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  1. AU="Hollander, Jonathan A"
  2. AU="Polidoro, Silvia"
  3. AU="Dausset, J"
  4. AU=Eijkholt Marleen
  5. AU=Sousa Braian L A AU=Sousa Braian L A
  6. AU="Fresel, Marielle"
  7. AU="Ilana Babaev"
  8. AU="Tang, Hang"
  9. AU="McBride, Erin"

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  1. Artikel ; Online: Seminar: Extracellular Vesicles as Mediators of Environmental Stress in Human Disease.

    Kalia, Vrinda / Baccarelli, Andrea A / Happel, Christine / Hollander, Jonathan A / Jukic, Anne Marie / McAllister, Kimberly A / Menon, Ramkumar / Merrick, Bruce A / Milosavljevic, Aleksander / Ravichandran, Lingamanaidu V / Roth, Matthew E / Subramanian, Anita / Tyson, Frederick L / Worth, Leroy / Shaughnessy, Daniel T

    Environmental health perspectives

    2023  Band 131, Heft 10, Seite(n) 104201

    Abstract: Background: Extracellular vesicles (EVs), membrane-bound particles containing a variety of RNA types, DNA, proteins, and other macromolecules, are now appreciated as an important means of communication between cells and tissues, both in normal cellular ... ...

    Abstract Background: Extracellular vesicles (EVs), membrane-bound particles containing a variety of RNA types, DNA, proteins, and other macromolecules, are now appreciated as an important means of communication between cells and tissues, both in normal cellular physiology and as a potential indicator of cellular stress, environmental exposures, and early disease pathogenesis. Extracellular signaling through EVs is a growing field of research for understanding fundamental mechanisms of health and disease and for the potential for biomarker discovery and therapy development. EVs are also known to play important roles in mediating the effects of exposure to environmental stress.
    Objectives: This seminar addresses the application of new tools and approaches for EV research, developed in part through the National Institutes of Health (NIH) Extracellular RNA Communication Program, and reflects presentations and discussions from a workshop held 27-28 September 2021 by the National Institute of Environmental Health Sciences (NIEHS) and the National Center for Advancing Translational Sciences (NCATS) on "Extracellular Vesicles, Exosomes, and Cell-Cell Signaling in Response to Environmental Stress." The panel of experts discussed current research on EVs and environmental exposures, highlighted recent advances in EV isolation and characterization, and considered research gaps and opportunities toward identifying and characterizing the roles for EVs in environmentally related diseases, as well as the current challenges and opportunities in this field.
    Discussion: The authors discuss the application of new experimental models, particularly organ-on-chip (OOC) systems and
    Mesh-Begriff(e) Humans ; Biomarkers/metabolism ; Environmental Exposure ; Exosomes/metabolism ; Extracellular Vesicles/metabolism ; RNA/metabolism
    Chemische Substanzen Biomarkers ; RNA (63231-63-0)
    Sprache Englisch
    Erscheinungsdatum 2023-10-20
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 195189-0
    ISSN 1552-9924 ; 0091-6765 ; 1078-0475
    ISSN (online) 1552-9924
    ISSN 0091-6765 ; 1078-0475
    DOI 10.1289/EHP12980
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: 2021 Workshop: Neurodegenerative Diseases in the Gut-Brain Axis-Parkinson's Disease.

    Mawe, Gary M / Browning, Kirsteen N / Manfredsson, Fredric P / Camilleri, Michael / Hamilton, Frank A / Hollander, Jonathan A / Sieber, Beth-Anne / Greenwel, Patricia / Shea-Donohue, Terez / Wiley, John W

    Gastroenterology

    2022  Band 162, Heft 6, Seite(n) 1574–1582

    Mesh-Begriff(e) Brain/diagnostic imaging ; Brain-Gut Axis ; Gastrointestinal Microbiome ; Humans ; Neurodegenerative Diseases ; Parkinson Disease/diagnosis
    Sprache Englisch
    Erscheinungsdatum 2022-02-08
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 80112-4
    ISSN 1528-0012 ; 0016-5085
    ISSN (online) 1528-0012
    ISSN 0016-5085
    DOI 10.1053/j.gastro.2022.02.004
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  3. Artikel: Abstinence from cocaine self-administration heightens neural encoding of goal-directed behaviors in the accumbens.

