAcSh-orexin neuron-rostral LH circuit regulate SPA. Overall, our data suggest that differences in orexin sensitivity in rostral LH and its modulation by GABA afferents from NAcSh contribute to individual SPA differences.

  • effects of the opioid antagonist naltrexone on feeding induced by damgo in the ventral tegmental area and in the Nucleus Accumbens Shell region in the rat
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2003
    Co-Authors: Amy F Macdonald, Charles J Billington, Allen S Levine
    Abstract:

    The Nucleus Accumbens Shell region (sNAcc) and the ventral tegmental area (VTA) are two major nodes in the mesolimbic dopamine pathway, which mediates reward for various survival behaviors, includi...

  • Peptides that regulate food intake effects of the opioid antagonist naltrexone on feeding induced by DAMGO in the ventral tegmental area and in the Nucleus Accumbens Shell region in the rat
    American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2003
    Co-Authors: Amy F Macdonald, Charles J Billington, Allen S Levine
    Abstract:

    The Nucleus Accumbens Shell region (sNAcc) and the ventral tegmental area (VTA) are two major nodes in the mesolimbic dopamine pathway, which mediates reward for various survival behaviors, including feeding. Opioids increase and maintain food intake when injected peripherally and centrally. Opioids in the VTA cause increased release of dopamine in the sNAcc, and when injected into either site, cause an increase in food intake. Animals in this study were double cannulated in the VTA and in the sNAcc and injected with various combinations of naltrexone (NTX) (2.5, 5, and 25 μg/side) and Tyr-D-Ala-Gly-(Me)Phe-Gly-ol (DAMGO) (0.1, 0.3, 1, 3, and 5 nmol/side) in both sites. DAMGO was found to dose dependently increase intake to an equal extent when injected into either site. DAMGO-induced increases in food intake when injected into the VTA were blocked to control levels with the highest dose of NTX injected bilaterally into the sNAcc; however, increases in intake when injected into the sNAcc were blocked only partially by the highest dose of NTX injected bilaterally into the VTA. These results indicate opioid-opioid communication between the two sites; however, the communication may be quite indirect, requiring other sites and transmitters to elicit a change in behavior.

Allen S Levine - One of the best experts on this subject based on the ideXlab platform.

R.c. Pierce - One of the best experts on this subject based on the ideXlab platform.

  • Deep brain stimulation of the Nucleus Accumbens Shell attenuates cocaine reinstatement through local and antidromic activation.
    The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013
    Co-Authors: Fair M. Vassoler, Samantha L. White, Thomas J. Hopkins, Leonardo A. Guercio, Julie Espallergues, Olivier Berton, Heath D. Schmidt, R.c. Pierce
    Abstract:

    Accumbal deep brain stimulation (DBS) is a promising therapeutic modality for the treatment of addiction. Here, we demonstrate that DBS in the Nucleus Accumbens Shell, but not the core, attenuates cocaine priming-induced reinstatement of drug seeking, an animal model of relapse, in male Sprague Dawley rats. Next, we compared DBS of the Shell with pharmacological inactivation. Results indicated that inactivation using reagents that influenced (lidocaine) or spared (GABA receptor agonists) fibers of passage blocked cocaine reinstatement when administered into the core but not the Shell. It seems unlikely, therefore, that intraShell DBS influences cocaine reinstatement by inactivating this Nucleus or the fibers coursing through it. To examine potential circuit-wide changes, c-Fos immunohistochemistry was used to examine neuronal activation following DBS of the Nucleus Accumbens Shell. IntraShell DBS increased c-Fos induction at the site of stimulation as well as in the infralimbic cortex, but had no effect on the dorsal striatum, prelimbic cortex, or ventral pallidum. Recent evidence indicates that Accumbens DBS antidromically stimulates axon terminals, which ultimately activates GABAergic interneurons in cortical areas that send afferents to the Shell. To test this hypothesis, GABA receptor agonists (baclofen/muscimol) were microinjected into the anterior cingulate, and prelimbic or infralimbic cortices before cocaine reinstatement. Pharmacological inactivation of all three medial prefrontal cortical subregions attenuated the reinstatement of cocaine seeking. These results are consistent with DBS of the Accumbens Shell attenuating cocaine reinstatement via local activation and/or activation of GABAergic interneurons in the medial prefrontal cortex via antidromic stimulation of cortico-accumbal afferents.

