Regulation of cytosolic calcium concentration in presynaptic nerve endings isolated from rat brain.

Abstract

SUMMARY1. The regulation of cytosolic Ca concentration ([Ca]i) was studied with the fluorescent Ca indicator, quin2, in pinched-off presynaptic nerve endings (synaptosomes) isolated from rat brain. [Ca]i increases by about 2-fold when the external Na concentration is lowered from 145 to 5 mm, and returns to its initial level when external Na is restored. This recovery occurs also in the presence of FCCP.5. These results suggest that Na/Ca exchange, but not mitochondrial Ca uptake, plays a role in regulating [Ca]i and in allowing the nerve terminals to recover from Ca loading.

Increased free intrasynaptosomal Ca2+ by neurotoxic organometals: Distinctive mechanisms

“…Inside Ca 2 + is bound to cytoplasmic Ca2+ binding and membrane proteins and is sequestered in the endoplasmic reticulum. The role of mitochondria in the regulation of synaptosomal resting [Ca 2 +]i is at present controversial (Akerman and Nicholls, 1981 b;Nachshen, 1985; present results) but they may take up Ca 2 + at elevated [Ca 2 +]j. Hence, there are many sites in Ca 2 + metabolism as possible targets for alkylmetals.…”

Roles of Na + –Ca 2+ exchange and of mitochondria in the regulation of presynaptic Ca 2+ and spontaneous glutamate release

“…The role of mitochondria in the regulation of [Ca 2+ ] i within nerve terminals is also controversial. Nachshen (1985) reported that Na +^C a 2+ exchange but not mitochondrial Ca 2+ uptake regulates [Ca 2+ ] i in synaptosomes, while other authors (Akerman & Nicholls 1981) showed that during KCl depolarization Ca 2+ accumulates in mitochondria of such isolated nerve terminals. However, the total synaptosomal Ca 2+ load that follows KCl depolarization is reduced when mitochondrial function is abolished (Akerman & Nicholls 1981).…”

Regulation of intracellular calcium and calcium buffering properties of rat isolated neurohypophysial nerve endings.

“…Moreover, the mechanisms involved may vary with the specific nerve ending type. For example, substantial variation exists among studies with regard to the importance ascribed to Na'-Ca2+ exchange activity in recovery from Ca2" loads and in regulating the resting [Ca2+]i (Nachshen, 1985;Nicholls 1989). In addition, while ATP-dependent Ca2+ sequestration into intracellular compartments has been suggested from studies on disrupted synaptosome preparations (Blaustein, Ratzlaff & Schweitzer, 1978 b) the generality and the subcellular site of this mechanism remains unclear.…”

“…These homeostatic mechanisms can be generally categorized into (1) cytosolic or membrane delimited proteins which bind calcium, (2) ATP-dependent calcium pumps of the plasnma membrane and of intracellular compartments, andl (3) non-ATP-dependent calcium transporters, such as the electrogenic plasma membrane Na'-Ca2+ exchanger and mitochondrial Ca2+ uptake. The presence of these mechanisms in nerve terminals has been well documented, although the relative contribution of each to calcium homeostasis is not clear and may vary considerably among nerve terminal types (Blaustein, Ratzlaff & Schweitzer, 1978b;Nordmann & Zyzek, 1982;Nachshen, 1985;Nicholls, 1989 Calcium regulation in secretory nerve endings homogenate was directly aliquoted onto a glass coverslip forming the bottom of an open recording chamber. Following a 5 min peiiod, during which the nerve endings settled and adhered to the chamber bottom, a continuous flow of physiological saline (15-2 ml min-) through the chamber was begun.…”