One element, potassium, can be identified as the connecting link in the research of Czech neurophysiologist Prof. František Vyskočil. It accompanied him from the first student experiments on the frog muscle (Solandt effect) via sodium-potassium pump and quantum and non-quantum release of neurotransmitters (e.g. acetylcholine) to the most appreciated work on the reversible leakage of K+ from brain neurons during the Leao´s spreading cortical depression, often preceding migraine. He used a wide range of methods at the systemic, cellular and genetic levels. The electrophysiology and biochemistry of nerve-muscle contacts and synapses in the muscles and brain led to a range of interesting findings and discoveries on normal, denervated and hibernating laboratory mammals and in tissue cultures. Among others, he co-discovered the facilitating effects of catecholamines (adrenaline in particular) by end-plate synchronization of individual evoked quanta. This helps to understand the general effectiveness of nerve-muscle performance during actual stress. After the transition of the Czech Republic to capitalism, together with Dr. Josef Zicha from our Institute, he was an avid promoter of scientometry as an objective system of estimating a scientist´s success in basic research (journal Vesmír, 69: 644-645, 1990 in Czech).

• MeSH
• dějiny 20. století MeSH
• dějiny 21. století MeSH
• lidé MeSH
• mozek * fyziologie   metabolismus   MeSH
• neurony * metabolismus   fyziologie   MeSH
• neurovědy * MeSH
• žáby MeSH
• zvířata MeSH
• Check Tag
• dějiny 20. století MeSH
• dějiny 21. století MeSH
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• historické články MeSH
• přehledy MeSH

Resting non-quantal acetylcholine (ACh) and probably glutamate (Glu) release from nerve endings activates M1- and NMDA receptor-mediated Ca2+ entry into the sarcoplasm with following activation of NOS and production of NO. This is a trophic message from motoneurons, which keeps the Cl- transport inactive in the innervated sarcolemma. After denervation, the secretion of ACh and Glu at the neuromuscular junction is eliminated within 3-4 h and the production of NO in the sarcoplasm is lowered. As a result, the Cl- influx is probably activated by dephosphorylation of the Cl- transporter with subsequent elevation of intracellular Cl- concentration. The equilibrium Cl- potential becomes more positive and the muscle membrane becomes depolarized.

• MeSH
• acetylcholin fyziologie   MeSH
• chloridy metabolismus   MeSH
• denervace svalu * MeSH
• elektrofyziologie MeSH
• kosterní svaly fyziologie   MeSH
• kyselina glutamová fyziologie   MeSH
• oxid dusnatý metabolismus   MeSH
• transportní proteiny fyziologie   MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• acetylcholin MeSH
• chloridy MeSH
• kyselina glutamová MeSH
• oxid dusnatý MeSH
• transportní proteiny MeSH

1. Rat hemidiaphragms were incubated in a physiological low-K+ medium without stimulation and the amount of acetylcholine (ACh) released was measured radioenzymatically. Cholinesterases were inhibited by paraoxon. 2. In the presence of 1 microM tetrodotoxin (TTX), the amount of ACh released during a 2 h incubation was lowered by 40%. A similar decrease was observed in the absence of Ca2+ and in the presence of 10 microM-d-tubocurarine (dTC). The effects of TTX combined with Ca2+ removal, and of TTX combined with dTC were no greater than those of TTX, dTC or Ca2+ removal alone. TTX and dTC had no effect on the release of ACh from diaphragms 4 days after denervation. 3. The reduction of spontaneous ACh release observed in the presence of TTX or dTC or in the absence of Ca2+ is best interpreted on the assumption that about 40% of the ACh release was due to the impulse activity known to be generated in intramuscular motor nerve branches by the ACh which accumulates after the inhibition of cholinesterases. 4. In the presence of 1 and 10 microM vesamicol (AH5183, 2-(4-phenylpiperidino)-cyclohexanol), the release of ACh was also diminished by approximately 40%. Vesamicol did not augment the inhibition of release produced by TTX or by the omission of Ca2+.(ABSTRACT TRUNCATED AT 250 WORDS)

• MeSH
• acetylcholin metabolismus   MeSH
• bránice MeSH
• časové faktory MeSH
• chemická deprese MeSH
• cholinesterasy fyziologie   MeSH
• denervace MeSH
• depolarizující myorelaxancia farmakologie   MeSH
• krysa rodu Rattus MeSH
• piperidiny farmakologie   MeSH
• potkani Wistar MeSH
• svaly inervace   metabolismus   MeSH
• techniky in vitro MeSH
• tetrodotoxin farmakologie   MeSH
• tubokurarin farmakologie   MeSH
• vápník fyziologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• acetylcholin MeSH
• cholinesterasy MeSH
• depolarizující myorelaxancia MeSH
• piperidiny MeSH
• tetrodotoxin MeSH
• tubokurarin MeSH
• vápník MeSH
• vesamicol MeSH Prohlížeč

