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  • Articles  (4)
  • Science. 234(4777): 738-40.  (1)
  • Science. 263(5147): 689-92.  (1)
  • Science. 266(5183): 291-4.  (1)
  • Science. 276(5316): 1265-8.  (1)
  • 25
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  • Articles  (4)
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  • 1
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    Adenosine: a mediator of the sleep-inducing effects of prolonged wakefulness (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-05-23
    Description: Both subjective and electroencephalographic arousal diminish as a function of the duration of prior wakefulness. Data reported here suggest that the major criteria for a neural sleep factor mediating the somnogenic effects of prolonged wakefulness are satisfied by adenosine, a neuromodulator whose extracellular concentration increases with brain metabolism and which, in vitro, inhibits basal forebrain cholinergic neurons. In vivo microdialysis measurements in freely behaving cats showed that adenosine extracellular concentrations in the basal forebrain cholinergic region increased during spontaneous wakefulness as contrasted with slow wave sleep; exhibited progressive increases during sustained, prolonged wakefulness; and declined slowly during recovery sleep. Furthermore, the sleep-wakefulness profile occurring after prolonged wakefulness was mimicked by increased extracellular adenosine induced by microdialysis perfusion of an adenosine transport inhibitor in the cholinergic basal forebrain but not by perfusion in a control noncholinergic region.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3599777/" 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/PMC3599777/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Porkka-Heiskanen, T -- Strecker, R E -- Thakkar, M -- Bjorkum, A A -- Greene, R W -- McCarley, R W -- R01 MH039683/MH/NIMH NIH HHS/ -- R37 MH39,683/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1997 May 23;276(5316):1265-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Harvard Medical School, Brockton Veterans Administration Medical Center (VAMC), 116 A, 940 Belmont Street, Brockton, MA 02401, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9157887" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/antagonists & inhibitors/*physiology ; Animals ; Cats ; Electrophysiology ; Microdialysis ; Prosencephalon/physiology ; Sleep/*physiology ; Sleep Deprivation ; Thioinosine/analogs & derivatives/pharmacology ; Time Factors ; Wakefulness/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Abnormal fear response and aggressive behavior in mutant mice deficient for alpha-calcium-calmodulin kinase II (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-10-14
    Description: Mice deficient for the gene encoding alpha-calcium-calmodulin-dependent kinase II (alpha-CaMKII knockout mice) provide a promising tool to link behavioral and cellular abnormalities with a specific molecular lesion. The heterozygous mouse exhibited a well-circumscribed syndrome of behavioral abnormalities, consisting primarily of a decreased fear response and an increase in defensive aggression, in the absence of any measured cognitive deficits. Unlike the heterozygote, the homozygote displayed abnormal behavior in all paradigms tested. At the cellular level, both extracellular and whole-cell patch clamp recordings indicated that serotonin release in putative serotonergic neurons of the dorsal raphe was reduced. Thus, alpha-CaMKII knockout mice, in particular the heterozygote, may provide a model for studying the molecular and cellular basis underlying emotional disorders involving fear and aggression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, C -- Rainnie, D G -- Greene, R W -- Tonegawa, S -- New York, N.Y. -- Science. 1994 Oct 14;266(5183):291-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Center for Cancer Research, Cambridge, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7939668" target="_blank"〉PubMed〈/a〉
    Keywords: *Aggression ; Animals ; Behavior, Animal ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/deficiency/genetics/*physiology ; *Fear ; Fluoxetine/pharmacology ; Gene Dosage ; Heterozygote ; Homozygote ; In Vitro Techniques ; Membrane Potentials ; Mice ; Mice, Knockout ; Mutation ; Neurons/metabolism ; Patch-Clamp Techniques ; Raphe Nuclei/metabolism ; Serotonin/metabolism/pharmacology ; Synaptic Transmission/drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Adenosine inhibition of mesopontine cholinergic neurons: implications for EEG arousal (1994)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1994-02-04
    Description: Increased discharge activity of mesopontine cholinergic neurons participates in the production of electroencephalographic (EEG) arousal; such arousal diminishes as a function of the duration of prior wakefulness or of brain hyperthermia. Whole-cell and extracellular recordings in a brainstem slice show that mesopontine cholinergic neurons are under the tonic inhibitory control of endogenous adenosine, a neuromodulator released during brain metabolism. This inhibitory tone is mediated postsynaptically by an inwardly rectifying potassium conductance and by an inhibition of the hyperpolarization-activated current. These data provide a coupling mechanism linking neuronal control of EEG arousal with the effects of prior wakefulness, brain hyperthermia, and the use of the adenosine receptor blockers caffeine and theophylline.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3612520/" 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/PMC3612520/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rainnie, D G -- Grunze, H C -- McCarley, R W -- Greene, R W -- R01 MH039683/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1994 Feb 4;263(5147):689-92.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Harvard University, Brockton, MA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8303279" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/*physiology ; Animals ; Arousal/*physiology ; Calcium/metabolism ; Electric Conductivity ; *Electroencephalography/drug effects ; Female ; Frontal Lobe/physiology ; In Vitro Techniques ; Male ; Membrane Potentials ; Neurons/*physiology ; Parasympathetic Nervous System/*physiology ; Potassium/metabolism ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    A low threshold calcium spike mediates firing pattern alterations in pontine reticular neurons (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-11-07
    Description: Intracellular electrical recordings in an in vitro slice preparation of the brainstem medial pontine reticular formation, a region thought to be important in mediation of desynchronized sleep phenomena, demonstrate a population of neurons that have a calcium-dependent, low threshold spike. This low threshold spike was inactivated at relatively depolarized membrane potential levels and, when this spike was deinactivated, it induced a burst of action potentials. The membrane potential dependence of the spike may underlie changes in action potential firing patterns associated with behavioral state change because the baseline membrane potential in neurons of the medial pontine reticular population depolarizes during passage from waking and slow wave sleep to desynchronized sleep, which is characterized by the absence of burst firing.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Greene, R W -- Haas, H L -- McCarley, R W -- MH 39,683/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1986 Nov 7;234(4777):738-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3775364" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Calcium/physiology ; Electric Stimulation ; In Vitro Techniques ; Membrane Potentials ; Pons/cytology/*physiology ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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