αLatrotoxin of black widow spider is known to bind with high affinity to surface sites of rat pheochromocytoma (PC12) cells, thereby causing depolarization, calcium influx and massive neurotransmitter release. We show here that the toxin causes the accumulation of inositol phosphates, the products of phosphoinositide breakdown. Inositol 1,4,5, trisphosphate was predominantly accumulated shortly after toxin application. Phosphoinositide breakdown appears to be a direct consequence of toxin binding because high K+ and ionophores (which induce depolarization, calcium influx and transmitter release by different mechanisms) were without such effect. Phosphoinositide breakdown is known as an event coupled to the activation of receptors of various hormons and transmitters. We suggest therefore that the αlatrotoxin binding site is a receptor coupled across the membrane to the phosphoinositide hydrolysing system.
|Number of pages||7|
|Journal||Biochemical and Biophysical Research Communications|
|Publication status||Published - Jun 15 1984|
ASJC Scopus subject areas
- Molecular Biology