by
DrErik Fransén(Computational Biology, School of Computer Science and Communication, Royal Inst of Tech)
→
Europe/Stockholm
122:028
122:028
Description
Synchronous activity is an integral part of brain function. For
instance, when solving a cognitive challaging taks such as traversing
a maze, human subjects show a correlation between task load and EEG
gamma band (40-80Hz) power (Howard et al 2003). Further, the degree of
synchronicity during encoding in a learning task correlates with
subsequent recall (Sederberg et al 2003).
It is however concievable that there is an optimum in regard to
synchronicity of brain activity, and that hyper synchronous firing, or
increased neural spike response to synchronous input, leads to
pathological states such as epileptic sezures. At the single neuron
level, there may under normal conditions be mechanisms that maximizes
processing while proving sufficient safety margins to undesirable
hypersynchronous states. In pathological cases, these mechanisms may
be compromized or insufficient.
In this project using quantitative modeling we are studying the
possibility of controlling a neurons bias to respond to synchronous
synaptic input by presence of an A-type potassium current. We find that the
channel is able to reduce the response to synchronous input while
sparing responses to desynchronized input. The effect originates from the
dynamic interplay between the input depolarization and the channel kinetics.
In vivo ion channels are under continious modulatory control, either
acting directly on the channel or indirectly via second messanger
pathways, phosphorylation or oxidative processes
(Johnston et al 2000). There are also pharmacological means of
affecting ion channel characteristics, i.e. shift of channel
steady-state activation curve, (Akins et al 1990, Saint et al 1990).
Thus, pharmacological manipulation of endogenous ion channel types might
provide possible ways of treatment of diseases where responses to
synchronicity is altered.