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  • 1
    Publication Date: 2008-03-28
    Description: Although information storage in the central nervous system is thought to be primarily mediated by various forms of synaptic plasticity, other mechanisms, such as modifications in membrane excitability, are available. Local dendritic spikes are nonlinear voltage events that are initiated within dendritic branches by spatially clustered and temporally synchronous synaptic input. That local spikes selectively respond only to appropriately correlated input allows them to function as input feature detectors and potentially as powerful information storage mechanisms. However, it is currently unknown whether any effective form of local dendritic spike plasticity exists. Here we show that the coupling between local dendritic spikes and the soma of rat hippocampal CA1 pyramidal neurons can be modified in a branch-specific manner through an N-methyl-d-aspartate receptor (NMDAR)-dependent regulation of dendritic Kv4.2 potassium channels. These data suggest that compartmentalized changes in branch excitability could store multiple complex features of synaptic input, such as their spatio-temporal correlation. We propose that this 'branch strength potentiation' represents a previously unknown form of information storage that is distinct from that produced by changes in synaptic efficacy both at the mechanistic level and in the type of information stored.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Losonczy, Attila -- Makara, Judit K -- Magee, Jeffrey C -- England -- Nature. 2008 Mar 27;452(7186):436-41. doi: 10.1038/nature06725.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Janelia Farm Research Campus, 19700 Helix Dr Ashburn, Virginia 20147, USA. losonczya@janelia.hhmi.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18368112" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/physiology ; Animals ; Cell Shape ; Dendrites/*physiology ; Ion Channel Gating ; Male ; Mice ; Models, Neurological ; Neuronal Plasticity/*physiology ; Pyramidal Cells/*cytology/*metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism ; Shal Potassium Channels/deficiency/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2009-10-17
    Description: Cortical information processing is under state-dependent control of subcortical neuromodulatory systems. Although this modulatory effect is thought to be mediated mainly by slow nonsynaptic metabotropic receptors, other mechanisms, such as direct synaptic transmission, are possible. Yet, it is currently unknown if any such form of subcortical control exists. Here, we present direct evidence of a strong, spatiotemporally precise excitatory input from an ascending neuromodulatory center. Selective stimulation of serotonergic median raphe neurons produced a rapid activation of hippocampal interneurons. At the network level, this subcortical drive was manifested as a pattern of effective disynaptic GABAergic inhibition that spread throughout the circuit. This form of subcortical network regulation should be incorporated into current concepts of normal and pathological cortical function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Varga, Viktor -- Losonczy, Attila -- Zemelman, Boris V -- Borhegyi, Zsolt -- Nyiri, Gabor -- Domonkos, Andor -- Hangya, Balazs -- Holderith, Noemi -- Magee, Jeffrey C -- Freund, Tamas F -- HHMI55005608/Howard Hughes Medical Institute/ -- MH-54671/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2009 Oct 16;326(5951):449-53. doi: 10.1126/science.1178307.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Experimental Medicine, Budapest 1083, Hungary. vargav@koki.hu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19833972" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Electric Stimulation ; Excitatory Postsynaptic Potentials ; Glutamic Acid/physiology ; Hippocampus/cytology/*physiology ; Inhibitory Postsynaptic Potentials ; Interneurons/*physiology ; Mice ; Neural Inhibition/physiology ; Neural Pathways/physiology ; Neurons, Afferent/*physiology ; Patch-Clamp Techniques ; Photic Stimulation ; Raphe Nuclei/cytology/*physiology ; Rats ; Rats, Sprague-Dawley ; Serotonin/*physiology ; Synapses/*physiology ; Synaptic Potentials/*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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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-01-10