    Hollander, Jonathan A / Carelli, Regina M

    Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

    2005  Band 30, Heft 8, Seite(n) 1464–1474

    Abstract: Cocaine addiction in humans is characterized by cycles of abstinence from drug-taking and relapse. Here, electrophysiological recording procedures were used to determine whether nucleus accumbens (Acb) neuronal firing properties are altered following ... ...

    Abstract Cocaine addiction in humans is characterized by cycles of abstinence from drug-taking and relapse. Here, electrophysiological recording procedures were used to determine whether nucleus accumbens (Acb) neuronal firing properties are altered following interruption and resumption of cocaine self-administration. Rats (n = 12) were trained to self-administer cocaine (2 h daily sessions) then divided into two groups. Acb activity was recorded for Group 1 (controls) during two additional self-administration sessions completed over the next 2 days (test sessions 1 and 2). Acb activity was recorded for Group 2 (1-month) during one self-administration session completed the next day (test 1), and during a second self-administration session 1 month later (test 2). As in prior reports, a subset of Acb neurons exhibited patterned discharges (short duration and/or long-term cyclic alterations, termed 'phasically active') relative to cocaine-reinforced responding during test session 1. Remarkably, the percentage of phasically active cells dramatically increased (nearly two-fold) following 1-month abstinence, in the core but not the shell of the Acb. Likewise, the strength of the neural correlates (determined via signal-to-baseline ratios) also increased as a function of abstinence. Extinction experiments in another set of rats (n = 12) revealed an increased motivational state for the drug following abstinence. The results show that abstinence from cocaine self-administration causes a dramatic increase in the number and strength of Acb neurons that encode cocaine-related information, thus representing the first neurophysiological correlate of heightened activation of the 'brain reward system' following abstinence and resumption (relapse) of cocaine consumption.
    Mesh-Begriff(e) Action Potentials/drug effects ; Action Potentials/physiology ; Animals ; Behavior, Animal ; Cocaine/administration & dosage ; Cocaine-Related Disorders/physiopathology ; Dopamine Uptake Inhibitors/administration & dosage ; Extinction, Psychological/drug effects ; Extinction, Psychological/physiology ; Male ; Neurons/classification ; Neurons/drug effects ; Neurons/physiology ; Nucleus Accumbens/cytology ; Nucleus Accumbens/drug effects ; Nucleus Accumbens/physiology ; Psychomotor Performance/drug effects ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Self Administration ; Time Factors
    Chemische Substanzen Dopamine Uptake Inhibitors ; Cocaine (I5Y540LHVR)
    Sprache Englisch
    Erscheinungsdatum 2005-08
    Erscheinungsland England
    Dokumenttyp Comparative Study ; Journal Article ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 639471-1
    ISSN 1740-634X ; 0893-133X
    ISSN (online) 1740-634X
    ISSN 0893-133X
    DOI 10.1038/sj.npp.1300748
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Hypocretin-1 receptors regulate the reinforcing and reward-enhancing effects of cocaine: pharmacological and behavioral genetics evidence.

    Hollander, Jonathan A / Pham, Don / Fowler, Christie D / Kenny, Paul J

    Frontiers in behavioral neuroscience

    2012  Band 6, Seite(n) 47

    Abstract: Considerable evidence suggests that transmission at hypocretin-1 (orexin-1) receptors (Hcrt-R1) plays an important role in the reinstatement of extinguished cocaine-seeking behaviors in rodents. However, far less is known about the role for hypocretin ... ...

