Morphine is an
opioid drug used as a painkiller which acts directly on cells in the CNS to
reduce the sensation of a nociceptive stimulus. The site of absorption for
morphine occurs in the gastrointestinal tract; after transportation it then
binds directly to the ?-opioid receptors in the membranes of nerve cells in the
Brain and Spinal Cord (within the CNS) which modulate pain within the nervous
system. It acts by mimicking natural compounds such as enkephalins and blocking
the processing of pain sensations. In order for this to occur, morphine
directly affects Calcium channels within a presynaptic nerve cell, reducing the
influx of Calcium ions into the cell and increasing the conduction of ions
through potassium channels in the same nerve cell. In turn, this causes an
inhibitory effect of neurotransmitter release from the presynaptic terminal of
a nerve cell; neurotransmitters such as noradrenaline and acetylcholine are
therefore not released from the neurone across the synaptic cleft to the
postsynaptic neurone, thus preventing an action potential to be stimulated and
transmitted through the axon on the post synaptic neurone. This all causes an
overall inhibition of the transmission of pain signals along the axon of a sensory
neuron to the control centre in the nervous system, therefore altering the individuals’
perception of the nociceptive stimulus and reducing the sensations. Overall,
the brain responds to the binding of morphine by synthesising an increased
number of G-proteins which are involved in the cellular effects of morphine and
blunting of the transmission of a nociceptive stimulus. However, over time
morphine can become addictive and more is needed to have the same pain-reducing
impact on the body; severe withdrawal symptoms may also occur after a long
period of time as the body’s usual pleasure system becomes blunted by excessive
G-protein synthesis.