    Description: The role of back-propagating dendritic action potentials in the induction of long-term potentiation (LTP) was investigated in CA1 neurons by means of dendritic patch recordings and simultaneous calcium imaging. Pairing of subthreshold excitatory postsynaptic potentials (EPSPs) with back-propagating action potentials resulted in an amplification of dendritic action potentials and evoked calcium influx near the site of synaptic input. This pairing also induced a robust LTP, which was reduced when EPSPs were paired with non-back-propagating action potentials or when stimuli were unpaired. Action potentials thus provide a synaptically controlled, associative signal to the dendrites for Hebbian modifications of synaptic strength.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Magee, J C -- Johnston, D -- MH44754/MH/NIMH NIH HHS/ -- NS09482/NS/NINDS NIH HHS/ -- NS11535/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Jan 10;275(5297):209-13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA. jmagee@ptp.bcm.tmc.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8985013" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Animals ; Axons/physiology ; Calcium/metabolism ; Calcium Channel Blockers/pharmacology ; Calcium Channels/drug effects/physiology ; Dendrites/*physiology ; Feedback ; In Vitro Techniques ; Long-Term Potentiation/drug effects/*physiology ; Patch-Clamp Techniques ; Pyramidal Cells/drug effects/*physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/*physiology ; *Synaptic Transmission/drug effects ; Tetrodotoxin/pharmacology
    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: 2012-11-13
    Description: Active dendrites provide neurons with powerful processing capabilities. However, little is known about the role of neuronal dendrites in behaviourally related circuit computations. Here we report that a novel global dendritic nonlinearity is involved in the integration of sensory and motor information within layer 5 pyramidal neurons during an active sensing behaviour. Layer 5 pyramidal neurons possess elaborate dendritic arborizations that receive functionally distinct inputs, each targeted to spatially separate regions. At the cellular level, coincident input from these segregated pathways initiates regenerative dendritic electrical events that produce bursts of action potential output and circuits featuring this powerful dendritic nonlinearity can implement computations based on input correlation. To examine this in vivo we recorded dendritic activity in layer 5 pyramidal neurons in the barrel cortex using two-photon calcium imaging in mice performing an object-localization task. Large-amplitude, global calcium signals were observed throughout the apical tuft dendrites when active touch occurred at particular object locations or whisker angles. Such global calcium signals are produced by dendritic plateau potentials that require both vibrissal sensory input and primary motor cortex activity. These data provide direct evidence of nonlinear dendritic processing of correlated sensory and motor information in the mammalian neocortex during active sensation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xu, Ning-long -- Harnett, Mark T -- Williams, Stephen R -- Huber, Daniel -- O'Connor, Daniel H -- Svoboda, Karel -- Magee, Jeffrey C -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Dec 13;492(7428):247-51. doi: 10.1038/nature11601. Epub 2012 Nov 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Janelia Farm Research Campus, Ashburn, Virginia 20147, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23143335" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/*physiology ; Calcium/metabolism ; Dendrites/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Motor Activity/*physiology ; Patch-Clamp Techniques ; Pyramidal Cells/physiology ; Sensation/*physiology ; Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2012-10-30
    Description: Dendritic spines are the nearly ubiquitous site of excitatory synaptic input onto neurons and as such are critically positioned to influence diverse aspects of neuronal signalling. Decades of theoretical studies have proposed that spines may function as highly effective and modifiable chemical and electrical compartments that regulate synaptic efficacy, integration and plasticity. Experimental studies have confirmed activity-dependent structural dynamics and biochemical compartmentalization by spines. However, there is a longstanding debate over the influence of spines on the electrical aspects of synaptic transmission and dendritic operation. Here we measure the amplitude ratio of spine head to parent dendrite voltage across a range of dendritic compartments and calculate the associated spine neck resistance (R(neck)) for spines at apical trunk dendrites in rat hippocampal CA1 pyramidal neurons. We find that R(neck) is large enough (~500 MOmega) to amplify substantially the spine head depolarization associated with a unitary synaptic input by ~1.5- to ~45-fold, depending on parent dendritic impedance. A morphologically realistic compartmental model capable of reproducing the observed spatial profile of the amplitude ratio indicates that spines provide a consistently high-impedance input structure throughout the dendritic arborization. Finally, we demonstrate that the amplification produced by spines encourages electrical interaction among coactive inputs through an R(neck)-dependent increase in spine head voltage-gated conductance activation. We conclude that the electrical properties of spines promote nonlinear dendritic processing and associated forms of plasticity and storage, thus fundamentally enhancing the computational capabilities of neurons.