initial axon segment
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2005 ◽  
Vol 206 (6) ◽  
pp. 535-542 ◽  
Author(s):  
Yan-Chao Li ◽  
Chang-Xie Cheng ◽  
Yong-Nan Li ◽  
Osamu Shimada ◽  
Saoko Atsumi

1994 ◽  
Vol 72 (2) ◽  
pp. 899-908 ◽  
Author(s):  
D. H. Edwards ◽  
S. R. Yeh ◽  
L. D. Barnett ◽  
P. R. Nagappan

1. The effect of growth on the electrotonic structure and synaptic integrative properties of the lateral giant (LG) interneuron was assessed from anatomic and electrophysiological measurements of LGs in small (1–2.4 cm) and large (9–11.2 cm) crayfish and from calculated responses of mathematical models of these neurons. Postsynaptic responses of small and large LGs were compared with model responses to determine whether the differences in the neurons' responses result from growth-related changes in their physical characteristics. 2. LG neurons in the terminal abdominal ganglia of small and large crayfish are similar in shape but differ in size according to an approximately isometric pattern of growth. The soma diameter of the large LG is 2.2 times larger than the small LG, the major ipsilateral dendrite is 2.8 times longer and 3.6 times greater in diameter, and the axon is 7.6 times longer and 4.5 times greater in diameter. The projected area of the major ipsilateral dendrite of LG in the horizontal plane of the terminal abdominal ganglion is 27 times larger in the large than in the small crayfish. 3. LG's input resistance was nearly 80% smaller in the large (167 K omega) than in the small (742 K omega) crayfish when measured at or near the initial axon segment. The cell's membrane time constant displayed an opposite relationship, with the value in the large crayfish (20.9 ms) nearly two-and-a-half times larger than the value in the small crayfish (8.6 ms). 4. Simultaneous recordings were made from the distal portion of the ipsilateral dendrite and the initial axon segment of small and large LGs to determine how excitatory postsynaptic potentials (EPSPs) are attenuated or filtered by the electrotonic properties of the different sized cells. In the small LG, the fast alpha and the slower beta components of compound EPSPs evoked by sensory nerve stimulation were similarly attenuated. In the large LG, the alpha component of the compound EPSP was much more attenuated and smoothed than the slower beta component. 5. Multicompartment models of small and large LGs were constructed and used to test whether differences in the two neurons' physical properties could account for the differences in their passive response properties.(ABSTRACT TRUNCATED AT 250 WORDS)


1955 ◽  
Vol 184 (1) ◽  
pp. 223-232 ◽  
Author(s):  
Adele E. U. Edisen

Spinal cord motoneurons of the cat were stimulated by a needle electrode and reflexly via dorsal root impulses. Responses to direct stimulation originated in dendrites, initial axon segment, or myelinated axon, but apparently not in the cell body. The sites were differentiated by latency changes of the response as needle position and stimulus strength are varied, by ability to follow repetitive stimulation, and by responses to asphyxia duration and anesthesia depth. Facilitatory afferent impulses increased the excitability of the motoneurons, whether the direct test stimulus was activating either dendrites or initial axon segment, but inhibitory afferent impulses decreased the direct response only when dendrites were being activated. Facilitation is therefore nonlocalized and can be accounted for by the usual eddy currents. Inhibition is interpreted as a partial depolarization and impedance decrease of the cell body, induced by afferents reaching it directly and resulting in a short circuiting of eddy currents from excited dendrites to initial axon segment. The central delay of the spinal cord monosynaptic response (about 0.8 msec.) is accounted for by conduction time in the afferent fibers (0.5 msec.), determined by antidromic stimulation of these and by the time lag of afferent conditioning effects, and in the motoneurons, 0.2–0.3 msec. It is thus doubtful if any true ‘synaptic delay’ exists. The long intramedullary afferent conduction time also fully accounts for the lag seen in afferent inhibition, in harmony with the existence of a direct inhibitory pathway.


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