Rat hypothalamic synaptosomes were exposed via superfusion to various stimuli and the release of neuropeptide Y-like immunoreactivity (NPY-LI) was measured by means of radioimmunoassay procedures. High KCl (15-50 mM) concentration dependently evoked NPY-LI release; the evoked overflow reached a plateau at 30 mM KCl and was abolished in the absence of Ca2+ ions. Furthermore, a remarkable NPY-LI overflow was obtained when extracellular Na+ ions were removed. Low external Na(+)-evoked NPY-LI release was independent of the presence of Ca2+ ions from the superfusion medium. It is well known that the reduction of external Na+ ions activates the release of several neurotransmitters through an inversion of the uptake-carrier working direction; but such mechanisms, involving Na(+)-dependent uptake, have never been described for neuropeptides. The alteration of the extracellular Na+ concentration is able to modify the concentration of the intracellular Ca2+ and H+ ions. In fact, the concentrations of these two ions are regulated through Na(+)-dependent exchange mechanisms across the membrane. Amiloride, blocking the Na+/H+ exchanger, was able to maintain low Na(+)-evoked NPY-LI release, underlying that the blockade of the exchanger preserves the H+ accumulation induced by the reduction of the external Na+ ions. NPY-LI release could also be stimulated by nigericine, a proton ionophore, showing that the intracellular acidification is responsible for NPY-LI release. Intracellular acidification may stimulate Ca2+ ion release from intracellular stores, as has been shown by other workers. Large dense-core vesicles containing the peptide appear to be more sensitive to local intracellular Ca2+ release compared with extracellular Ca2+ ion entry through voltage-dependent channels.

Martire, M., Preziosi, P., Cannizzaro, C., Mores, N., Fuxe, K., Extracellular sodium removal increases release of neuropeptide Y-like immunoreactivity from rat brain hypothalamic synaptosomes: involvement of intracellular acidification, <<SYNAPSE>>, 1997; 27 (3): 191-198. [doi:10.1002/(SICI)1098-2396(199711)27:3<191::AID-SYN5>3.0.CO;2-8] [http://hdl.handle.net/10807/9175]

Extracellular sodium removal increases release of neuropeptide Y-like immunoreactivity from rat brain hypothalamic synaptosomes: involvement of intracellular acidification

Martire, Maria;Preziosi, Paolo;Mores, Nadia;
1997

Abstract

Rat hypothalamic synaptosomes were exposed via superfusion to various stimuli and the release of neuropeptide Y-like immunoreactivity (NPY-LI) was measured by means of radioimmunoassay procedures. High KCl (15-50 mM) concentration dependently evoked NPY-LI release; the evoked overflow reached a plateau at 30 mM KCl and was abolished in the absence of Ca2+ ions. Furthermore, a remarkable NPY-LI overflow was obtained when extracellular Na+ ions were removed. Low external Na(+)-evoked NPY-LI release was independent of the presence of Ca2+ ions from the superfusion medium. It is well known that the reduction of external Na+ ions activates the release of several neurotransmitters through an inversion of the uptake-carrier working direction; but such mechanisms, involving Na(+)-dependent uptake, have never been described for neuropeptides. The alteration of the extracellular Na+ concentration is able to modify the concentration of the intracellular Ca2+ and H+ ions. In fact, the concentrations of these two ions are regulated through Na(+)-dependent exchange mechanisms across the membrane. Amiloride, blocking the Na+/H+ exchanger, was able to maintain low Na(+)-evoked NPY-LI release, underlying that the blockade of the exchanger preserves the H+ accumulation induced by the reduction of the external Na+ ions. NPY-LI release could also be stimulated by nigericine, a proton ionophore, showing that the intracellular acidification is responsible for NPY-LI release. Intracellular acidification may stimulate Ca2+ ion release from intracellular stores, as has been shown by other workers. Large dense-core vesicles containing the peptide appear to be more sensitive to local intracellular Ca2+ release compared with extracellular Ca2+ ion entry through voltage-dependent channels.
1997
Inglese
Martire, M., Preziosi, P., Cannizzaro, C., Mores, N., Fuxe, K., Extracellular sodium removal increases release of neuropeptide Y-like immunoreactivity from rat brain hypothalamic synaptosomes: involvement of intracellular acidification, <<SYNAPSE>>, 1997; 27 (3): 191-198. [doi:10.1002/(SICI)1098-2396(199711)27:3<191::AID-SYN5>3.0.CO;2-8] [http://hdl.handle.net/10807/9175]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10807/9175
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