i88o 



HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY III 



sure or respiration was observed. It the calcium con- 

 centration was reduced sufficiently a severe state of 

 tetany supervened (117). "The animal (dog) showed 

 marked opisthotonus, pleurothotonus, and dorsal 

 curvature of the tail, as well as extensor rigidity of the 

 legs and contracted abdominal musculature. The 

 neck and foreleg phenomena came on Hist. Accom- 

 panying these symptoms, there was an elevation of 

 blood pressure with a slowed heart. (After curare 

 these circulatory effects were much less marked and 

 the pronounced neuromuscular changes were abol- 

 ished. ) Respiration was markedly increased, and dur- 

 ing severe attacks it became very dyspneic." 



Increased central calcium ion has been demon- 

 strated to have the opposite effect from potassium ion, 

 to directly oppose the action of raised central potas- 

 sium concentration, or to do both, on all of the 

 autonomic functions described previously. 



The effect of increased central potassium ion on 

 the higher frequency electrical activity of the brain 

 appears to be biphasic. Small increases in potassium 

 ion raise the frequency and decrease the amplitude of 

 the EEG (17, 22, 32, 69, too, 126), indicating a 

 modification of cortical excitability. Larger increases 

 in potassium ion decrease the frequency and increase 

 the amplitude of the EEG (17, 32). Investigations of 

 both evoked and spontaneous potentials show a 

 differential susceptibility of these to changes in potas- 

 sium concentration. Small intracarotid injections of 

 potassium chloride have no effect on the primary 

 response of the auditory cortex to clicks but intensify 

 the after-discharge. Higher intracarotid doses of 

 potassium ion will block the after-discharge. Auditory 

 cortical responses to a continuous sound are rein- 

 forced with low potassium chloride doses and de- 

 creased with higher doses 



Increased central calcium ion decreases the fre- 

 quency and increases the amplitude of the EEG 

 (17, 32, 69, 1 -'()), indicating a decrease in cortical 

 excitability comparable to that achieved 1>\ large 

 increases in central potassium. Work on both evoked 

 in. I spontaneous potentials indicates that raised 

 calcium ion concentration has no effect on the primal \ 

 evoked cortical response but blocks the . 1 1 1 < r-clis- 



charge Heppenstall & Greville (69) conclude that 

 neithei potassium nor calcium ions cm influence 



sensory transmission 10 tin- cortex, but neurons which 



o-spond to the arrival <>l afferenl impulses at the cor- 

 tex, probably internuncial neurons in upper cortical 

 layers, can l><- excited or depressed l>\ these ions. 

 Horsten & KJopper (83), however, believe that the 

 . 01 in ,il effects oi ion si 1 ilts an- not achieved \ i.i direct 



cortical action but rather via effects of these ions on 

 the reticular formation. They argue that all effects of 

 altered cerebrospinal fluid ionic composition on brain 

 electrical responses which are reported in the litera- 

 ture can be viewed as consequences of ionic action on 

 brain-stem centers, and that the observed cortical 

 waves arise from synchronous fluctuations in mem- 

 brane potentials governed by subcortical structures. 



As with the autonomic effects of imposed central 

 ionic shifts, the effects of altered central potassium on 

 EEG can be opposed by calcium (17, 32, 69, 104, 

 126). These authors agree that the inhibitory action 

 of calcium ion occurs more slowly than the blocking 

 produced by large potassium ion increases. 



The evidence points to the importance of the potas- 

 sium-calcium ratio, rather than either ion per se, in 

 these modifications of electrical activity. Gerard 

 (53) points out that potassium ion and calcium ion, 

 both inhibitory in high concentrations, nevertheless 

 cancel each other's effects on the EEG, which can be 

 interpreted as an indication that two independent 

 and antagonistic mechanisms exist for the suppression 

 of cortical electrical activity. 



The effects of altered central nervous system ionic 

 concentrations on the gross behavior of the intact 

 unancsthetized animal have not been extensively 

 investigated. The occurrence of seizures after adminis- 

 tration of intracisternal (96), intracerebral (115) or 

 hypothalamic (24, 29) potassium has been reported. 

 Koenigstern described scratching attacks in eats after 

 intracisternal potassium ion, which were reversible 

 with calcium ion administered via the same route 

 (96). Calcium injected into the cisterna magna (9I)), 

 the lateral ventricles (40), or the infundibular region 

 1 j I, 29) has been reported to cause sleep or uncon- 

 sciousness. One worker (96) reports convulsive 

 episodes on some occasions after calcium injections 

 into the cisterna magna. John and co-workers (86) 

 studied the effects of intraventricular injections of 

 cations on conditioned responses in unanesthetized 

 cats trained to avoid shock on the presentation ol 

 visual or auditory stimuli or both, and to discriminate 

 visual patterns for food. Both calcium and potassium 

 markedly interfered with the performance of learned 

 tasks, and in similar ways. Furthermore, calcium did 

 not counteract the effect of potassium in this regard, 



leading these authors to conclude that the crucial 



factor sensitive to central potassium and calcium injec- 

 tions is not the threshold of .1 neuron to ,tn impinging 

 stimulus, but the phasing of signals to arrive at some 

 integrating structure in propei time relationship. 