1. Acetylcholine (ACh), 7.5 x 10(-5) M, and carbachol, 5 x 10(-6) M (CCh) depressed the frequency of miniature endplate potentials (m.e.p.ps) in the frog (Rana temporaria) sartorius neuromuscular junction with active acetylcholinesterase to about 50-55% of the controls. 2. A similar depression was produced by the nicotinic agonists, nicotine, suberyldicholine and tetramethylammonium. 3. The muscarinic agonists, oxotremorine, methylfurmethide and methacholine were without effect on m.e.p.p. frequency. The muscarinic antagonist, atropine and the nicotinic antagonist, (+)-tubocurarine, had no effect on the depression of m.e.p.p. frequency evoked by CCh. 4. The ganglionic blockers, benzhexonium and IEM-1119, were also without effect on the CCh-evoked depression of m.e.p.p. frequency. 5. Pretreatment of muscles with anticholinesterases did not prevent the CCh-induced drop in m.e.p.p. frequency. 6. The effect of CCh was proportionally the same as in the controls in preparations where the m.e.p.p. frequency was changed by elevation of K+ and in the presence of theophylline, noradrenaline, dibutyryl adenosine 3':5'-cyclic monophosphate (db cyclic AMP) and db cyclic GMP. 7. An inhibitor of Na+,K(+)-ATPase, ouabain, 5 x 10(-5) mol l-1, prevented or reversed the depression of m.e.p.p. frequency by CCh. However, the depression was present in a nominally K(+)-free medium. Insulin and adrenaline, which are considered to be Na+,K(+)-ATPase activators, were without effect on depression of m.e.p.p. frequency. 8. The depression of m.e.p.p. frequency by 5 x 10(-6) M CCh was the same at temperatures between 5 and 30 degrees C with a Q10 near to 1.0. When threshold amounts of CCh were used (6 x 10-7 and 3 x 10-7 M), the depression was less at higher temperatures.9. The receptive structures responsible for the CCh (or ACh)-evoked depression of m.e.p.p. frequency differ pharmacologically from muscarinic, nicotinic ganglionic and neuromuscular junction ACh-receptors as well as from the synaptic cholinesterase, in contrast to previous reports (Duncan & Publicover, 1979).The low temperature-dependence points to the possibility that physical rather than biochemical processes are limiting in this presynaptic effect of cholinomimetics.

• MeSH
• acetylcholin analogy a deriváty   farmakologie   MeSH
• aktivace enzymů účinky léků   MeSH
• chemická deprese MeSH
• chloridy metabolismus   MeSH
• dibutyryl cyklický AMP farmakologie   MeSH
• dibutyryl cyklický GMP farmakologie   MeSH
• draslík metabolismus   MeSH
• karbachol farmakologie   MeSH
• membránové potenciály účinky léků   MeSH
• nervosvalová ploténka účinky léků   MeSH
• nervosvalové spojení účinky léků   MeSH
• parasympatolytika farmakologie   MeSH
• parasympatomimetika farmakologie   MeSH
• Rana temporaria MeSH
• sodík metabolismus   MeSH
• sodíko-draslíková ATPasa metabolismus   MeSH
• techniky in vitro MeSH
• teplota MeSH
• theofylin farmakologie   MeSH
• vápník metabolismus   MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• acetylcholin MeSH
• chloridy MeSH
• dibutyryl cyklický AMP MeSH
• dibutyryl cyklický GMP MeSH
• draslík MeSH
• karbachol MeSH
• parasympatolytika MeSH
• parasympatomimetika MeSH
• sodík MeSH
• sodíko-draslíková ATPasa MeSH
• theofylin MeSH
• vápník MeSH

1. Local endplate depolarization induced by anticholinesterase application to mouse nerve-diaphragm preparations was taken as a measure of non-quantal release of acetylcholine. 2. Non-quantal acetylcholine release occurred within 20-60 s after anticholinesterase application, either spontaneously or evoked by nerve stimulation. Non-quantal release declined with time and disappeared after 3-5 min. 3. The amplitude of stimulation-evoked non-quantal release increased with the frequency of stimulation and was maximal at frequencies above 50 Hz. Two stimuli were sufficient to evoke the maximal effect. 4. Micromolar concentrations of atropine, pirenzepine and vesamicol reduced the amplitude and shortened the duration of non-quantal release. Oxotremorine (10(-8) M) enhanced the amplitude and ouabain (10(-4) M) prolonged the duration of non-quantal release. 5. Our results support the idea that the non-quantal release is due to the vesicular acetylcholine transport system which becomes transiently a part of the nerve terminal during exocytotic release of quantal acetylcholine.

• MeSH
• acetylcholin metabolismus   MeSH
• atropin farmakologie   MeSH
• cholinesterasové inhibitory farmakologie   MeSH
• elektrická stimulace MeSH
• myši MeSH
• nervosvalová ploténka fyziologie   MeSH
• nervosvalové spojení účinky léků   metabolismus   fyziologie   MeSH
• nervová zakončení účinky léků   metabolismus   fyziologie   MeSH
• ouabain farmakologie   MeSH
• oxotremorin farmakologie   MeSH
• techniky in vitro MeSH
• zvířata MeSH
• Check Tag
• myši MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• acetylcholin MeSH
• atropin MeSH
• cholinesterasové inhibitory MeSH
• ouabain MeSH
• oxotremorin MeSH