  • deep brain stimulation of the Nucleus Accumbens Shell attenuates cocaine priming induced reinstatement of drug seeking in rats
    The Journal of Neuroscience, 2008
    Co-Authors: Fair M. Vassoler, Heath D. Schmidt, Katie R Famous, M E Gerard, Domenic A Ciraulo, Conan Kornetsky, Clifford M Knapp, R.c. Pierce
    Abstract:

    Increasing evidence suggests that deep brain stimulation (DBS), which is currently being used as a therapy for neurological diseases, may be effective in the treatment of psychiatric disorders as well. Here, we examined the influence of DBS of the Nucleus Accumbens Shell on cocaine priming-induced reinstatement of drug seeking, an animal model of relapse. Rats were allowed to self-administer cocaine (0.25 mg, i.v.) 2 h daily for 21 d and then cocaine-seeking behavior was extinguished by replacing cocaine with saline. During the reinstatement phase, DBS was administered bilaterally to the Nucleus Accumbens Shell through bipolar stainless steel electrodes. Biphasic symmetrical pulses were delivered at a frequency of 160 Hz and a current intensity of 150 μA. DBS began immediately after a priming injection of cocaine (0, 5, 10, or 20 mg/kg, i.p.) and continued throughout each 2 h reinstatement session. Results indicated that only the higher doses of cocaine (10 and 20 mg/kg) produced robust and reliable reinstatement of cocaine seeking. DBS of the Nucleus Accumbens Shell significantly attenuated the reinstatement of drug seeking precipitated by these higher cocaine doses. Additional experiments indicated that this DBS effect was both anatomically and reinforcer specific. Thus, DBS of the dorsal striatum had no influence on cocaine reinstatement and DBS of the Accumbens Shell did not affect the reinstatement of food seeking. Together, these results suggest that DBS of the Nucleus Accumbens Shell may be a potential therapeutic option in the treatment of severe cocaine addiction.

  • D1-like and D2 dopamine receptor antagonists administered into the Shell subregion of the rat Nucleus Accumbens decrease cocaine, but not food, reinforcement.
    Neuroscience, 2005
    Co-Authors: Ausaf A. Bari, R.c. Pierce
    Abstract:

    Cocaine self-administration experiments were designed to assess the respective roles of D1-like and D2-like dopamine receptors in the ventral forebrain in cocaine reinforcement. D1-like or D2-like dopamine receptor antagonists were microinjected into the Nucleus Accumbens core, Nucleus Accumbens Shell, neostriatum or lateral septum prior to sessions in which cocaine was self-administered under a progressive ratio schedule by rats. The results indicated that administration of a D1/5 (SCH-23390) or a D2/D3/D4 (eticlopride), but not a D3 (U99194A) or D4 (L-750,667), dopamine receptor antagonist into the core and Shell of the Nucleus Accumbens decreased the reinforcing efficacy of cocaine. However, in control experiments intra-accumbal core administration of SCH-23390 or eticlopride decreased food self-administration, whereas administration of these drugs into the Accumbens Shell had no effect on food reinforcement. Neither SCH-23390 nor eticlopride influenced cocaine reinforcement when administered into the neostriatum or lateral septum. Collectively, these results indicate that D1-like and D2 dopamine receptors in the Nucleus Accumbens Shell selectively modulate the reinforcing efficacy of cocaine, whereas D1-like and D2 dopamine receptors in the Accumbens core have a more general influence on reinforced behaviors.