    Abstract Considerable evidence suggests that transmission at hypocretin-1 (orexin-1) receptors (Hcrt-R1) plays an important role in the reinstatement of extinguished cocaine-seeking behaviors in rodents. However, far less is known about the role for hypocretin transmission in regulating ongoing cocaine-taking behavior. Here, we investigated the effects of the selective Hcrt-R1 antagonist SB-334867 on cocaine intake, as measured by intravenous (IV) cocaine self-administration in rats. The stimulatory effects of cocaine on brain reward systems contribute to the establishment and maintenance of cocaine-taking behaviors. Therefore, we also assessed the effects of SB-334867 on the reward-enhancing properties of cocaine, as measured by cocaine-induced lowering of intracranial self-stimulation (ICSS) thresholds. Finally, to definitively establish a role for Hcrt-R1 in regulating cocaine intake, we assessed IV cocaine self-administration in Hcrt-R1 knockout mice. We found that SB-334867 (1-4 mg/kg) dose-dependently decreased cocaine (0.5 mg/kg/infusion) self-administration in rats but did not alter responding for food rewards under the same schedule of reinforcement. This suggests that SB-334867 decreased cocaine reinforcement without negatively impacting operant performance. SB-334867 (1-4 mg/kg) also dose-dependently attenuated the stimulatory effects of cocaine (10 mg/kg) on brain reward systems, as measured by reversal of cocaine-induced lowering of ICSS thresholds in rats. Finally, we found that Hcrt-R1 knockout mice self-administered far less cocaine than wildtype mice across the entire dose-response function. These data demonstrate that Hcrt-R1 play an important role in regulating the reinforcing and reward-enhancing properties of cocaine and suggest that hypocretin transmission is likely essential for establishing and maintaining the cocaine habit in human addicts.
    Sprache Englisch
    Erscheinungsdatum 2012-07-24
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article
    ZDB-ID 2452960-6
    ISSN 1662-5153 ; 1662-5153
    ISSN (online) 1662-5153
    ISSN 1662-5153
    DOI 10.3389/fnbeh.2012.00047
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Cocaine-associated stimuli increase cocaine seeking and activate accumbens core neurons after abstinence.

    Hollander, Jonathan A / Carelli, Regina M

    The Journal of neuroscience : the official journal of the Society for Neuroscience

    2003  Band 27, Heft 13, Seite(n) 3535–3539

    Abstract: Electrophysiological recordings were completed in rats (n = 14) trained to self-administer cocaine to determine whether activation of nucleus accumbens (Acb) neurons (core vs shell) by cocaine-associated stimuli is enhanced after 1 month of cocaine ... ...

    Abstract Electrophysiological recordings were completed in rats (n = 14) trained to self-administer cocaine to determine whether activation of nucleus accumbens (Acb) neurons (core vs shell) by cocaine-associated stimuli is enhanced after 1 month of cocaine abstinence. After self-administration training, 170 cells were recorded during a single test session conducted either the next day or 1 month later. The test session consisted of three phases during which (1) the cocaine cue was presented unexpectedly to rats, (2) rats responded for the same cue in the absence of the drug (extinction), and (3) the cocaine cue was presented randomly between cocaine-reinforced responding during resumption of self-administration. The cocaine stimulus significantly increased activation of Acb core (not shell) neurons after 1 month of cocaine abstinence (compared with 1 d); this finding occurred regardless of contingency of cue presentation or cocaine availability. Acb core activation was not observed in other rats (n = 7) presented with the same stimulus never paired with cocaine. The results reflect a cellular neuroadaptation in the Acb core related to cocaine-associated cues that is observed during initial cue exposure and sustained during extinction and resumption of self-administration after prolonged drug abstinence.
    Mesh-Begriff(e) Animals ; Behavior, Addictive/physiopathology ; Cocaine/pharmacology ; Cocaine-Related Disorders/physiopathology ; Conditioning, Operant/drug effects ; Cues ; Extinction, Psychological/physiology ; Male ; Neurons/drug effects ; Nucleus Accumbens/cytology ; Nucleus Accumbens/drug effects ; Nucleus Accumbens/physiopathology ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Self Administration
    Chemische Substanzen Cocaine (I5Y540LHVR)
    Sprache Englisch
    Erscheinungsdatum 2003-12-11
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 604637-x
    ISSN 1529-2401 ; 0270-6474
    ISSN (online) 1529-2401
    ISSN 0270-6474
    DOI 10.1523/JNEUROSCI.3667-06.2007
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel: Decreased brain reward function during nicotine withdrawal in C57BL6 mice: evidence from intracranial self-stimulation (ICSS) studies.

    Johnson, Paul M / Hollander, Jonathan A / Kenny, Paul J

    Pharmacology, biochemistry, and behavior

    2008  Band 90, Heft 3, Seite(n) 409–415

    Abstract: Deficits in brain reward function during nicotine withdrawal may serve as an important substrate for negative reinforcement that contributes to the persistence of the tobacco habit in human smokers. The ability to assess withdrawal-associated reward ... ...

