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Notes: [Auszug] Factor I has now been found to be present in an occult, inactive condition in brain from which it can be released by heat, hypotonicity, or mild acid or alkali. Its production by brain is indicated by the fact that the activity found in brain suspensions increases with time. It has previously been ...

Notes: Zusammenfassung Im Zentralnervensystem der Wirbeltiere wird die Erregung sensibler Nerven durch eine eigene, von ihnen gebildete Erregungssubstanz vermittelt, welche durch ein Ferment rasch wieder abgebaut wird (Hellauer und Umrath 49). Das Ferment läßt sich durch Strychnin, Pikrotoxin, Brucin und Cardiazol hemmen (Hellauer und Umrath 50). Diese Pharmaka bewirken daher Erregung und charakteristische Krämpfe. Durch einen neuen Test an Bienen konnte gezeigt werden, daß die sensiblen Nerven der Arthropoden eine von der der Wirbeltiere etwas verschiedene Erregungssubstanz bilden. Ihr fermentativer Abbau wird durch Pikrotoxin und Cardiazol gehemmt, nicht aber durch Strychnin. An einer großen Anzahl von Arten aus dem ganzen Tierreich wurden die Reaktionen auf Strychnin, Pikrotoxin und Cardiazol geprüft. Es zeigte sich, daß bestimmte Tiergruppen jeweils verschiedene sensible Erregungssubstanzen und dementsprechend verschiedene abbauende Fermente besitzen. Es ergaben sich interessante Beziehungen zur Systematik: Die Deuterostomier (Vertebraten, Tunikaten, Echinodermen, Chätognathen) erwiesen sich hinsichtlich der sensiblen Erregungssubstanz und des sie abbauenden Fermentes als einheitliche Gruppe (Hemmung des Abbaues durch Strychnin, Pikrotoxin und Cardiazol). Einheitlich sind auch die Arthropoden (Hemmung durch Pikrotoxin und Cardiazol). Bei Mollusken hemmt ausschließlich Strychnin, das auch bei verschiedenen anderen Gruppen der Protostomier diese Wirkung hat, wenn auch zum Teil schwächer. Pikrotoxin hemmt außer bei Deuterostomiern und Arthropoden nur noch bei Turbellarien und Nemertinen, bei denen auch Strychnin und Cardiazol wirksam sind. Die sensible Erregungssubstanz der Clitellaten ist Acetylcholin. Bei Cölenteraten erwiesen sich die Pharmaka als unwirksam. Bei Ciliaten ist das Vorkommen einer sensiblen Erregungssubstanz mit fermentativem Abbau (Hemmung durch Strychnin) möglich. Die Wirkungsweise von Strychnin, Pikrotoxin, Brucin und Cardiazol wird besprochen.

Notes: Summary 1. Slow and fast contractions, as well as the corresponding excitatory junctional potentials (ejp's), were recorded from the closer muscle of walking legs subjected to temperatures ranging from 10 to 35 °C. 2. Maximal ejp amplitudes and tension occurred at temperatures between 22° and 28°. The temperature of the animals in the field was between 26° and 27.5 °C. 3. When the temperature was raised above 27° tension development and ejp amplitude declined. At 31° the values of both were usually less than half those recorded at 27°, and they declined to zero when the temperature was raised above 34.5°. 4. At temperatures below 22° tension development and ejp amplitude declined also. The half-time of the decay of ejp's increased with decreasing temperature, causing summation of ejp's at low frequencies. 5. The membrane potential of the muscle fibers increased with increasing temperature above 12 °C by about 1 mV/l°. 6. The running speed of intact animals tested in the field decreased when body temperature was lowered below the ambient temperature. The typical flight response could not be elicited when animals were cooled by only 3°, to 23°. Rewarming to 26° restored normal behavior. Animals cooled to 10° or less were incapable of any movement, even when prodded. They usually recovered within a few minutes after being warmed to 26°. 7. The observed temperature effects are discussed in terms of altered transmitter output and transmitter re-uptake by nerve terminals and in terms of the significance of changes in synaptic efficiency and conduction time for the neural mechanisms underlying behavior. The results suggest several mechanisms by which temperature effects on nerve-muscle systems might be compensated in crustaceans adapted to more widely fluctuating temperatures.

Notes: Zusammenfassung Die Wirkung einer Reihe von Substanzen auf den isolierten Enddarm von Gambarus clarcii Girard wurde geprüft. Es ergab sich, daß Acetylcholin bis zu einer Verdünnung von 10-11 die Spontanaktivität spezifisch fördert und daß die untersuchten Därme eine echte Acetylcholinesterase besitzen. Adrenalin und Noradrenalin steigern ebenfalls bis zu einer Verdünnung von 10-7 die Spontanaktivität der Därme, mitunter bewirken sie aber periodenweise eine Hemmung. Es ist möglich, daß an ihrer Stelle normalerweise eine andere adrenalinähnliche Substanz wirksam ist. Die Wirkung von gereinigtem Faktor I (Florey 1953a, b) läßt auf eine hemmende Darminnervation schließen. Zerschneidungsversuche ergaben, daß die angewendeten Substanzen, abgesehen von Faktor I, Atropin und Eserin, auf dem Wege über Nerven auf die Darmmuskulatur wirken.

