Document Detail


An increase in AMPA and a decrease in SK conductance increase burst firing by different mechanisms in a model of a dopamine neuron in vivo.
MedLine Citation:
PMID:  16885519     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A stylized, symmetric, compartmental model of a dopamine neuron in vivo shows how rate and pattern can be modulated either concurrently or differentially. If two or more parameters in the model are varied concurrently, the baseline firing rate and the extent of bursting become de-correlated, which provides an explanation for the lack of a tight correlation in vivo and is consistent with some independence of the mechanisms that generate baseline firing rates versus bursts. We hypothesize that most bursts are triggered by a barrage of synaptic input and that particularly meaningful stimuli recruit larger numbers of synapses in a more synchronous way. An example of concurrent modulation is that increasing the short-lived AMPA current evokes additional spikes without regard to pattern, producing comparable increases in spike frequency and fraction fired in bursts. On the other hand, blocking the SK current evokes additional bursts by allowing a depolarization that previously produced only a single spike to elicit two or more and elongates existing bursts by the same principle, resulting in a greater effect on pattern than rate. A probabilistic algorithm for the random insertion of spikes into the firing pattern produces a good approximation to the pattern changes induced by increasing the AMPA conductance, but not by blocking the SK current, consistent with a differential modulation in the latter case. Furthermore, blocking SK produced a longer burst with a greater intra-burst frequency in response to a simulated meaningful input, suggesting that reduction of this current may augment reward-related responses.
Authors:
C C Canavier; R S Landry
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2006-08-02
Journal Detail:
Title:  Journal of neurophysiology     Volume:  96     ISSN:  0022-3077     ISO Abbreviation:  J. Neurophysiol.     Publication Date:  2006 Nov 
Date Detail:
Created Date:  2006-10-16     Completed Date:  2006-12-06     Revised Date:  2014-09-20    
Medline Journal Info:
Nlm Unique ID:  0375404     Medline TA:  J Neurophysiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2549-63     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Algorithms
Dendrites / physiology
Dopamine / physiology*
Electrophysiology
Excitatory Postsynaptic Potentials / physiology
Extracellular Space / physiology
Glutamates / physiology
Ion Channels / physiology
Membrane Potentials / physiology
Models, Neurological*
Models, Statistical
Neurons / physiology*
Receptors, AMPA / physiology*
Receptors, N-Methyl-D-Aspartate / physiology
Small-Conductance Calcium-Activated Potassium Channels / physiology*
gamma-Aminobutyric Acid / physiology
Grant Support
ID/Acronym/Agency:
NS-37963/NS/NINDS NIH HHS; R01 NS037963/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Glutamates; 0/Ion Channels; 0/Receptors, AMPA; 0/Receptors, N-Methyl-D-Aspartate; 0/Small-Conductance Calcium-Activated Potassium Channels; 56-12-2/gamma-Aminobutyric Acid; VTD58H1Z2X/Dopamine
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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