    Abstract Deficits in brain reward function during nicotine withdrawal may serve as an important substrate for negative reinforcement that contributes to the persistence of the tobacco habit in human smokers. The ability to assess withdrawal-associated reward deficits in genetically modified mice may facilitate understanding of the neurobiological mechanisms of nicotine dependence. Here, we assessed the effects of nicotine withdrawal on brain reward function in mice, as measured by intracranial self-stimulation (ICSS) thresholds. Male C57BL6 mice were trained in a discrete-trial current-threshold ICSS procedure until stable reward thresholds were obtained. Mice then received experimenter-administered saline or nicotine (2 mg/kg/injection salt; x4 daily) injections for 7 consecutive days, and ICSS thresholds assessed for 3 days after cessation of injections. Thresholds were unaltered in nicotine- and saline-treated mice after cessation of injections, indicating that this treatment regimen was not sufficient to induce withdrawal-associated reward deficits. Next, mice were implanted subcutaneously with osmotic minipumps delivering a constant daily amount of saline or nicotine (24 mg/kg/day; free-base), with pumps surgically removed 13 days later. The nicotinic receptor antagonist mecamylamine (2 mg/kg) elevated ICSS thresholds in nicotine- but not saline-treated mice when administered 8-10 days after pump implantation. Similarly, reward thresholds were elevated in nicotine-treated mice 12-72 h after minipump removal. These data demonstrate that antagonist-precipitated or spontaneous withdrawal from nicotine delivered via osmotic minipumps induced reward deficits in mice. Further, these findings highlight the potential utility of the ICSS procedure for assessing this important affective component of nicotine withdrawal in genetically modified mice.
    Mesh-Begriff(e) Animals ; Brain/physiology ; Drug Implants ; Electrodes, Implanted ; Male ; Mecamylamine/pharmacology ; Mice ; Mice, Inbred C57BL ; Nicotine/adverse effects ; Nicotinic Agonists/adverse effects ; Nicotinic Antagonists/pharmacology ; Reward ; Self Stimulation ; Substance Withdrawal Syndrome/psychology ; Tobacco Use Disorder/psychology
    Chemische Substanzen Drug Implants ; Nicotinic Agonists ; Nicotinic Antagonists ; Mecamylamine (6EE945D3OK) ; Nicotine (6M3C89ZY6R)
    Sprache Englisch
    Erscheinungsdatum 2008-04-04
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 191042-5
    ISSN 1873-5177 ; 0091-3057
    ISSN (online) 1873-5177
    ISSN 0091-3057
    DOI 10.1016/j.pbb.2008.03.024
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: MeCP2 controls BDNF expression and cocaine intake through homeostatic interactions with microRNA-212.

    Im, Heh-In / Hollander, Jonathan A / Bali, Purva / Kenny, Paul J

    Nature neuroscience

    2010  Band 13, Heft 9, Seite(n) 1120–1127

    Abstract: The X-linked transcriptional repressor methyl CpG binding protein 2 (MeCP2), known for its role in the neurodevelopmental disorder Rett syndrome, is emerging as an important regulator of neuroplasticity in postmitotic neurons. Cocaine addiction is ... ...

    Abstract The X-linked transcriptional repressor methyl CpG binding protein 2 (MeCP2), known for its role in the neurodevelopmental disorder Rett syndrome, is emerging as an important regulator of neuroplasticity in postmitotic neurons. Cocaine addiction is commonly viewed as a disorder of neuroplasticity, but the potential involvement of MeCP2 has not been explored. Here we identify a key role for MeCP2 in the dorsal striatum in the escalating cocaine intake seen in rats with extended access to the drug, a process that mimics the increasingly uncontrolled cocaine use seen in addicted humans. MeCP2 regulates cocaine intake through homeostatic interactions with microRNA-212 (miR-212) to control the effects of cocaine on striatal brain-derived neurotrophic factor (BDNF) levels. These data suggest that homeostatic interactions between MeCP2 and miR-212 in dorsal striatum may be important in regulating vulnerability to cocaine addiction.
    Mesh-Begriff(e) Animals ; Brain-Derived Neurotrophic Factor/genetics ; Brain-Derived Neurotrophic Factor/metabolism ; Cocaine/pharmacology ; Cocaine-Related Disorders/genetics ; Cocaine-Related Disorders/metabolism ; Compulsive Behavior/genetics ; Compulsive Behavior/metabolism ; Corpus Striatum/drug effects ; Corpus Striatum/metabolism ; Dopamine Uptake Inhibitors/pharmacology ; Gene Expression Regulation ; Gene Knockdown Techniques ; Male ; Methyl-CpG-Binding Protein 2/genetics ; Methyl-CpG-Binding Protein 2/metabolism ; MicroRNAs/metabolism ; Rats ; Rats, Wistar ; Self Administration
    Chemische Substanzen Brain-Derived Neurotrophic Factor ; Dopamine Uptake Inhibitors ; MIRN212 microRNA, rat ; Mecp2 protein, rat ; Methyl-CpG-Binding Protein 2 ; MicroRNAs ; Cocaine (I5Y540LHVR)
    Sprache Englisch
    Erscheinungsdatum 2010-08-15
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1420596-8
    ISSN 1546-1726 ; 1097-6256
    ISSN (online) 1546-1726
    ISSN 1097-6256
    DOI 10.1038/nn.2615
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: Beyond the looking glass: recent advances in understanding the impact of environmental exposures on neuropsychiatric disease.