Notes: Summary 1. Slow and fast contractions, as well as the corresponding excitatory junction potentials (ejp's) were recorded from the closer muscle (adductor of the dactylopodite) of the third walking legs, subjected to temperatures ranging from +6 °C to +32 °C. In addition, the effect of temperature on resting potential and resting tension was studied, and in several preparations we investigated the effect of temperature on the efficacy of the inhibitory axon. The experimental animals had been acclimated at 12 °C. 2. The membrane potential was found to increase with temperature. In the lower temperature range (e.g., between 6°C and 14–18 °C) the slope was usually steeper; the maximal rate of change was 2 mV/°C. 3. The amplitude of facilitated slow ejp's (10/s) changes only insignificantly over the temperature span from 6 °C to about 22 °C and declines at higher temperatures. Fast ejp's have maximal amplitudes at 20 °C and decline at lower and higher temperatures, the decline being insignificant, however, below 14 °C. 4. Facilitation rate also changes little with temperature; a significant increase occurs near 30 °C in the case of fast ejp's, and between 15 °C and 20 °C in the case of slow ejp's. Above 28 °C, facilitation of slow ejp's declines. 5. As the temperature is lowered, many muscles develop a contracture which may reach 10% of maximal tension at 6 °C. These temperature-induced contractures can be abolished by stimulation of the inhibitory axon. 6. The effectiveness of the inhibitory axon in reducing the contraction caused by the slow motor axon increases with decreasing temperature. 7. The time course of the decay of both slow and fast ejp's increases with falling temperature, particularly in the temperature range below 12 °C. 8. At a given frequency (1–30/s), both slow and fast contractions increased with falling temperature over the entire temperature range tested. This increased efficiency of the neuro-muscular system is attributed to the depolarization and the prolonged time course of the ejp's.

Notes: Summary The muscle fibers of brown and red chromatophores in the skin of the squid, Loligo opalescens, respond to motor nerve stimulation with non-propagating excitatory postsynaptic potentials (e.p.s.p.'s) of fluctuating amplitude. Depending on the strength of stimulation several size classes of e.p.s.p.'s are found, indicating polyneuronal innervation. Facilitation and summation are minimal even though the reversal potential of the e.p.s.p.'s is close to zero. Acetylcholine (ACh) and 5-hydroxytryptamine (5-HT) have no effect on membrane characteristics of the muscle fiber, but ACh greatly augments the “spontaneous” quantal release of transmitter [increase in the frequency of miniature postsynaptic potentials (m.p.s.p.'s)] and thereby causes tonic contraction (“miniature tetanus”). 5-HT reduces the frequency of miniature potentials and abolishes tonic contraction. Inhibition of cholinesterase by eserine does not affect the amplitude or time course of e.p.s.p.'s and of m.p.s.p.'s. High concentrations of cholinergic blocking agents (atropine, banthine) reduce the postsynaptic effects of nerve stimulation in some cases. The natural transmitter substance of the motoneurones may not be ACh. The action of 5-HT appears to be intracellular. Neighboring muscle fibers are electrically coupled through low resistance pathways. These are most likely provided by the close junctions that form part of the myo-muscular junctions. The specific membrane resistance of the regular muscle fiber membrane was found to range from 1,056 to 1,320 Ohm×cm2, that of the close junctions ranges from 12.8 to 22.6 Ohm×cm2. The area occupied by close junctions is small, however, and only 10% of the current injected into one cell passes into the next. Some of the e.p.s.p.'s observed in a given muscle fiber most likely represent the electrotonic spread of the e.p.s.p.'s of the neighbor fibers. Of the six classes of e.p.s.p.'s observed in some muscle fibers, only two may originate in these fibers themselves. Chromatophores in aged preparations often exhibit pulsations. These are caused by spike potentials arising within muscle fibers whose membranes have become electrically excitable. Each spike is preceded by a generator depolarization. The electrical coupling of neighboring muscle cells permits conduction of the spike potentials throughout the set of muscle fibers of a pulsating chromatophore. Altered conditions within such preparations also lead to tonic contractions and contractures that are not necessarily accompanied by electrical activity. Several arguments are presented in support of the hypothesis that the “tonic condition” of nerve terminals (characterized by enhanced spontaneous transmitter release) and of muscle fibers (characterized by inability to relax) is due to an abnormal condition of intracellular calcium (lack of Ca-binding by sarcoplasmic reticulum or other storage sites). No evidence could be found for an inhibitory innervation of the chromatophore muscles. The nerve-induced relaxation of tonically contracted muscle fibers is caused by the action of motoneurones. Preliminary experiments on muscle fibers of the anterior byssus retractor muscle of Mytilus support the hypothesis that the tonic behavior (“catch”) of other molluscan muscles is due to mechanisms similar to those found in the chromatophore muscles.

Notes: Summary 1. A method is described for the perfusion of the thoracic ganglia of crabs (Cancer, Pugettia, Portunus, Callinectes, Eriphia) through the sternal artery. 2. Administration of acetylcholine (ACh)via perfusion elicits leg movements. The effect is enhanced by the anticholinesterase eserine. Eserine alone causes great enhancement of reflex activity. 3. Eserinized perfusate collected during periods of sensory stimulation (optical or tactile stimuli) contained ACh as detected by bioassay on isolated mollusc ventricles. Up to 2 × 10−9 g of ACh were liberated per minute. No ACh was detectable in perfusates collected from quiescent, unstimulated crabs (detection limit 1−10 × 10−11g/ml) or from stimulated crabs when the perfusion fluid contained no eserine. Eserine itself had no effect on the heart preparations used. 4. The demonstration of a release of ACh from the central nervous system of crabs during sensory stimulation represents the last missing link in the evidence (which is fully reviewed) that ACh is the transmitter substance of sensory neurons in decapod crustacea and, presumably, in other arthropod groups as well.