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Titolo:
THE REGULATION OF CHLORIDE HOMEOSTASIS IN THE SMALL NONSPIKING VISUALINTERNEURONS OF THE FLY COMPOUND EYE
Autore:
UUSITALO RO; WECKSTROM M;
Indirizzi:
UNIV OULU,DEPT PHYSIOL,KAJAANINTIE 52A SF-90220 OULU FINLAND UNIV OULU,DEPT PHYSIOL SF-90220 OULU FINLAND
Titolo Testata:
Journal of neurophysiology
fascicolo: 4, volume: 71, anno: 1994,
pagine: 1381 - 1389
SICI:
0022-3077(1994)71:4<1381:TROCHI>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTRACELLULAR PH REGULATION; PLASMA-MEMBRANE VESICLES; SINGLE MICROELECTRODE; BASOLATERAL MEMBRANE; BLOWFLY CALLIPHORA; APLYSIA INTESTINE; MONOPOLAR NEURONS; PROXIMAL TUBULE; MUSCA-DOMESTICA; TRANSPORT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
50
Recensione:
Indirizzi per estratti:
Citazione:
R.O. Uusitalo e M. Weckstrom, "THE REGULATION OF CHLORIDE HOMEOSTASIS IN THE SMALL NONSPIKING VISUALINTERNEURONS OF THE FLY COMPOUND EYE", Journal of neurophysiology, 71(4), 1994, pp. 1381-1389

Abstract

We have used intracellular recordings and ionophoretic injections in vivo to investigate the ion exchange mechanisms responsible for the maintenance of the ion gradients in the large monopolar cells ( LMCs) ofthe first optic ganglion of the blowfly, Calliphora vicina. Ionophoretic chloride injections caused a rapid similar to 20-mV depolarizationof the resting potential (E(rp)) and abolished or even reversed the light-on response (OR), which is caused by histamine-gated chloride conductance, as the chloride equilibrium potential (E(cl)) was increased beyond the E(rp) i.e., 50 mV upward. Ionophoretic sodium injections were found to mimic the action of the ionophoretic chloride injections and thus also to cause chloride accumulation inside the cell. Ionophoretic injections of bicarbonate only had the effect of hyperpolarizing the E(rp) by 5-15 mV for 1-25 s, but chloride gradient, i.e., E(cl) remained unchanged. Intracellular proton load caused depolarization of the E(rp) by 15 +/- 5 mV (mean +/- SE) for 20-25 s and a slight 15 +/- 5-mV decrease of the peak OR. Ionophoretic injections of potassium, acetate, and furosemide failed to cause any physiological effect. The time constant for the recovery of the peak OR after sodium load increasedlinearly as a function of injected charge whereby the time constant for the recovery after chloride accumulation increased slowly up to 50 nC of injected charge, after which it increased rapidly, possibly indicating substrate inhibition. The time constant for the recovery of peak OR after sodium load was from 5 to 65 nC greater than that of chloride. The results indicate that the one possible mechanism responsible for chloride extrusion and thus the maintenance of the inward-directed chloride gradient in LMCs could be a Cl- adenosinetriphosphatase. At this stage the possibility remained, however, that the eradication of the sodium gradient by intracellular sodium accumulation could have a direct effect on the chloride extrusion, albeit by hitherto unknown mechanisms. One synaptic adaptation mechanism is proposed to be the change in E(cl) by intracellular chloride accumulation.

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Documento generato il 05/12/20 alle ore 01:27:02