    Hollander, Jonathan A / Cory-Slechta, Deborah A / Jacka, Felice N / Szabo, Steven T / Guilarte, Tomás R / Bilbo, Staci D / Mattingly, Carolyn J / Moy, Sheryl S / Haroon, Ebrahim / Hornig, Mady / Levin, Edward D / Pletnikov, Mikhail V / Zehr, Julia L / McAllister, Kimberly A / Dzierlenga, Anika L / Garton, Amanda E / Lawler, Cindy P / Ladd-Acosta, Christine

    Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

    2020  Band 45, Heft 7, Seite(n) 1086–1096

    Abstract: The etiologic pathways leading to neuropsychiatric diseases remain poorly defined. As genomic technologies have advanced over the past several decades, considerable progress has been made linking neuropsychiatric disorders to genetic underpinnings. ... ...

    Abstract The etiologic pathways leading to neuropsychiatric diseases remain poorly defined. As genomic technologies have advanced over the past several decades, considerable progress has been made linking neuropsychiatric disorders to genetic underpinnings. Interest and consideration of nongenetic risk factors (e.g., lead exposure and schizophrenia) have, in contrast, lagged behind heritable frameworks of explanation. Thus, the association of neuropsychiatric illness to environmental chemical exposure, and their potential interactions with genetic susceptibility, are largely unexplored. In this review, we describe emerging approaches for considering the impact of chemical risk factors acting alone and in concert with genetic risk, and point to the potential role of epigenetics in mediating exposure effects on transcription of genes implicated in mental disorders. We highlight recent examples of research in nongenetic risk factors in psychiatric disorders that point to potential shared biological mechanisms-synaptic dysfunction, immune alterations, and gut-brain interactions. We outline new tools and resources that can be harnessed for the study of environmental factors in psychiatric disorders. These tools, combined with emerging experimental evidence, suggest that there is a need to broadly incorporate environmental exposures in psychiatric research, with the ultimate goal of identifying modifiable risk factors and informing new treatment strategies for neuropsychiatric disease.
    Mesh-Begriff(e) Environmental Exposure/adverse effects ; Humans ; Mental Disorders/etiology
    Sprache Englisch
    Erscheinungsdatum 2020-02-28
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 639471-1
    ISSN 1740-634X ; 0893-133X
    ISSN (online) 1740-634X
    ISSN 0893-133X
    DOI 10.1038/s41386-020-0648-5
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel: Insular hypocretin transmission regulates nicotine reward

    Hollander, Jonathan A / Lu, Qun / Cameron, Michael D / Kamenecka, Theodore M / Kenny, Paul J

    Proceedings of the National Academy of Sciences of the United States of America. 2008 Dec. 9, v. 105, no. 49

    2008  

    Abstract: Damage to the insular cortex can profoundly disrupt tobacco addiction in human smokers, reflected in spontaneous cessation of the tobacco habit and persistently decreased urge to smoke. Little is known concerning the neurobiological mechanisms through ... ...

