Path: utzoo!utgpu!news-server.csri.toronto.edu!bonnie.concordia.ca!uunet!bu.edu!slehar From: slehar@park.bu.edu (Steve Lehar) Newsgroups: bionet.neuroscience Subject: Re: Auditory Impulse Travel and Distance Message-ID: Date: 18 Jun 91 12:45:20 GMT References: <9106171949.AA20716@genbank.bio.net> <1991Jun18.033141.11511@agate.berkeley.edu> Sender: news@bu.edu Distribution: bionet Organization: Boston University Center for Adaptive Systems Lines: 75 In-reply-to: brp@dino.berkeley.edu's message of 18 Jun 91 03:31:41 GMT The reason why the brain uses neural spiking, and encodes signal magnitude as spiking frequency is exactly to avoid the degredation with distance that is experienced by the alternative method of neural signaling, i.e. the density of ions of a particular charge. The ions, injected at the site of neural input must diffuse passively along the neuron, which works ok as long as they don't have to diffuse too far. When you get one of those neurons with an extremely long axon however, there may be little or no charge left by the time the signal gets to the end, so the signal decays with distance. In a spiking neuron, the diffusion must only travel the distance from the dendrites to the axon hillock. There, the ions either have enough charge density to trigger an action potential, or they don't. Once the action potential is triggered, it is guaranteed to travel the whole length of the axon, and since each spike is a complete depolarization of the membrane, there is no distinction between "weak spikes" and "strong spikes", all spikes are essentially the same. ========[ end of quick answer- beginning of more detail ]============= Here is a simplistic explaination designed to clarify the dynamics of neural firing without delving into deep technicalities. The sodium pump constantly and steadily pumps sodium (+) ions from inside the cell to outside, until a negative charge is built up inside the cell relative to the outside. There are a few passive channels around that allow some of the charge to leak back in at a rate proportional to the potential difference across the membrane, so that even though the pumps run continuously, the charge can never build up too great, but settles at some equilibrium value, where the rate at which the pumps pump it out is exactly balanced by the rate at which it flows back in through the passive channels. Electrically gated channels are also scattered about, and these will open if the membrane is DE-polarized, i.e. if the potential begins to break down, the electrically gated channels will make it break down even more. This creates an unstable situation, because a little local depolarization near an electrically gated channel, say, from a chemically gated channel that has just locked on to a transmitter molecule, will create a larger local depolarization. The electrically gated channel has a refactory period, so that it can only allow a little gulp of positive ions back into the cell before it slams shut again to recover. That gulp of ions diffuses outward, and what happens next depends critically on the density of electrically gated channels in the local viscinity. If the next one is too far away, then the charge will not be strong enough to trigger it, and the charge diffuses slowly in space and time. If enough of these events occur however, and close enough in time, then the total positive charge in the cell will become high enough to trigger even the more remote channels. Now the axon hillock is richly endowed with electrically gated channels in close proximity to each other, so that if a single one of these were to open, it will set off a cascade of channel openings that will flood the cell with positive charge in one great pulse. Now along the axon there are more ion pumps and electrically gated channels, (positioned at the nodes of Ranvier so that they have access to the extracellular environment) so that a similar event occurs all along the axon. You can see that a saturation event like this cannot occur half-way, either the system fires or it does not. At the output end of the neuron these spasms of depolarization trigger the release of pulses of transmitter which cause the injection of gulps of ions into the postsynaptic cell, thereby automatically performing a frequency - to - magnitude, or digital - to - analog conversion of the phasic pulsed signal into an "analog" magnitude of charge in the postsynaptic cell. -- (O)((O))(((O)))((((O))))(((((O)))))(((((O)))))((((O))))(((O)))((O))(O) (O)((O))((( slehar@park.bu.edu )))((O))(O) (O)((O))((( Steve Lehar Boston University Boston MA )))((O))(O) (O)((O))((( (617) 424-7035 (H) (617) 353-6741 (W) )))((O))(O) (O)((O))(((O)))((((O))))(((((O)))))(((((O)))))((((O))))(((O)))((O))(O)