Abstract
Mammalian spinal monosynaptic Ia EPSP and its postsynaptic reciprocal depolarizing inhibition was studied using NEURON simulator in a morphologically and physiologically characterised α-motoneuron. Low g Na and g K located at the dendrites greatly enhanced EPSP A+N maximal amplitude and its reciprocal inhibition. A small area of active dendrite is sufficient for obtaining the maximal increase in excitatory response for each g Na. EPSP peak is monotonically augmented by raising g Na, whereas inhibition is enhanced until a specific g Na and a further increase diminishes the inhibitory effect. Computer simulations performed at four additional α-motoneurons yielded similar results.
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