    Abstract Damage to the insular cortex can profoundly disrupt tobacco addiction in human smokers, reflected in spontaneous cessation of the tobacco habit and persistently decreased urge to smoke. Little is known concerning the neurobiological mechanisms through which the insula may control the maintenance of the tobacco habit. Emerging evidence suggests that hypocretin (orexin) transmission may play an important role in drug reinforcement processes, but its role in the rewarding actions of nicotine, considered the key addictive component of tobacco smoke, remains largely unexplored. Here we show that blockade of hypocretin transmission at hypocretin-1 (Hcrt-1; orexin-1) receptors decreases i.v. nicotine self-administration in rats and the motivation to obtain the drug. Blockade of Hcrt-1 receptors also abolished the stimulatory effects of nicotine on brain reward circuitries, as measured by reversal of nicotine-induced lowering of intracranial self-stimulation thresholds. In addition, we show that hypocretin-containing fibers innervate the insula, Hcrt-1 receptors are located on insular cells, and blockade of Hcrt-1 receptors in the insula but not in the adjacent somatosensory cortex decreases nicotine self-administration. These data demonstrate that insular hypocretin transmission plays a permissive role in the motivational properties of nicotine, and therefore may be a key neurobiological substrate necessary for maintaining tobacco addiction in human smokers.
    Schlagwörter brain ; cortex ; drugs ; humans ; motivation ; nicotine ; rats ; receptors ; smoking (habit) ; tobacco
    Sprache Englisch
    Erscheinungsverlauf 2008-1209
    Umfang p. 19480-19485.
    Erscheinungsort National Academy of Sciences
    Dokumenttyp Artikel
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.0808023105
    Datenquelle NAL Katalog (AGRICOLA)

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  10. Artikel ; Online: Basolateral amygdala neurons encode cocaine self-administration and cocaine-associated cues.

    Carelli, Regina M / Williams, Jefferson G / Hollander, Jonathan A

    The Journal of neuroscience : the official journal of the Society for Neuroscience

    2003  Band 23, Heft 23, Seite(n) 8204–8211

    Abstract: Electrophysiological recording procedures were used to examine basolateral amygdala (BLA) cell firing during cocaine self-administration and relative to response-independent presentations of cocaine-associated stimuli. Of 72 neurons (n = 10 rats), 31 ... ...

    Abstract Electrophysiological recording procedures were used to examine basolateral amygdala (BLA) cell firing during cocaine self-administration and relative to response-independent presentations of cocaine-associated stimuli. Of 72 neurons (n = 10 rats), 31 cells (43%) were classified as phasically active, exhibiting one of three types of patterned discharges relative to the drug-reinforced response, similar to that previously described for nucleus accumbens (Acb) neurons (Carelli, 2002). Briefly, neurons exhibited increased firing rates within seconds preceding the response [termed preresponse (PR)], increased activity within seconds after the response [termed reinforcement excitation (RFe)] or an inhibition in cell firing before and/or after the response for intravenous cocaine [termed reinforcement inhibition (RFi)]. To examine the responsiveness of these same neurons to cocaine-associated stimuli, the stimulus "probe" procedure was used. Specifically, probe trials (18-20) were presented in which the audiovisual (tone-house light) stimulus associated with intravenous cocaine delivery during self-administration was randomly presented by the computer, interspersed between reinforced lever press responses. Neurons classified as type PR or type RFi were not activated by the stimulus. In contrast, neurons that exhibited increased firing immediately after the response (type RFe neurons) were significantly activated by the audiovisual cue. These findings are discussed with respect to the role of the BLA in cocaine addiction as well as previous studies characterizing Acb cell firing during cocaine self-administration.
    Mesh-Begriff(e) Acoustic Stimulation ; Amygdala/cytology ; Amygdala/drug effects ; Amygdala/physiology ; Animals ; Behavior, Animal/drug effects ; Cocaine/administration & dosage ; Cocaine-Related Disorders/physiopathology ; Conditioning, Operant ; Cues ; Electrodes, Implanted ; Electrophysiology ; Neurons/cytology ; Neurons/drug effects ; Neurons/physiology ; Photic Stimulation ; Rats ; Reinforcement (Psychology) ; Self Administration
    Chemische Substanzen Cocaine (I5Y540LHVR)
    Sprache Englisch
    Erscheinungsdatum 2003-09-10
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 604637-x
    ISSN 1529-2401 ; 0270-6474
    ISSN (online) 1529-2401
    ISSN 0270-6474
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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