Modeling Na+- and Ca2+-dependent mechanisms of rhythmic bursting in excitatory neural networks
© Rybak et al; licensee BioMed Central Ltd. 2012
Published: 16 July 2012
The mechanisms generating neural oscillations in the mammalian brainstem, particularly in the pre-Bötzinger complex (pre-BötC) involved in control of respiration, and the spinal cord (e.g. circuits controlling locomotion) that persist after blockade of synaptic inhibition, remain poorly understood. Experimental studies in medullary slices from neonatal rodents containing the pre-BötC identified two mechanisms that could potentially contribute to generation of rhythmic bursting in the pre-BötC: one based on the persistent sodium current (I NaP ) [1, 2], and the other involving the voltage-gated calcium (I Ca )  and/or the calcium-activated nonspecific cation current (I CAN ), activated by intracellular Ca2+ accumulated from extra- and/or intracellular sources . However, the involvement and relative roles of these mechanisms in rhythmic bursting are still under debate.
The existence of multiple oscillatory regimes and their state-dependency may provide explanations for different rhythmic activities observed in the brainstem and spinal cord under different experimental conditions.
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