Re: saxitoxin, why action potential in sensory fibre of normal duration

Saxitoxin is a highly toxic natural chemical found in the phytoplankton 
that causes red tide.  Saxitoxin exerts it’s toxic effect by interfering 
with the transmission of signals through the nervous system.  Nerve cells 
maintain a charge difference between the inside and the outside of the 
cell.  When ion channels open, ions enter and eliminate the local charge 
difference in a process called depolarization.  This depolarization tends 
to open nearby channels of the neuron membrane, starting a wave that 
propagates down the nerve cell as a nerve impulse.  Saxitoxin binds 
specifically to the voltage-gated sodium ion channels and prevents their 
normal function.  This blocks the creation of a proper action potential 
and the nerve cell no longer has the means to transmit a signal.

Saxitoxin has become a useful tool in neuroscience research because it is 
a very selective inhibitor of sodium ion channels but has little or no 
effect on other ion channels (such as potassium or calcium channels.)  

I’m not sure exactly what you are asking in your question, so if you need 
more specific information I would suggest looking at sources in the 
primary literature.  The following references may give you a place to 
start:


Effect of neurotoxins on the electrical and mechanical activity of heart 
muscle.     Sauviat, Martin-Pierre.    C. R. Seances Soc. Biol. Ses Fil.  
(1997),  191(3),  451-471.

Effects of saxitoxin and tetrodotoxin on brainstem auditory evoked 
potentials in the rat.     Moore, E. L.; Carter, D. J.; Kling, C. E..    
Med. Def. Biosci. Rev., Proc.  (1996),  3  1556-1565.  Publisher: National 
Technical Information Service,  Springfield, Va.

Presynaptic initiation of action potentials of retrograde signals in 
developing neurons.     Primi, Marie-Pierre; Clarke, Peter G. H.    J. 
Neurosci.  (1997),  17(11),  4253-4261. 

Saxitoxin binding and "fast" sodium channel inhibition in sheep heart 
plasma membrane.     Doyle, Donald D.; Brill, David M.; Wasserstrom, J. 
A.; Karrison, Theodore; Page, Ernest.  Am. J. Physiol.  (1985),  249(2, 
Pt. 2),  H328-H336.