Morphine coupling to invertebrate immunocyte nitric oxide release is dependent on intracellular calcium transients.

Morphine significantly stimulated invertebrate immunocyte intracellular calcium level increases in a concentration-dependent manner in cells preloaded with Fura 2/AM. Morphine's action was blocked by prior exposure of the cells to the opiate receptor antagonist naloxone. Various opioid peptides did not exhibit this ability, indicating a morphine-mu 3 mediated process.

Endomorphin-1 and -2 inhibit human vascular sympathetic norepinephrine release: lack of interaction with mu 3 opiate receptor subtype.

Aim: To determine if endomorphin-1 (End-1) and -2 (End-2) interact with mu 3 opiate receptor subtype and in this way cause vascular hypotension.

Methods: Amperometric nitric oxide (NO) determinations associated with opiate binding displacement analysis and preloaded [3H]norepinephrine KCl stimulated release in human vascular tissues from sympathetic nerve fibers in vitro.

Results: The endomorphins did not release NO from human monocytes, granulocytes, saphenous vein, and internal thoracic artery endothelium and did not displace opiate alkaloid binding to mu 3 receptor.

Selective effects of human immunodeficiency virus (HIV) gp120 on invertebrate neurons.

1. HIV gp120 selectively reduces the glutamate-induced inward current and the acetylcholine-induced outward current in specific and identified Aplysia neurons without affecting dopamine (DA)- and serotonin (5-HT)-induced responses. 2.