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Rat motor nerve terminals and the endplates they interact with exhibit changes to varying patterns of use, as when exposed to increased activation in the form of endurance exercise training. The extent to which these changes affect neuromuscular transmission efficacy is uncertain. In this study, the effects of habitual exercise on the electrophysiological properties of neuromuscular transmission in rat soleus muscle were investigated using a novel in situ approach. Consistent with previous reports, miniature endplate potential frequency was enhanced by habitual exercise. Other passive properties, such as resting membrane potential, miniature endplate potential amplitude, and "giant" miniature endplate potential characteristics were unaltered by the training program. Full-size endplate potentials were obtained by blocking soleus muscle action potentials with mu-conotoxin GIIIb. Quantal content values were 91.5 and 119.9 for control and active groups, respectively (P < 0.01). We also measured the rate and extent of endplate potential amplitude rundown during 3-s trains of continuous stimulation at 25, 50, and 75 Hz; at 50 and 75 Hz, we found both the rate and extent of rundown to be significantly attenuated (10--20%) in a specific population of cells from active rats (P < 0.05). The results establish the degree of activity-dependent plasticity as it pertains to neuromuscular transmission in a mammalian slow-twitch muscle.

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Summary K+ efflux from Umbilicaria muhlenbergii was not affected following the uptake of known amounts (< 20 μmol g‐1) of Ca2+, Mg2+, Sr2+ and Zn2+, but was increased in the cases of Cu2+ and Pb2+. In a number of samples that had taken up increasing amounts of Cu2+, a discontinuity in K+ release during metal incubation correlated with a decrease in subsequent 14C fixation. Some of the binding sites associated with the first phase of Cu2+ uptake (up to 12 μmol g‐1) are interpreted to occur near, on or within the algal cells. The larger K+ loss associated with higher Cu2+ uptake levels indicated that a component of the second Cu2+ uptake phase involved binding at or penetration of the fungal membranes. The uptake of Sr2+, Ni2+ and Zn2+ conferred some protection to samples subsequently exposed to 75 p.p.m. aqueous SO2 for 1 h, while Mg2+, and Ca2+ had no effect. The combined effects of Cu2+ uptake and SOS exposure (and also Pb2+ and SO8) were approximately cumulative. Finally, the results are explained by reference to a classification that separates metal ions into three chemically and biologically significant categories. It is concluded that class A metal ions (those with a preference for ionic interactions) and borderline metal ions with class A character tend to protect lichens against SO2 damage, while borderline metal ions with class B character (a preference for covalent interactions) have the opposite effect.

We have used a resting (5 mM K+) or depolarizing (60 mM K+) choline-based medium, and a nondepolarizing sodium-based or choline-based medium, to characterize the inhibitory potential of tricyclic antidepressants against the voltage-dependent calcium channels or the Na(+)-Ca2+ exchange process, respectively, in synaptosomes from rat brain cortex. Imipramine, desipramine, amitriptyline, and clomipramine inhibited net K(+)-induced 45Ca uptake with similar IC50 values (26-31 microM), and this uptake was also inhibited by diltiazem with an IC50 of 36 microM; these results indicate an inhibition of voltage-dependent calcium channels by tricyclic antidepressants. The net uptake of 45Ca induced by Na(+)-Ca2+ exchange was also inhibited by the four tricyclic antidepressants tested, but not by diltiazem; imipramine (IC50 = 94 microM) was a more potent inhibitor of this process than desipramine (IC50 = 151 microM), and the IC50 values of amitriptyline (107 microM) and clomipramine (97 microM) were similar to that of imipramine. Some degree (approximately 25%) of brain calcium channel blockade could be present at the steady-state concentrations of tricyclic antidepressants expected to occur therapeutic use of these compounds to treat depression or panic disorder.

The presence of a requirement for calcium during the fast transport of [3H]protein in axons was assessed in desheathed spinal nerves of bullfrog. The nerves were desheathed locally along 4 mm of their length, and desheathing was judged effective on the basis of an enhanced uptake of [3H]leucine into that region of nerve trunk. Desheathing per se had a slight inhibitory effect on transport. Incubation of desheathed nerve trunks in calcium‐free medium reduced transport by 60‐80% relative to that in desheathed nerves incubated in normal medium. Addition of Mg2+ or Sr2+ to the calcium‐free medium allowed transport to proceed normally. Addition of Co2+ or Mn2+ to normal medium did not affect transport in desheathed isolated nerve trunks. When ganglia and nerve trunks were both incubated in medium containing 0.18 mM‐CoCl2, transport was depressed to a similar extent proximal and distal to the desheathed region. This again indicates that Co2+ does not inhibit transport in desheathed nerves, whereas it does inhibit transport in the ganglia. Additive inhibitory effects were observed when ganglia were incubated in medium containing 0.018 mM‐CoCl2, and desheathed nerves were incubated in calcium‐free medium. Differences in the divalent cation specificities of the axonal and ganglionic calcium requirements suggest that calcium supports transport in nerves in a manner distinct from its role in maintaining transport in spinal ganglia. It is concluded that the ganglionic calcium requirement involves initiation of axonal transport in the soma rather than translocation in the intraganglionic region of axon.

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