Zachary A Rodd - One of the best experts on this subject based on the ideXlab platform.

  • Adolescent Intermittent Ethanol (AIE) Enhances the Dopaminergic Response to Ethanol within the Mesolimbic Pathway during Adulthood: Alterations in Cholinergic/Dopaminergic Genes Expression in the Nucleus Accumbens Shell
    'MDPI AG', 2021
    Co-Authors: Sheketha R Hauser, Eric A Engleman, Patrick J. Mulholland, William A. Truitt, Aaron R. Waeiss, Richard L. Bell, Zachary A Rodd
    Abstract:

    A consistent preclinical finding is that exposure to alcohol during adolescence produces a persistent hyperdopaminergic state during adulthood. The current experiments determine that effects of Adolescent Intermittent Ethanol (AIE) on the adult neurochemical response to EtOH administered directly into the mesolimbic dopamine system, alterations in dendritic spine and gene expression within the Nucleus Accumbens Shell (AcbSh), and if treatment with the HDACII inhibitor TSA could normalize the consequences of AIE. Rats were exposed to the AIE (4 g/kg ig; 3 days a week) or water (CON) during adolescence, and all testing occurred during adulthood. CON and AIE rats were microinjected with EtOH directly into the posterior VTA and dopamine and glutamate levels were recorded in the AcbSh. Separate groups of AIE and CON rats were sacrificed during adulthood and Taqman arrays and dendritic spine morphology assessments were performed. The data indicated that exposure to AIE resulted in a significant leftward and upward shift in the dose-response curve for an increase in dopamine in the AcbSh following EtOH microinjection into the posterior VTA. Taqman array indicated that AIE exposure affected the expression of target genes (Chrna7, Impact, Chrna5). The data indicated no alterations in dendritic spine morphology in the AcbSh or any alteration in AIE effects by TSA administration. Binge-like EtOH exposure during adolescence enhances the response to acute ethanol challenge in adulthood, demonstrating that AIE produces a hyperdopaminergic mesolimbic system in both male and female Wistar rats. The neuroadaptations induced by AIE in the AcbSh could be part of the biological basis of the observed negative consequences of adolescent binge-like alcohol exposure on adult drug self-administration behaviors

  • reduced ethanol consumption by alcohol preferring p rats following pharmacological silencing and deep brain stimulation of the Nucleus Accumbens Shell laboratory investigation
    Journal of Neurosurgery, 2014
    Co-Authors: Jessica A Wilden, William J Mcbride, Kurt Y Qing, Sheketha R Hauser, Pedro P Irazoqui, Zachary A Rodd
    Abstract:

    Object There is increasing interest in deep brain stimulation (DBS) for the treatment of addiction. Initial testing must be conducted in animals, and the alcohol-preferring (P) rat meets the criteria for an animal model of alcoholism. This study is composed of 2 experiments designed to examine the effects of 1) pharmacological inactivation and 2) DBS of the Nucleus Accumbens Shell (AcbSh) on the consumption of alcohol by P rats. Methods In the first experiment, the effects of reversible inactivation of the AcbSh were investigated by administering intracranial injections of γ–aminobutyric acid (GABA) agonists. Bilateral microinjections of drug were administered to the AcbSh in P rats (8–10 rats/group), after which the animals were placed in operant chambers containing 2 levers—one used to administer water and the other to administer 15% EtOH—to examine the acquisition and maintenance of oral EtOH self-administration. In the second experiment, a DBS electrode was placed in each P rat's left AcbSh. The anima...

