Origin of transmitters released by electrical stimulation from a small metabolically very active vesicular pool of cholinergic synapses in guinea-pig cerebral cortex.
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Biomedical subjects
Publications and source records attributed to I von Schwarzenfeld.
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1 per cent Picrotoxin placed on cortex of rat caused paroxysmal ECoG discharges with concomitant increase in [Ke"] from 3 to 6.7 mM with oscillations corresponding to ictal (maximum) and interictal (minimum) spiking. Invasion of the epileptogenic focus by spreading depression was blocked when the amplitude of oscillations of [Ke+] reached 2.6 mM. Epileptogenic activity induced by topical 10 per cent pentazol caused a less marked increase in [Ke+] (4.6 mM) and did not prevent depression from invading the focal area, but did diminish [Ke+] from the normal of 60 to 70 mM to 39 mM. It is concluded that seizure-induced depolarization of neural elements in deep cortical layers, though inadequate to trigger spreading depression, does prevent it from spreading, in part by activating the sodium pump.
Centrally acting cholinomimetic drugs like arecoline stimulate active ion transport processes in the synaptic region. Regarding the connection between cellular metabolism and active Na"-K+-transport the effect of arecoline on the cerebral metabolic status was proved. Arecoline decreased the level of high energic phosphates and glycogen (energy charge diminished from 0,57 to 0,48) and increased the glucose consumption and lactate production. Thus, the increased rate of CoA acetylation via oxidative breakdown of pyruvate seems to be prerequisite for the cholinergically stimulated ACh synthesis.
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