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3504647/" 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/PMC3504647/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harnett, Mark T -- Makara, Judit K -- Spruston, Nelson -- Kath, William L -- Magee, Jeffrey C -- 090915/Wellcome Trust/United Kingdom -- NS-046064/NS/NINDS NIH HHS/ -- NS-077601/NS/NINDS NIH HHS/ -- R01 NS046064/NS/NINDS NIH HHS/ -- R01 NS077601/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Nov 22;491(7425):599-602. doi: 10.1038/nature11554. Epub 2012 Oct 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉HHMI Janelia Farm Research Campus, Ashburn, Virginia 20147, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23103868" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dendritic Spines/*physiology ; Electric Impedance ; Excitatory Postsynaptic Potentials/physiology ; Male ; Models, Neurological ; Pyramidal Cells/*physiology ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Synapses/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1995-04-14
    Description: Activation of dendritic voltage-gated ion channels by local synaptic input was tested by simultaneous dendrite-attached patch-clamp recordings and whole-cell somatic voltage recordings made from CA1 pyramidal neurons in hippocampal slices. Schaffer collateral stimulation elicited subthreshold excitatory postsynaptic potentials (EPSPs) that opened voltage-gated sodium and calcium channels in the apical dendrites. The EPSP-activated sodium channels opened near the peak of the EPSP, whereas low voltage-activated calcium channels opened near the EPSP peak and during the decay phase. Dendritic high voltage-activated channels required somatic action potential generation or suprathreshold synaptic trains for activation. Dendritic voltage-gated channels are, therefore, likely to participate in dendritic integration of synaptic events.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Magee, J C -- Johnston, D -- MH44754/MH/NIMH NIH HHS/ -- NS09482/NS/NINDS NIH HHS/ -- NS11535/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1995 Apr 14;268(5208):301-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7716525" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Calcium Channels/metabolism ; Dendrites/*physiology ; *Ion Channel Gating ; Patch-Clamp Techniques ; Pyramidal Cells/*physiology ; Rats ; Rats, Sprague-Dawley ; Sodium Channels/metabolism ; Synapses/*physiology ; Synaptic Transmission ; Tetrodotoxin/pharmacology
    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
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Neuroscience 19 (1996), S. 165-186 
    ISSN: 0147-006X
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Mathematische Zeitschrift 195 (1987), S. 409-413 
    ISSN: 1432-1823
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mathematics
    Type of Medium: Electronic Resource
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  • 9
    Publication Date: 2017-09-08
    Description: Learning is primarily mediated by activity-dependent modifications of synaptic strength within neuronal circuits. We discovered that place fields in hippocampal area CA1 are produced by a synaptic potentiation notably different from Hebbian plasticity. Place fields could be produced in vivo in a single trial by potentiation of input that arrived seconds before and after complex spiking. The potentiated synaptic input was not initially coincident with action potentials or depolarization. This rule, named behavioral time scale synaptic plasticity, abruptly modifies inputs that were neither causal nor close in time to postsynaptic activation. In slices, five pairings of subthreshold presynaptic activity and calcium (Ca 2+ ) plateau potentials produced a large potentiation with an asymmetric seconds-long time course. This plasticity efficiently stores entire behavioral sequences within synaptic weights to produce predictive place cell activity.
    Keywords: Neuroscience
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 1996-03-01
    Print ISSN: 0147-006X
    Electronic ISSN: 1545-4126
    Topics: Biology , Medicine
    Published by Annual Reviews
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