One cell, two bursting mechanisms. In vivo conditions change the in vitroburst in pyramidal cells of the ElectroLateral Lobe (ELL) of electric fish
© Toporikova and Chacron; licensee BioMed Central Ltd. 2008
Published: 11 July 2008
One of the striking differences between in vivo and in vitro conditions is the absence of glutamatergic input to the cells in vitro which might provide the major source of Ca2+ to the cell via NMDA receptors. To test this hypothesis, we injected the calcium chelator, BAPTA, in pyramidal cell in vivo. The resulting removal of intracellular Ca2+ changed the cell bursting pattern to one characteristic of in vitro recordings.
To understand these observations, we have used a computational approach to propose a cellular mechanism for burst generation in vivo. In our computational model, which is based on the in vitro ghost-burst model, Ca2+ enters the cell through NMDA channels in the dendrites. When Ca2+ diffuses into the soma, it affects the Ca-activated potassium current. Gradual increases in Ca2+ concentration increases this current and eventually terminates the burst. This current also creates a spike shape characteristic to an in vivo burst, with a strong hyperpolarization after every spike within a burst.
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