Anomalous and Apparently Anomalous Diffusion in the Area of Neurophysiology

1. Introduction In the central nervous system information is transmitted from neuron to neuron due to functional contacts, or synapses, where a chemical intermediary, or neurotransmitter, releases following electrical signals in presynaptic cells; its binding to surface receptors triggers an influx of ions into the postsynaptic cells causing the shift of membrane potential away from the resting state. Glutamate releases in majority of brain synapses. The glutamate concentration time course in the synaptic cleft is influenced markedly by the geometry of the space that surrounds the synapse and the properties of glutamate diffusion in this geometry. Intracellular signals that lead to regulation of cell processes are transmitted by a limited number of small molecules, which are called second messengers. Their diffusion ensures the spreading of the signal all over the cell. Ca 2+ is a unique molecule that relays signals mediated by membrane potential changes to the cell interior. Furthermore, in response to the binding of glutamate with metabotropic glutamate receptors, inositol 1,4,5-triphosphate (IP 3) is generated that releases Ca 2+ from the intracellular stores. Recently first communications that neurotransmitters in the extracellular space and second messengers in the dendrites of neurons can undergo anomalous diffusion appeared [1, 2]. Earlier diffusion kernel with fractional dimension was used for approximation glutamate diffusion in calyx of Held synapses [3]. Diffusion of IP 3 in the spiny dendrites was proven to occur owing to trapping of molecules in these structures [2]. Nevertheless the causes of anomalous diffusion of both IP 3 in smooth dendrites, and glutamate in the extracellular medium are not evident. Can the diffusion of neurotransmitters and second messengers be only apparently anomalous?