basic question

Jeroen Schaap Schaap at rullf2.medfac.leidenuniv.nl
Thu Oct 10 02:44:20 EST 1996


In article <52ov40$4q2 at gap.cco.caltech.edu>,
   hdvorak at cns.caltech.edu (Hannah Dvorak) wrote:
[snip]
>in dendrites are generated by the binding of neurotransmitter to 
>specialized receptors, and these potentials may spread passively to
>the soma, or be amplified by voltage-dependent Na or Ca channels.
>
>As for directionality of signal propagation:  An isolated axon can
>conduct action potentials in either direction, as can be easily
>demonstrated in the laboratory.  However, in the intact neuron, 
>action potentials are generated near the soma and propagate towards
>the axon terminals.  I don't believe it would be possible to take
>an isolated segment of axon and determine which way it was originally
>oriented relative to the soma.  Synaptic potentials in dendrites
>will spread in all directions away from the site at which they were
>generated.  Traditionally, the soma has been seen as the site of
>integration of synaptic potentials, but there has been recent interest
>in the propagation of signals, including action potentials, back into
>the dendrites.  (See e.g. the work of B. Sakmann and collaborators.)
>
>Hope this starts to answer your question!
>


Maybe it is theoretically possible to take a segment of an axon an 
determine which the direction is. But I am not mentioning any 
electrophysiological properties. I am not very sure, but I believe the 
cytoskeleton grows in one direction, with helices turning in a special 
direction. Theoretically, I stress, it might be possible to determine 
the direction of the cytoskeleton in an axon-segment and with that the 
direction of the propagation of action potentials in 'normal' 
situations. 
	Second, I can also imagine  antidromic ap's could have an 
influence on the membrane potential of the soma/ axon hillock by means 
of electrotonic interaction. But results will be very difficult to 
interpretate. Because the different potentials involved in an ap as a 
function of time, there will be no simple elevation of depression of 
membrane potential. I don't know whether some slow channels have been 
proved on axons -please help me with this- but they could de- or 
hyperpolarize the soma.
	Third, why couldn't any action potential be generated on an 
axon, by means of axo-axonic synapses etc. Off course the axons don't 
have the ap generating mechanism, axon hillock, but nevertheless, why 
couldn't the 'axonic synapses' depolarize enough in order to generate an 
action potential.

Things are never that simple they seem to be.

Jeroen



More information about the Neur-sci mailing list