The effects of ten cations and fifteen anions on the excitability of the squid giant axon were studied. The method of intracellular perfusion used in these investigations is described in detail. Empirical criteria were established for evaluating the relative favorability of any salt solution for maintaining the normal excitability of the membrane of the axon. It was found that both cations and anions could be ordered in sequences of relative favorability, which are directly related to the classic lyotropic sequences found for protein macromolecules and in colloid chemistry in general. The effects of concentration, salt mixtures, non-electrolyte carriers, enzymes, metabolic inhibitors, pH, and external media were also studied. The results are interpreted in terms of current concepts of the interactions between water structure, charged macromolecules, and their ionic environments. A macromolecular approach is given to the physicochemical nature of the "two stable states" of the excitable membrane, to describe the time-dependent potential changes observed.

Chick collapsin‐1, a member of the semaphorin family, has been implicated in axonal pathfinding as a repulsive guidance cue. Collapsin‐1 induces growth cone collapse via a pathway which may include CRMP‐62 and heterotrimeric G proteins. CRMP‐62 protein is related to UNC‐33, a nematode neuronal protein required for appropriately directed axonal extension. Mutations in unc‐33 affect neural microtubules, the basic cytoskeletal elements for axoplasmic transport. Using computer‐assisted video‐enhanced differential interference contrast microscopy, we now demonstrate that collapsin‐1 potently promotes axoplasmic transport. Collapsin‐1 doubles the number of antero‐ and retrograde‐transported organelles but not their velocity. Collapsin‐1 decreases the number of stationary organelles, suggesting that the fraction of time during which a particle is moving is increased. Collapsin‐1‐stimulated transport occurs by a mechanism distinct from that causing growth cone collapse. Pertussis toxin (PTX) but not its B oligomer blocks collapsin‐induced growth cone collapse. The holotoxin does not affect collapsin‐stimulated axoplasmic transport. Mastoparan and a myelin protein NI‐35 induce PTX‐sensitive growth cone collapse but do not stimulate axoplasmic transport. These results provide evidence that collapsin has a unique property to activate axonal vesicular transport systems. There are at least two distinct pathways through which collapsin exerts its actions in developing neurons. © 1997 John Wiley & Sons, Inc. J Neurobiol 33: 316–328, 1997

Idiopathic normal-pressure hydrocephalus (iNPH) has become socially significant in Japan. Japanese guidelines for iNPH in 2011 described the diagnostic importance of "disproportionately enlarged subarachnoid space hydrocephalus" (DESH) on magnetic resonance imaging (MRI). However, some patients with iNPH have equivocal or no features of DESH. To clarify the diversity of MRI findings in iNPH, we classified iNPH into three types based on MRI findings. Using this, we investigate predictable MRI findings for shunt effectiveness in iNPH. A total of 83 patients with suspected iNPH who were treated with shunt surgery were reviewed in this study. All patients had a positive cerebrospinal fluid (CSF) tap test. Among the 83 patients, DESH was noted in 64 %, incomplete DESH in 23 %, and no DESH in 13 % (see Fig. 3). Among the three types of incomplete DESH, incomplete DESH-v (ventricle) was 0 %, DESH-c (convexity) in 13 %, and DESH-s (Sylvian fissure) in 10 %. A high improvement rate after the shunt surgery was noted in the DESH and incomplete DESH-s groups, showing 73.5 % and 87.5 %, respectively. The non-DESH group showed a fairly large improvement of 63.6 %. A common MRI finding in DESH and incomplete DESH-s was high convexity tightness with ventriculomegaly. This combination was promising for shunt effectiveness in patients with suspected iNPH. Further study is necessary to elucidate the pathogenesis.

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