  • microinjections of acetaldehyde or salsolinol into the posterior ventral tegmental area increase dopamine release in the Nucleus Accumbens Shell
    Alcoholism: Clinical and Experimental Research, 2013
    Co-Authors: Gerald A Deehan, Eric A Engleman, Zhengming Ding, William J Mcbride, Zachary A Rodd
    Abstract:

    Background Published findings indicate that acetaldehyde (ACD; the first metabolite of ethanol [EtOH]) and salsolinol (SAL; formed through the nonenzymatic condensation of ACD and dopamine [DA]) can be formed following EtOH consumption. Both ACD and SAL exhibit reinforcing properties within the posterior ventral tegmental area (pVTA) and both exhibit an inverted “U-shaped” dose–response curve. The current study was undertaken to examine the dose–response effects of microinjections of ACD or SAL into the pVTA on DA efflux in the Nucleus Accumbens Shell (AcbSh). Methods For the first experiment, separate groups of male Wistar rats received pulse microinjections of artificial cerebrospinal fluid (aCSF) or 12-, 23-, or 90-μM ACD into the pVTA, while extracellular DA levels were concurrently measured in the AcbSh. The second experiment was similarly conducted, except rats were given microinjections of aCSF or 0.03-, 0.3-, 1.0-, or 3.0-μM SAL, while extracellular levels of DA were measured in the AcbSh. Results Both ACD and SAL produced a dose-dependent inverted “U-shaped” response on DA release in the AcbSh, with 23-μM ACD (200% baseline) and 0.3-μM SAL (300% baseline) producing maximal peak responses with higher concentrations of ACD (90 μM) and SAL (3.0 μM) producing significantly lower DA efflux. Conclusions The findings from the current study indicate that local application of intermediate concentrations of ACD and SAL stimulated DA neurons in the pVTA, whereas higher concentrations may be having secondary effects within the pVTA that inhibit DA neuronal activity. The present results parallel the studies on the reinforcing effects of ACD and SAL in the pVTA and support the idea that the reinforcing effects of ACD and SAL within the pVTA are mediated by activating DA neurons.

G Di Chiara - One of the best experts on this subject based on the ideXlab platform.

  • Nucleus Accumbens Shell and core dopamine responsiveness to sucrose in rats role of response contingency and discriminative conditioned cues
    European Journal of Neuroscience, 2015
    Co-Authors: Valentina Bassareo, Daniele Lecca, Flavia Cucca, P Musio, Roberto Frau, G Di Chiara
    Abstract:

    This study investigated by microdialysis the role of response contingency and food-associated cues in the responsiveness of dopamine transmission in the Nucleus Accumbens Shell and core to sucrose feeding. In naive rats, single-trial non-contingent presentation and feeding of sucrose pellets increased dialysate Shell dopamine and induced full habituation of dopamine responsiveness to sucrose feeding 24 and 48 h later. In rats trained to respond for sucrose pellets on a fixed ratio 1 (FR1) schedule, dialysate dopamine increased in the Shell but not in the core during active responding as well as under extinction in the presence of sucrose cues. In rats yoked to the operant rats, the presentation of sucrose cues also increased dialysate dopamine selectively in the Shell. In contrast, non-contingent sucrose presentation and feeding in FR1-trained and in yoked rats increased dialysate dopamine to a similar extent in the Shell and core. It is concluded that, whereas non-contingent sucrose feeding activated dopamine transmission in the Shell and core, response-contingent feeding activated, without habituation, dopamine transmission selectively in the Shell as a result of the action of sucrose conditioned cues. These observations are consistent with a critical role of conditioned cues acquired during training and differential activation of Shell vs. core dopamine for response-contingent sucrose feeding.

  • drug addiction as dopamine dependent associative learning disorder
    European Journal of Pharmacology, 1999
    Co-Authors: G Di Chiara
    Abstract:

