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  • 1
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1991-01-04
    Description: The N-methyl-D-aspartate (NMDA) subtype of the glutamate receptor is an important mediator of several forms of neural and behavioral plasticity. The present studies examined whether NMDA receptors might be involved in the development of opiate tolerance and dependence, two examples of behavioral plasticity. The noncompetitive NMDA receptor antagonist MK-801 attenuated the development of tolerance to the analgesic effect of morphine without affecting acute morphine analgesia. In addition, MK-801 attenuated the development of morphine dependence as assessed by naloxone-precipitated withdrawal. These results suggest that NMDA receptors may be important in the development of opiate tolerance and dependence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Trujillo, K A -- Akil, H -- DA02265/DA/NIDA NIH HHS/ -- DA05336/DA/NIDA NIH HHS/ -- MH422251/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1991 Jan 4;251(4989):85-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mental Health Research Institute, University of Michigan, Ann Arbor 48109-0720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1824728" target="_blank"〉PubMed〈/a〉
    Keywords: *Analgesia ; Animals ; Behavior, Animal/drug effects ; Dizocilpine Maleate/*pharmacology ; Drug Tolerance ; Male ; *Morphine ; Naloxone/pharmacology ; Pain Measurement ; Rats ; Rats, Inbred Strains ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/*physiology ; *Substance-Related Disorders
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2010-12-15
    Description: Individuals make choices and prioritize goals using complex processes that assign value to rewards and associated stimuli. During Pavlovian learning, previously neutral stimuli that predict rewards can acquire motivational properties, becoming attractive and desirable incentive stimuli. However, whether a cue acts solely as a predictor of reward, or also serves as an incentive stimulus, differs between individuals. Thus, individuals vary in the degree to which cues bias choice and potentially promote maladaptive behaviour. Here we use rats that differ in the incentive motivational properties they attribute to food cues to probe the role of the neurotransmitter dopamine in stimulus-reward learning. We show that intact dopamine transmission is not required for all forms of learning in which reward cues become effective predictors. Rather, dopamine acts selectively in a form of stimulus-reward learning in which incentive salience is assigned to reward cues. In individuals with a propensity for this form of learning, reward cues come to powerfully motivate and control behaviour. This work provides insight into the neurobiology of a form of stimulus-reward learning that confers increased susceptibility to disorders of impulse control.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058375/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058375/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flagel, Shelly B -- Clark, Jeremy J -- Robinson, Terry E -- Mayo, Leah -- Czuj, Alayna -- Willuhn, Ingo -- Akers, Christina A -- Clinton, Sarah M -- Phillips, Paul E M -- Akil, Huda -- 5P01-DA021633-02/DA/NIDA NIH HHS/ -- F32-DA24540/DA/NIDA NIH HHS/ -- P01 DA021633/DA/NIDA NIH HHS/ -- P01 DA021633-02/DA/NIDA NIH HHS/ -- R00 MH085859/MH/NIMH NIH HHS/ -- R00 MH085859-02/MH/NIMH NIH HHS/ -- R01 DA027858/DA/NIDA NIH HHS/ -- R01 MH079292/MH/NIMH NIH HHS/ -- R01-DA027858/DA/NIDA NIH HHS/ -- R01-MH079292/MH/NIMH NIH HHS/ -- R37-DA04294/DA/NIDA NIH HHS/ -- T32-DA07278/DA/NIDA NIH HHS/ -- England -- Nature. 2011 Jan 6;469(7328):53-7. doi: 10.1038/nature09588. Epub 2010 Dec 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Behavioral Neuroscience Institute, University of Michigan, Michigan, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21150898" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conditioning, Classical/drug effects/physiology ; *Cues ; Disruptive, Impulse Control, and Conduct Disorders/physiopathology ; Dopamine/*metabolism ; Dopamine Antagonists/pharmacology ; Flupenthixol/pharmacology ; Food ; Learning/drug effects/*physiology ; Male ; Microelectrodes ; *Models, Neurological ; Motivation/drug effects ; Nucleus Accumbens/metabolism ; Phenotype ; Probability ; Rats ; Rats, Sprague-Dawley ; *Reward ; Signal Transduction ; Synaptic Transmission
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2010-03-27
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3091000/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3091000/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akil, Huda -- Brenner, Sydney -- Kandel, Eric -- Kendler, Kenneth S -- King, Mary-Claire -- Scolnick, Edward -- Watson, James D -- Zoghbi, Huda Y -- P01 DA021633/DA/NIDA NIH HHS/ -- P01 DA021633-01A2/DA/NIDA NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Mar 26;327(5973):1580-1. doi: 10.1126/science.1188654.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular and Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, MI 48109, USA. akil@umich.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20339051" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*pathology/*physiopathology ; Forecasting ; Genetic Predisposition to Disease ; Genome, Human ; Genomics ; Humans ; Mental Disorders/*genetics/pathology/physiopathology ; Neural Pathways/pathology/physiopathology ; Sequence Analysis, DNA/economics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2011-02-12
