What is the primary action of morphine on presynaptic nerve terminals?

Morphine primarily acts on presynaptic nerve terminals by decreasing calcium entry. This action occurs through its binding to the mu-opioid receptors located on these terminals. When morphine binds to these receptors, it triggers a series of intracellular signaling events that culminate in the inhibition of voltage-gated calcium channels.

As a result, there is a reduction in the influx of calcium ions when the neuron is depolarized, which in turn decreases the release of neurotransmitters like substance P and glutamate—a crucial step in pain transmission. By diminishing calcium entry, morphine effectively reduces the excitability of the presynaptic neuron, contributing to its analgesic properties.

This mechanism highlights why morphine is effective in pain management, as it interrupts the transmission of pain signals at the level of the presynaptic neuron, inhibiting their propagation to the postsynaptic targets in the nervous system.