    Natural rewards preferentially stimulate dopamine transmission in the Nucleus Accumbens Shell. This effect undergoes adaptive changes (one-trial habituation, inhibition by appetitive stimuli) that are consistent with a role of Nucleus Accumbens Shell dopamine in associative reward-related learning. Experimental studies with a variety of paradigms confirm this role. A role in associative stimulus-reward learning can provide an explanation for the extinction-like impairment of primary reinforcement that led Wise to propose the 'anhedonia hypothesis'. Addictive drugs share with natural rewards the property of stimulating dopamine transmission preferentially in the Nucleus Accumbens Shell. This response, however, in contrast to that to natural rewards, is not subjected to one-trial habituation. Resistance to habituation allows drugs to activate dopamine transmission in the Shell non-decrementally upon repeated self-administration. It is hypothesized that this process abnormally strengthens stimulus-drug associations thus resulting in the attribution of excessive motivational value to discrete stimuli or contexts predictive of drug availability. Addiction is therefore the expression of the excessive control over behaviour acquired by drug-related stimuli as a result of abnormal associative learning following repeated stimulation of dopamine transmission in the Nucleus Accumbens Shell.

  • drug addiction as a disorder of associative learning role of Nucleus Accumbens Shell extended amygdala dopamine
    Annals of the New York Academy of Sciences, 1999
    Co-Authors: G Di Chiara, Gianluigi Tanda, Valentina Bassareo, Francesco E Pontieri, Elio Maria Gioachino Acquas, Sandro Fenu, C Cadoni, E Carboni
    Abstract:

    Conventional reinforcers phasically stimulate dopamine transmission in the Nucleus Accumbens Shell. This property undergoes one-trial habituation consistent with a role of Nucleus Accumbens Shell dopamine in associative learning. Experimental studies with place- and taste-conditioning paradigms confirm this role. Addictive drugs share with conventional reinforcers the property of stimulating dopamine transmission in the Nucleus Accumbens Shell. This response, however, undergoes one-trial habituation in the case of conventional reinforcers but not of drugs. Resistance to habituation allows drugs to repetitively activate dopamine transmission in the Shell upon repeated self-administration. This process abnormally facilitates associative learning, leading to the attribution of excessive motivational value to discrete stimuli or contexts predictive of drug availability. Addiction is therefore the expression of the excessive control over behavior acquired by drug-related stimuli as a result of abnormal strenghtening of stimulus-drug contingencies by nondecremental drug-induced stimulation of dopamine transmission in the Nucleus Accumbens Shell.

  • reciprocal changes in dopamine responsiveness in the Nucleus Accumbens Shell and core and in the dorsal caudate putamen in rats sensitized to morphine
    Neuroscience, 1999
    Co-Authors: Cristina Cadoni, G Di Chiara
    Abstract:

    Abstract In this study, we describe a model of opiate sensitization characterized by a brief schedule of treatment with repeated morphine administrations. In this model, we investigated the changes produced by repeated morphine treatment on dopamine transmission at the level of the two major terminal dopaminergic areas, the dorsolateral caudate–putamen and the Nucleus Accumbens in its two subdivisions, the Shell and the core. Rats were treated twice a day for three days with increasing doses of morphine (10, 20 and 40 mg/kg, s.c.) or with saline. After 15 days of withdrawal, rats were challenged with 1 and 5 mg/kg (s.c.) of morphine, and dopamine transmission was monitored by microdialysis. In this model, we show that repeated morphine produces a strong behavioral sensitization accompained by increased stimulation of dopamine transmission in the core of the Nucleus Accumbens and in the caudate–putamen, and by a decreased stimulation of dopamine transmission in the Shell of the Nucleus Accumbens, as compared to control rats. Moreover, we administered to these animals amphetamine (0.5 mg/kg, s.c.) and cocaine (10 mg/kg, i.p.) to assess whether cross-sensitization occurs between opiates and psychostimulants in conditions independent of the context. In the present study, we did not observe either behavioral or biochemical sensitization to amphetamine and to cocaine in rats sensitized to morphine. These results suggest that rats behaviorally sensitized to morphine show opposite changes in the stimulant effect of morphine in the Nucleus Accumbens Shell and core and in the dorsal caudate–putamen. Moreover, this study suggests that sensitization of the dopamine system to a given agent does not necessarily extend to drugs of abuse of different pharmacological classes.

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