    Description: Understanding the brain requires a broad range of approaches and methods from the domains of biology, psychology, chemistry, physics, and mathematics. The fundamental challenge is to decipher the "neural choreography" associated with complex behaviors and functions, including thoughts, memories, actions, and emotions. This demands the acquisition and integration of vast amounts of data of many types, at multiple scales in time and in space. Here we discuss the need for neuroinformatics approaches to accelerate progress, using several illustrative examples. The nascent field of "connectomics" aims to comprehensively describe neuronal connectivity at either a macroscopic level (in long-distance pathways for the entire brain) or a microscopic level (among axons, dendrites, and synapses in a small brain region). The Neuroscience Information Framework (NIF) encompasses all of neuroscience and facilitates the integration of existing knowledge and databases of many types. These examples illustrate the opportunities and challenges of data mining across multiple tiers of neuroscience information and underscore the need for cultural and infrastructure changes if neuroinformatics is to fulfill its potential to advance our understanding of the brain.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3102049/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3102049/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akil, Huda -- Martone, Maryann E -- Van Essen, David C -- 1U54MH091657-01/MH/NIMH NIH HHS/ -- 5P01-DA021633-02/DA/NIDA NIH HHS/ -- HHSN271200800035C/PHS HHS/ -- P01 DA021633/DA/NIDA NIH HHS/ -- P01 DA021633-01A2/DA/NIDA NIH HHS/ -- R01 MH060974/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2011 Feb 11;331(6018):708-12. doi: 10.1126/science.1199305.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Molecular and Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, MI, USA. akil@umich.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21311009" target="_blank"〉PubMed〈/a〉
    Keywords: Access to Information ; Animals ; Brain/anatomy & histology/*physiology ; *Computational Biology ; *Data Mining ; *Databases, Factual ; Humans ; Internet ; *Neural Pathways ; Neurons/physiology ; *Neurosciences ; Online Systems ; Terminology as Topic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 1978-05-26
    Description: There is compelling evidence that behavioral events after neurochemical function and that altered neurochemical function can change behavior. Such processes have been related both to neurotransmitters and to neuromodulators, together termed neuroregulators. Available research tools and theoretical constructs have begun to permit studies of certain types of behavior, primarily those related to emotional states and drives. This work is changing long-held concepts about severe mental disorders and the treatment of them.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barchas, J D -- Akil, H -- Elliott, G R -- Holman, R B -- Watson, S J -- New York, N.Y. -- Science. 1978 May 26;200(4344):964-73.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25486" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior/*physiology ; Cell Communication ; Depression/physiopathology ; Endorphins/physiology ; Enkephalins/physiology ; Hormones/physiology ; Humans ; Mental Disorders/physiopathology ; *Nervous System Physiological Phenomena ; Neurons/physiology ; Neurotransmitter Agents/physiology ; Schizophrenia/physiopathology ; Synapses/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 1978-07-07
    Description: Endogenous opiate-like peptides (endorphins) are putative neuroregulators located throughout the mammalian brainstem. There is some evidence for their role in pain, stress, and affect. We report that the opiate antagonist, naloxone, alters some schizophrenic symptoms. In a double-blind, cross-over study, naloxone produced decreases in auditory hallucinations in some schizophrenic patients. This finding supports the hypothesis that the endorphins may play a roll in modulating hallucinations in a highly selected subgroup of chronically hallucinating schizophrenic patients.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Watson, S J -- Berger, P A -- Akil, H -- Mills, M J -- Barchas, J D -- New York, N.Y. -- Science. 1978 Jul 7;201(4350):73-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/351804" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Chronic Disease ; Clinical Trials as Topic ; Dose-Response Relationship, Drug ; Double-Blind Method ; Endorphins/physiology ; Hallucinations/*drug therapy ; Humans ; Male ; Naloxone/administration & dosage/*therapeutic use ; Schizophrenia/*drug therapy/physiopathology ; Schizophrenia, Paranoid/drug therapy ; Time Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 1978-08-04
