Dihydromorphine is a semisynthetic opioid analgesic. Dihydromorphine binds on pre-synaptic mu opioid receptors. Opiate receptors are coupled with G-protein receptors and function as both positive and negative regulators of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as GABA. Less GABA leads to disinhibition of dopamine cell firing in the spinal cord pain transmission neurons. This leads to less pain signaling and analgesia. Opioids close N-type voltage-operated calcium channels and open calcium-dependent inwardly rectifying potassium channels. This results in hyperpolarization and reduced neuronal excitability. The inhibition of A delta and C pain fibres in the dorsal horn of the spinal cord is very important as it slows the signaling of pain into the spinal cord.

Dihydromorphine Opioid Agonist Pathway References