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IIWDHOUK OF PHYSIOLOGY 



M UROPHYSIOLOGY III 



the axon segment is controlled by the chemical field 

 bathing ii and by polarization currents reaching it, 



mainly, from other portions of the soma and den- 

 drites. These currents depend on the chemical en- 

 vironment of dendrites (and soma) [e.g. (120)], on ex- 

 ternal currents that flow through them, on membrane 

 conductance, and on local potential differences along 

 the neuron surface, mainly produced by incoming im- 

 pulses which constitute briefly enduring sources or 

 sinks for clectrotonic currents that invoke the axon 

 [Chang; Bishop (27)]. A final point: it is usually as- 

 sumed that, left to itself, the neuron threshold is high 

 enough to ensure inactivity, but the converse may 

 well he possible. Many neurons do show rhythmic 

 spontaneous activity under physiologic conditions. 

 Brain damage, including developmental abnormality 

 (Hicks), is commonly associated with convulsive or 

 other overactivity. Learning, at the motor or social 

 level alike, involves differential inhibition. Sleep 

 rather than alertness is the equilibrium state. Causal- 

 gic and related pains involve a decreased somesthetic 

 input ( 184). Inhibitory recurrents from motor neurons 

 seem important. High cord-section or anesthesia 

 increases the responses in spinal afferent tracts pro- 

 duced by a miven dorsal root stimulus (Livingston), 

 while stimulating several limbic or cortical structures 

 decreases cord responses (French). Blocking the pre- 

 sumptive inhibitory transmitter, GABA or factor I, 

 as by strychnine (Grundfcst), gives generalized dis- 

 charges to minimal stimuli. A steady outflow of 

 impulses keeps the external sphincter of the bladder 

 closed; these arc inhibited during micturition (Ruch). 

 Perhaps neuron thresholds are kept up by a continued 

 rain of inhibitory impulses. 



DENDRITIC (SOMATIC) POTENTIAL. The threshold of the 

 neuron, then, is primarily controlled over the long 

 run by chemicals in the intercellular fluid and currents 

 passing through it, over the short run by impulses 

 reaching the neuron far from the axon hillock and 

 summing spatially and temporally to give the dendri- 

 te or somatic potential. 3 Excitation, in contrast to 



'The concept ol an integrating somatic potential, under- 

 lying facilitation and inhibition, arosi from reading Sherring- 

 papei ■'" central ex< itatorv and inhibitory states and u.is 

 accepted by him in .1 discussion in 1927 (to8). The idea was 

 published in 193a (83, |> 547) It was supported experimentally 

 and furthei developed theoretically in the late thirties and 

 b Libet and Gerard (1 18, 174, 175) Hie sugges- 

 tion thai inhibition and excitation miulit depi nd on thi position 

 ill synap - ncai the dendritic 01 axonic pole "I the somatic 

 potential wa made at this time (89 After years of dormancy, 



threshold control, depends primarily on impulses 

 reaching the axonal pole of the neuron and acting 

 with little spatial summation and with even less, per- 

 haps no, temporal summation. 



The slow, cumulated, nonpropagated dendrite po- 

 tential, like a generator potential (Bartley, Chang, 

 Eccles, Gray, O'Leary & Goldring), is an ideal inte- 

 grating and storage mechanism. Impulses reaching 

 any part of the dendrite-soma system could sum alge- 

 braically and pool their clectrotonic influences on the 

 axon. Further, over a longer range, changes in re- 

 sponsiveness of these neuron parts to impinging im- 

 pulses, or to ambient conditions, afford a simple link 

 between past experience and current activity. Not 

 only in the cerebral cortex, where steady potential 

 changes parallel activity in projection areas (176), 

 spreading depression waves and the more complex 

 behavioral states (O'Leary & Goldring; 179), and in 

 the cerebellum, where polarization alters tonic activ- 

 ity (Brookhart), but also in older and simpler struc- 

 tures, potentials parallel state on a lasting basis [e.g. 

 with temperature or carbon dioxide (Strom)]. The 

 single cell layer of the hippocampus shows marked 

 potential shift with seizures (Green), or amygdalar 

 tetanization (Gloor). Amygdala potentials build easily 

 (Gloor), and enduring seizure discharges result from 

 short stimulation (8); and, in the frog telencephalon, 

 the steadv potential and waves of activity arc closelv 

 related (1 75). 



Ultimately, of course, the membrane and related 

 changes reduce to physical chemistry (Peters). Eccles 

 relates hv perpolarization, by inhibitory synapses and 

 presumably that following axon discharge, to a rela- 

 tive increase in permeability to K + and CI - of the 

 dendrite membrane. For end-plate activation, Fait 

 sees no ion flow across the membrane Inn electron 

 shift along enzyme molecules palisaded in the receptor 

 site. Gray boldly relates die Weber-Fechner law to 

 the ion ratio across relevant membranes. 



Whether at special electroactive receptor sites in 

 the membrane, in the palisaded layers of molecules in 

 the membrane at large, or involving the ion and mole- 

 cule flow within the cell as controlled by interior or- 

 ganelles, the neuron threshold depends on chemical 

 architecture, rhe frequency and magnitude ol waves 

 of spontaneous threshold change are dependent on 



cell metabolism, probably acting through an ionic 



iliis, work helped triggei extensive simlirs of dendrite potentials 

 ili.it have redirected thought in recent years O'Learj & 

 Goldring, Bartley; see also Hislicip (27), Bremei (29) and 

 O'Lea. 