    Description: Enkephalin-like activity has been measured in the ventricular cerebrospinal fluid of patients with intractable pain. Electrical stimulation of periventricular brain sites resulted in significant decrease in persistent pain in these subjects. This analgesia, which was blocked by naloxone in 80% of the cases, was accompanied by a significant rise in ventricular enkephalin-like activity, as measured by two different methods. The results present evidence of in vivo release of enkephalin-like material in humans and suggest that stimulation analgesia may be partially due to this release.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akil, H -- Richardson, D E -- Hughes, J -- Barchas, J D -- New York, N.Y. -- Science. 1978 Aug 4;201(4354):463-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/663668" target="_blank"〉PubMed〈/a〉
    Keywords: Brain/*physiopathology ; Cerebral Aqueduct ; Electric Stimulation ; Endorphins/*cerebrospinal fluid ; Enkephalins/*cerebrospinal fluid ; Female ; Humans ; Male ; Pain/*cerebrospinal fluid/physiopathology ; Pain Management
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1982-12-10
    Description: Intracerebroventricular administration of dynorphin produced potent and long-lasting effects on motor function and the electroencephalogram in rats. In addition, local iontophoretic or pressure ejection of dynorphin consistently inhibited hippocampal unit activity. None of these effects were significantly affected by naloxone even at high doses. Moreover, a fragment of dynorphin that failed to displace any of a number of tritiated narcotics from rat brain homogenates produced similar effects on these physiological measures in vivo. On the basis of a variety of criteria for "opiate action," the results suggest that a second biologically active site within the dynorphin sequence is capable of quite potent but nonopiate effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Walker, J M -- Moises, H C -- Coy, D H -- Baldrighi, G -- Akil, H -- 1F32DA04183/DA/NIDA NIH HHS/ -- DA02265/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1982 Dec 10;218(4577):1136-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6128791" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Amino Acid Sequence ; Animals ; Dynorphins ; Endorphins/*physiology ; Hippocampus/*physiology ; Male ; Pain/*physiopathology ; Rats ; Structure-Activity Relationship
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 1982-12-10
    Description: A study of the anatomical distribution of the endogenous opioid dynorphin in rat brain showed that the peptide is localized in a widespread system with multiple cell groups and projections. This network is revealed by the use of multiple antiserums against dynorphin and can be distinguished from the system containing methionine-enkephalin and leucine-enkephalin, which is mapped by the use of antiserums against the enkephalins and biosynthetically related peptides in the adrenal. It thus appears that the brain contains at least three separate opioid neuronal networks: an enkephalin family with components similar to those found in the adrenal, a beta-endorphin family, and a dynorphin family.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Watson, S J -- Khachaturian, H -- Akil, H -- Coy, D H -- Goldstein, A -- DA00154/DA/NIDA NIH HHS/ -- DA02265/DA/NIDA NIH HHS/ -- MH15794/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1982 Dec 10;218(4577):1134-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6128790" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*physiology ; Brain Mapping ; Dynorphins ; Endorphins/*physiology ; Enkephalins/*physiology ; Immunologic Techniques ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 1982-04-02
    Description: The opioid peptide dynorphin is widely distributed in neuronal tissue of rats. By immunocytochemical methods, it was shown previously that dynorphin-like immunoreactivity is present in the posterior pituitary and the cells of the hypothalamic neurosecretory magnocellular nuclei which also are responsible for the synthesis of oxytocin, vasopressin, and their neurophysins. By using an affinity-purified antiserum to the non-enkephalin part of the dynorphin molecule it has now been demonstrated that dynorphin and vasopressin occur in the same hypothalamic cells of rats, whereas dynorphin and oxytocin occur in separate cells. Homozygous Brattleboro rats (deficient in vasopressin) have magnocellular neurons that contain dynorphin separate from oxytocin. Thus dynorphin and vasopressin, although they occur in the same cells, appear to be under separate genetic control and presumably arise from different precursors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Watson, S J -- Akil, H -- Fischli, W -- Goldstein, A -- Zimmerman, E -- Nilaver, G -- van wimersma Griedanus, T B -- DA 00254/DA/NIDA NIH HHS/ -- DA 02265/DA/NIDA NIH HHS/ -- DA1199/DA/NIDA NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1982 Apr 2;216(4541):85-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6121376" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine Vasopressin/*metabolism ; Dynorphins ; Endorphins/*metabolism ; Enkephalin, Leucine ; Enkephalins/metabolism ; Hypothalamus/cytology/*metabolism ; Immunologic Techniques ; Male ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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