| Autor: |
Chaplain, R., Dinse, H., Fallert, M. |
| Zdroj: |
Pflügers Archiv: European Journal of Physiology; 1976, Vol. 365 Issue 1, p49-59, 11p |
| Abstrakt: |
The property of the neuronal membrane to be permeable to metabolic modifiers of two regulatory enzymes has been utilized to manipulate the spike activity of inspiratory (I) and expiratory-inspiratory (EI) neurons of the bulbar respiratory centre. The neurons have been classified according to their response to lung distension or collapse (α- or β-type) and to hyperventilation (tonic firing denoted by '+', cessation of activity by '−'). Using extracellular microelectrodes for single unit recording, the medulla oblongata was superfused with a metabolite-containing CSF. The various neuronal sub-types exhibited a differential activating or inhibitory response to one or several metabolic effectors. For example I units were activated by 5 mM glucose-6-phosphate (G-6-P) and 3.5 mM 3-phosphoglycerate (3-PGA), which both inhibited I neurons, while 5 mM AMP inhibited I much more strongly than I cells. The spike density of I and I neurons was increased in the presence of 2.5 mM fructose-6-phosphate and 3.5-5 mM AMP, but became reduced by G-6-P. In contrast, 3 mM fructose-1,6-diphosphate and 5 mM 3-PGA activated the I but inhibited the I neurons. The EI units were characteristically activated by 10 mM citrate, which inhibited all I-type neurons. Activations of the I and I neurons led to an accelerated respiratory rate and a higher tidal volume, while the opposite was true for EI neurons. Intravenous injection of metabolites could not duplicate the striking effects under local applications. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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