SUMMARY1. Transmitter release at neuromuscular junctions of extensor digitorum longus (EDL) muscle in mice was studied after 2-8 month periods of unforced running in wrheels.2. Intracellular recordings at 10 Hz stimulation revealed that the quantal content of endplate potentials (EPPs) in Mg2+-blocked preparations was larger by 30% in trained (mean number of quanta, m = 175+019, n = 7) than in untrained control EDL muscles (m = 135+0-35, n = 7). Similarly the amplitudes of the first, maximum and plateau EPPs during tetanic stimulation (100 Hz for 1 s or 400 ms) in curare-blocked preparations were increased by 28 % each; muscle fibre diameters did not differ while other postsynaptic effects were not excluded.3. Training effects became particularly evident in two pairs of monozygotic twins, in which the time courses of facilitation and depression were changed as well: at 100 Hz stimulation the maximum EPP amplitude was reached on average at 2-6 impulses in controls but at 2 0 impulses in runners, and the following decline below the value of the first EPP at 5 0 and 3-8 impulses respectively.4. Block resistance, as monitored by isometric tension measurements in different presynaptic (Mg2+) and postsynaptic (curare) blocking solutions, was higher in trained than in control EDL muscles. Depression in a train of four nerve-evoked single twitches at 2 Hz was lower.5. As expected from the unchanged fibre diameters (see above) isometric tetanic force was similar in trained and control EDL muscles. Muscle fatigue resistance was larger in trained animals and succinic dehydrogenase activity was higher in fibres of trained muscles indicating an endurance training of the EDL muscle.6. It is concluded that besides changes in muscle fibre properties, prolonged elevated activity causes increased transmitter release in EDL muscles. As a consequence, the safety margin of transmission in trained EDL muscles is markedly elevated.

In the present study the sexually dimorphic, androgen-sensitive flexor carpi radialis muscle (FCR) in male Xenopus laevis was viewed repeatedly in vivo to assess the influence of testosterone on muscle fiber size over a period of up to 12 weeks. Regions of the muscle innervated by different spinal nerves responded differently to testosterone treatment. Muscle fibers innervated by spinal nerve 2 (SN2) hypertrophied within 7 days in frogs that had been castrated and given testosterone-filled implants. This initial hypertrophy was followed by a return to normal fiber size a week later, after which fiber size slowly increased again. In castrated males with empty implants, muscle fibers innervated by SN2 gradually atrophied. Fibers innervated by spinal nerve 3 (SN3) were not affected by androgen replacement or withdrawal. The sartorius, a control muscle that is neither sexually dimorphic nor particularly androgen sensitive, was also unaffected. The in vivo observations were confirmed by measurements of muscle fiber cross-sectional areas in frozen sections of whole forelimbs. At 8 and 12 weeks after castration, cross-sectional areas of fibers innervated by SN2 were significantly larger in frogs provided with testosterone than in castrates without testosterone. No difference was found in the SN3 region or in the anconeus caput scapulare (triceps), another control muscle. Immunocytochemistry employing an antibody against the androgen receptor (AR) indicated that the receptor is present in myonuclei of all muscles of the forelimb. While no difference in labeling intensity was detected, the number of AR-containing nuclei per muscle fiber cross-section was higher in fibers innervated by SN2 than in those innervated by SN3, and was yet lower in the triceps. This suggests that regulation of androgen sensitivity may occur via muscle fiber ARs, although an influence of the nerve may also contribute.

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Phototransduction, Current Components, Light Adaptation, Bumps, CPA 1. Single-photon responses (bumps) and small macroscopic photocurrents were studied in ventral photoreceptors of the horseshoe crab Limulus. Lowering the calcium concentration in the bath from 10 mM to 250 fiM led to increased bump size. Adaptation of the cells by a moderately bright conditioning flash was not impaired.2. Pressure-injection of 1.2 mM EG TA into the dark-adapted cells resulted in reduced bump size. EG TA weakened the effect of the conditioning light flash although it did not completely abolish light adaptation.3. The microsomal calcium-ATPase inhibitor cyclopiazonic acid strongly desensitized the cells, and bumps were suppressed below detection. When the bathing saline contained 10 m M calcium, macroscopic photoresponses after extracellular application of the agent had ampli tudes smaller than under control conditions but normal response kinetics: The response to a light step still consisted of a fast transient photocurrent and a much smaller plateau. How ever, when applied in calcium-free bathing saline, cyclopiazonic acid additionally influenced the waveform of the photoresponse. The clear distinction between transient and plateau was no longer possible, and the photocurrent appeared "square".4. Our results support the idea that a transient elevation of the cytosolic calcium concentra tion is obligatory for light adaptation in the ventral photoreceptor. It is also obligatory for the generation of the so-called C2 component of the photocurrent which is represented by "standard" bumps and the fast transient phase of a prolonged response. However, a rise in cytosolic calcium appears not necessary for the initiation of a slow electrical photoresponse.