Cocaine affects the dynamics of cytoskeletal proteins via sigma(1) receptors

Trends Pharmacol Sci. 2001 Sep;22(9):456-8. doi: 10.1016/s0165-6147(00)01740-5.

Abstract

Cytoskeletal proteins are important in protein trafficking, membrane protein clustering, dendrite growth and the morphological maintenance of neurons. Sigma(1) receptors are unique endoplasmic reticular (ER) proteins that bind (+)benzomorphans, neurosteroids and psychotropic drugs such as cocaine. Cocaine, via sigma(1) receptors, can cause the dissociation of a cytoskeletal adaptor protein ankyrin from inositol (1,4,5)-trisphosphate [Ins(1,4,5)P(3)] receptors on the ER as a sigma(1)-receptor-ankyrin complex, which then translocates to the plasma membrane and nucleus. The dissociation of sigma(1)-receptor-ankyrin from Ins(1,4,5)P(3) receptors also increases the intracellular Ca(2+) concentration [[Ca(2+)](i)], which affects the activity of cytoskeletal proteins. Furthermore, cocaine might increase [Ca(2+)](i) via phospholipase C (PLC)-linked dopamine D1 receptors. We hypothesize that cocaine might cause life-long changes in neurons via cytoskeletal proteins by interacting with both D1 receptors and sigma(1) receptors.

MeSH terms

  • Animals
  • Calcium / physiology*
  • Cocaine / adverse effects*
  • Cytoskeletal Proteins / drug effects*
  • Cytoskeletal Proteins / metabolism
  • Dopamine Uptake Inhibitors / adverse effects*
  • Humans
  • Receptors, Dopamine D1 / drug effects*
  • Receptors, sigma / drug effects*
  • Sigma-1 Receptor

Substances

  • Cytoskeletal Proteins
  • Dopamine Uptake Inhibitors
  • Receptors, Dopamine D1
  • Receptors, sigma
  • Cocaine
  • Calcium