Morphine - Anatomy and Physiology

Anatomy and Physiology

MORPHINE

        Morphine is a highly addictive substance because it reduces the way one feels pain, alleviating feelings or fear and anxiety. Morphine also has a sense of euphoria, making the drug more alluring and even more addictive. Psychologically, morphine is relaxing, causes drowsiness, disconnectedness, self-absorption, mental clouding, and delirium. Physiologically it causes a low heart rate, respiratory depression, CNS depression, nausea and vomiting, reduced gastrointestinal motility, constipation, flushing of face and neck due to dilatation of subcutaneous blood vessels, cramping, sweating, pupils fixed and constricted, diminished reflexes, and depressed consciousness. Withdrawal from the morphine also causes tearing, yawning, chills, and sweating for up to three days.

        Morphine affects the Central Nervous System of the body. Morphine is an opiate found in opium, the juice secreted by the seedpods of poppies. It is a potent pain reliever and is similar in structure to other opiate analgesics. Morphine first acts on the mu-opioid receptors. The mechanism of respiratory depression involves a reduction in the responsiveness of the brain stem respiratory centers to increases in carbon dioxide tension and to electrical stimulation. It has been shown that morphine binds to and inhibits GABA inhibitory interneurons. These interneurons normally inhibit the descending pain inhibition pathway. So, without the inhibitory signals, pain modulation can proceed downstream. By attaching to their mu receptors, exogenous opioids reduce the amount of GABA released. Normally, GABA reduces the amount of dopamine released in the nucleus. By inhibiting this inhibitor, the opiates ultimately increase the amount of dopamine produced and the amount of pleasure felt. By binding to mu (µ) receptors, opiates like morphine enhance the pain-killing effects of encephalin neurons.

        Morphine inhibits action potential in some of the myenteric neurons. All synaptic responses are eliminated or greatly reduced. Dopamine is an important neurotransmitter involved in this experience. Dopamine is produced in the neuron and then packaged into vesicles. As an electrical impulse arrives at the neuron’s terminal, the vesicle moves to the neural membrane and releases its load of dopamine into the synaptic cleft. The dopamine crosses the gap and binds to the receptors. After the dopamine has bound to the receptor, eventually it comes off again and is removed from the synaptic cleft and back into the first neuron by reuptake pumps.