Morphine has many effects on the central nervous system:

• Analgesia: Morphine is effective for both acute and chronic pain, and is often used before and after surgery. While morphine is effective against nociceptive pain (pain resulting from tissue damage), it is also able to reduce the affective or psychological part of pain perception.
• Respiratory depression: The normal analgesic doses of opiates result in respiratory depression and increased concentration of CO2 in arterial blood. Both effects result from action at MOR: the respiratory center in the brain becomes less sensitive to the concentration of CO2 and fails to signal for more intense breathing. This is not usually accompanied by a decrease in the cardiovascular output, so it can be tolerated better than if both had been depressed, as for some other classes of drugs. However respiratory depression does occur at therapeutic doses of opiates and is the most common cause of death with opiate overdose.
• Euphoria: Morphine is able to induce a sense of contentment and well-being, which is key to its analgesic benefit. When anxiety and agitation are reduced, the patient can relax. If given intravenously (IV), morphine or heroin can produce a euphoric “rush.” The euphoria is dependent on the original state; if the patient has become used to chronic pain, there is usually no euphoria with the pain relief (commonly the case for cancer patients). The euphoria results from opioids at the MOR, while KOR mediates the opposite dysphoria. Therefore a particular drug can have widely varying effects. Codeine and pentazocine do not usually produce euphoria, while nalorphine is associated with dysphoria.
• Depression of cough reflex: Cough suppression does not correlate well with pain relief or respiratory depression and thus may use another receptor type. Certain substitutions on the morphine molecule increase the antitussive effects relative to analgesic effects such that codeine is commonly used in cough medicines at sub-analgesic doses. Pholcodine is a more selective antitussive, though it can also cause increased constipation.
• Nausea, vomiting: This happens in up to 40% of morphine patients and does not appear to be separable from the analgesic relief. The emetic effect of morphine can be reduced by giving a counteracting antagonist such as naloxone. The nausea and vomiting induced by morphine usually fades away with repeated use.
• Pupillary constriction: This is centrally mediated by MOR and KOR receptors stimulating the oculomotor nucleus. Pinpoint pupils is a useful diagnostic in detecting overdosage of opiates because most other causes of coma and respiratory depression are associated with dilated pupils.
• Effects on GI tract: Morphine causes an increased tone and decreased motility in the gastrointestinal tract, leading to potentially severe constipation. In addition, this may retard the absorption of other drugs given orally. Patients with pain associated with gallstones may not benefit and, in fact, have more pain, with slowed GI motility.
• Other actions of opioids: Morphine releases histamines from mast cells and may cause itching or urticaria (hives) at the injection site, or exhibit other systemic effects such as bronchoconstriction and hypotension from vasodilation; therefore, asthma patients should not be given morphine or the close structurally related opioids, but may be given synthetic opiates that do not release histamines. There also appears to be some immunosuppression with long-term opioid use, leading to possible increase of infections.